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Roles of taurine in cognitive function of physiology, pathologies and toxication
Abstract
Taurine is a key functional amino acid with many functions in the nervous system. The effects of taurine on cognitive function have aroused increasing attention. First, the fluctuations of taurine and its transporters are associated with cognitive impairments in physiology and pathology. This may help diagnose and treat cognitive impairment though mechanisms are not fully uncovered in existing studies. Then, taurine supplements in cognitive impairment of different physiologies, pathologies and toxicologies have been demonstrated to significantly improve and restore cognition in most cases. However, elevated taurine level in cerebrospinal fluid (CSF) by exogenous administration causes cognition retardations only in physiologically sensitive period between the perinatal to early postnatal period. In this review, taurine levels are summarized in different types of cognitive impairments. Subsequently, the effects of taurine supplements on cognitions in physiology, different pathologies and toxication of cognitive impairments (e.g. aging, Alzheimer' disease, streptozotocin (STZ)-induced brain damage, ischemia model, mental disorder, genetic diseases and cognitive injuries of pharmaceuticals and toxins) are analyzed. These data suggest that taurine can improve cognition function through multiple potential mechanisms (e.g. restoring functions of taurine transporters and γ-aminobutyric acid (GABA) A receptors subunit; mitigating neuroinflammation; up-regulating Nrf2 expression and antioxidant capacities; activating Akt/CREB/PGC1α pathway, and further enhancing mitochondria biogenesis, synaptic function and reducing oxidative stress; increasing neurogenesis and synaptic function by pERK; activating PKA pathway). However, more mechanisms still need explorations.
... Figure 1 summarizes the main functions of glutathione and cysteine in astrocytes and dopaminergic neurons in PD. Taurine (Tau) is a semi-essential amino acid that contains a sulfur group, endogenously produced from Cys (Chen et al. 2019;Jakaria et al. 2019). The body has different alternatives to get Tau; one is by dietary intake, and from de novo synthesis through the catabolism of Cys which however is limited by the oxidation of hypotaurine to Tau (Wojcik et al. 2010). ...
... Tau is mainly produced in the liver and kidney; however, it has also been found in other tissues, including the brain (El Idrissi 2019; Park et al. 2014). In the rat brain, Tau is expressed in all regions (Chen et al. 2019). Tau content in the brain is mainly transported from the periphery and by the local synthesis from de novo catabolism of Cys, both in neurons and astrocytes (Vitvitsky et al. 2011). ...
... Studies in mice reported that tissue depletion of Tau leads to a shorter lifespan (Ito et al. 2014). In the brain, Tau is involved in numerous processes in brain cells, acting as an anti-inflammatory, neuromodulator, and osmoregulator (Chen et al. 2019;Niu et al. 2018;Rafiee et al. 2022). Tau has been reported as a neuroprotective agent against excitotoxicity, apoptosis death, reticulum endoplasmic stress, mitochondrial stress, and oxidative stress (Leon et al. 2009;Pan et al. 2010;Pan et al. 2012;Rafiee et al. 2022;Wu et al. 2005). ...
The transsulfuration pathway (TSP) is a metabolic pathway involving sulfur transfer from homocysteine to cysteine. Transsulfuration pathway leads to many sulfur metabolites, principally glutathione, H2S, taurine, and cysteine. Key enzymes of the TSP, such as cystathionine β-synthase and cystathionine γ-lyase, are essential regulators at multiple levels in this pathway. TSP metabolites are implicated in many physiological processes in the central nervous system and other tissues. TSP is important in controlling sulfur balance and optimal cellular functions such as glutathione synthesis. Alterations in the TSP and related pathways (transmethylation and remethylation) are altered in several neurodegenerative diseases, including Parkinson's disease, suggesting their participation in the pathophysiology and progression of these diseases. In Parkinson's disease many cellular processes are comprised mainly those that regulate redox homeostasis, inflammation, reticulum endoplasmic stress, mitochondrial function, oxidative stress, and sulfur content metabolites of TSP are involved in these damage processes. Current research on the transsulfuration pathway in Parkinson's disease has primarily focused on the synthesis and function of certain metabolites, particularly glutathione. However, our understanding of the regulation of other metabolites of the transsulfuration pathway, as well as their relationships with other metabolites, and their synthesis regulation in Parkinson´s disease remain limited. Thus, this paper highlights the importance of studying the molecular dynamics in different metabolites and enzymes that affect the transsulfuration in Parkinson's disease.
... The most commonly reported side effect was severe dyskinesia; other commonly reported side effects were loss of lean body mass, malnutrition due to deficiency of protein or specific vitamins (B 2 [riboflavin] and B 3 [niacin]) or minerals (namely, calcium, phosphorus, and zinc) that rely on regulation by specific AAs. 28,29 Furthermore, published clinical trials of these diets reported some participants experienced sporadic psychiatric disorders, hallucinations, marked reduction in serum albumin levels, and orthostatic hypotension. 21 Given EAAs are needed throughout the day to perform their biological function, and protein absorption is impaired when consumed in large boluses, additional research is needed about the long-term effects of protein-restricted diets on overall health of people with PD. ...
... Taurine is a nonessential AA that functions as an antioxidant, neuromodulator, membrane stabilizer, and calcium regulator. 29 Decreased CSF concentrations have been found in people with PD, and decreased plasma levels are positively associated with disease symptoms and inversely associated with cumulative levodopa dosage. 26,109 As such, altered AA profiles of people with PD suggest that natural biological synthesis of taurine is either disrupted or inadequate. ...
... [71][72][73]110 Although human trials of taurine and PD are lacking, studies have found dietary consumption provides generalized neuroprotection and reduces the risk of developing Alzheimer's disease. 29,74 Given the information outlined above, taurine supplementation may be beneficial for people with PD, but research is needed to explore if such supplementation decreases the risk of dementia development among people with PD. ...
For individuals with Parkinson’s disease (PD), dietary habits affect disease symptoms, progression, and overall health. Protein consumption is of great interest because of the direct and indirect effects of specific amino acids (AAs) on disease progression and interference with levodopa medication. Proteins comprise 20 distinct AAs with varying effects on overall health, disease progression, and medication interference. Therefore, it is important to consider both the potential beneficial and detrimental effects of each AA when considering supplementation for an individual with PD. Such consideration is of particular importance because PD pathophysiology, altered dietary patterns associated with PD, and competitive absorption with levodopa have been shown to result in characteristically altered AA profiles (eg, some AAs are stored in excess while others are deficient). To address this problem, considerations for the development of a precision nutritional supplement that targets AAs specific to the needs of people with PD are discussed. The objective of this review is to provide a theoretical framework for such a supplement, detailing the current state of knowledge relating relevant evidence to such a supplement, and highlighting areas of future research. Specifically, the general need for such a supplement is discussed before a systematic examination is provided of the potential benefits and risks of dietary supplementation of each AA in people with PD. As a part of this discussion, evidence-based recommendations are provided regarding the inclusion or exclusion of each AA for such a supplement for people with PD, and areas are highlighted where additional research is needed.
... This insensitive variation of plasma taurine level corresponding to AD suggest the this variation of plama taurine level is not a significant prediction of Occurrence of AD. In comparison to controls, it was found in post mortem studies of AD subjects that there is significant decrease in taurine level in special regions of brain like temporal cortex [60]. Another study has demonstrated that in more advanced symptoms of AD, taurine level decreased in CSF [61]. ...
... Citation: Shah Waliullah., et al. "Role of Taurine and its Analogs Against Various Disorders and its Beneficial Effects: A Review Article". Acta Scientific chloride ions, the high affinity and the low capacity against its substrates, in various organs of body like placenta and skeletal muscle, thyroid, heart, lung, brain, liver, kidney, gut, osteoblast this transporter is distributed [60]. ...
... Gut, heart, skeletal muscle, liver, kidney, placenta, lung, brain, stomach, spleen and testis are the different organs where PAT1 transporter is identified. Besides these two transporters there are some other carriers involved in taurine transport.one of them is GABA transporters found in kidney can also accept taurine as the substance for transporting [60], but still the process and mechanism of transport is still ...
Taurine (Tau), a sulphur containing amino acid, chemically known as 2 aminoethane sulphonic acid, it's a non-proteinogenic β-amino acid, often referred to as semi essential amino acid as new born mammals have very limited ability to synthesize taurine and they have to depend on dietary sources, it is not incorporated into proteins as no aminoacyl tRNA synthetase has yet been identified and is not oxidized in mammalian cells, it attains an important place because of the antioxidant defence network. It has multiple function in the CNS, it serves as an osmoregulator, antioxidant, inhibitory neuromodulator, and regulator of intracellular Ca2flux.First time when it was discovered from ox bile by the German professors Friedrich Tiedemann and Leopold Gmelin they named it GallenAsparagin, later it was known as taurus, in latin Bos taurus means Ox, but it attains its current name (Taurine) in 1838 by von H. Demarcay. Because of presence of sulphonic acid instead of carboxylic acid it is not metabolized and not involved in gluconeogenesis and thus not envolve in direct energy sources. Taurine is produced by liver and kidney including retina, brain, heart and placenta. Taurine plays extensive role against different disorders of the body and in deadly diseases like cancer, liver cirrhosis etc. Human body contains about 0.1% of body weight as taurine. It has a number of physiological and pharmacological actions. In case of spinal cord injury elevated level of taurine has been seen, In methyl prednisolone (MP), treatment in case of SCI, elevation in level of taurine is observed, this elevated level seems to be involved in protection and regeneration of tissues following injury. In this review we try to cover every possible role of taurine which may provide enough information for future research.
... It also functions as an antioxidant, anti-inflammatory agent, neuromodulator, calcium modulator and osmoregulator (Schaffer and Kim, 2018). Animal and human studies have suggested that deficiency of taurine leads to numerous adverse health outcomes including reduced life and health spans (McGaunn and Baur, 2023;Singh et al., 2023), cardiomyopathy (Sagara et al., 2015), inflammatory diseases (Marcinkiewicz and Kontny, 2014), retinal degenerative disorders (Castelli et al., 2021) and cognitive impairment (Chen et al., 2019). ...
... Pregnant cats fed taurine-free diets were frequently unable to complete full-term pregnancies, whilst the kittens which did survive had neurological abnormalities (Sturman et al., 1985b, Sturman, 1991, Sturman et al., 1985a, Sturman et al., 1986, Sturman and Messing, 1992. In humans, studies have shown that taurine concentrations in adults are associated with cognitive function (Chen et al., 2019;Oh et al., 2020;Kim et al., 2003); however, limited research has been carried out investigating cognitive development and function in infants. Wharton et al. (2004) reported a positive correlation between neonatal taurine concentrations and neurodevelopmental outcomes at age 7 years in a study of 157 children (Wharton et al., 2004). ...
Background:
High concentrations of taurine are present in the developing human brain and maternal breast milk. Taurine is thought to influence fetal growth and brain development based on experimental rodent studies. As fish is an important dietary source of taurine, we investigated associations between taurine concentrations and child outcomes in a high fish consuming population.
Objective:
To examine associations between maternal and cord serum taurine concentrations and birth anthropometric measures and cognitive development in children at 20 months of age.
Methods:
Pregnant women were recruited between 2008 and 2011 as part of Nutrition Cohort 2 (NC2) of the Seychelles Child Development Study (SCDS). Maternal taurine serum concentrations were measured at 28 week's gestation and in cord serum. Child weight, length and head circumference were measured at birth and neurodevelopment was assessed using Bayley Scales of Infant Development II (BSID-II) at 20 months of age. Associations between taurine status, birth measures and neurodevelopmental outcomes were examined (n= 300) using regression models and adjusted for relevant covariates.
Results:
Mean (SD) maternal and cord taurine concentrations were 124.9 (39.2) µmol/L (range 28.2-253.9 µmol/L) and 187.6 (60.0) µmol/L (range 55.0-417.4 µmol/L) respectively. We found no associations between maternal taurine concentrations and child anthropometric and neurodevelopmental measures (weight β=-0.001, SE=0.001; length β=-0.006, SE=0.006; head circumference β=-0.002, SE=0.002; MDI β=-0.005, SE=0.015; PDI β=-0.004, SE=0.016; all P>0.05), or between cord taurine concentrations and outcomes (weight β=-0.001, SE<0.000; length β=-0.001, SE=0.004; head circumference β<0.000, SE=0.002; MDI β=0.004, SE=0.010; PDI β=-0.015, SE=0.012; all P>0.05).
Conclusion:
The Seychellois population have high maternal and cord taurine concentrations owing to their high fish intake and may be considered taurine replete compared to individuals who consume a Westernised diet. This high taurine status may explain why there were no significant associations between maternal and cord taurine concentrations and outcomes after adjusting for covariates.
... Taurine also alters immune response genes. Many studies have demonstrated that taurine can control the expression of cytokines and chemokines, which regulate immunological responses Chen et al. (2019). Taurine also boosts the innate immune response's natural killer cells and macrophages. ...
... Oxidative stress protection requires these enzymes. Chen et al. (2019). Taurine regulates gene expression and is very flexible. ...
This study reviews taurine amino acid research on brain development. Taurine, a brain-abundant non-protein amino acid, is essential for neuronal differentiation, migration, and survival. This research reviews the effects of taurine depletion and supplementation on brain development and their processes. The report also discusses current knowledge gaps and offers future research on taurine's role in brain development.
... The main substrate of SLC6A6 protein is taurine, which participates in osmoregulation, bile acid conjugation, calcium level modulation anti-oxidation processes, and immunomodulation [26][27][28]. Taurine also plays an important role in the nervous system functioning as a GABA agonist and NMDA partial agonist through the glycine site [29,30]. For humans, taurine is a non-essential amino acid which could be synthesized from methionine or cysteine, or retrieved from dietary sources [31]. ...
... Analysis of SLC6A6 ligands, their structure, and biological activity may help in the discovery of new taurine transporter inhibitors. Taurine is β-amino acid (2-aminoethanosulfonic acid) which plays a crucial role in nervous system development [29]. TauT takes the major role in taurine transport, although transporters GAT-2 (SLC6A13) and PAT1 (SLC36A1) help in the taurine delivery system [66]. ...
Cancer cells are characterized by uncontrolled growth, proliferation, and impaired apoptosis. Tumour progression could be related to poor prognosis and due to this fact, researchers have been working on novel therapeutic strategies and antineoplastic agents. It is known that altered expression and function of solute carrier proteins from the SLC6 family could be associated with severe diseases, including cancers. These proteins were noticed to play important physiological roles through transferring nutrient amino acids, osmolytes, neurotransmitters, and ions, and many of them are necessary for survival of the cells. Herein, we present the potential role of taurine (SLC6A6) and creatine (SLC6A8) transporters in cancer development as well as therapeutic potential of their inhibitors. Experimental data indicate that overexpression of analyzed proteins could be connected with colon or breast cancers, which are the most common types of cancers. The pool of known inhibitors of these transporters is limited; however, one ligand of SLC6A8 protein is currently tested in the first phase of clinical trials. Therefore, we also highlight structural aspects useful for ligand development. In this review, we discuss SLC6A6 and SLC6A8 transporters as potential biological targets for anticancer agents.
... Our results showed that the levels of taurine and cholesterol were significantly increased, and the Slc10a1 gene (encoding taurocholate co-transporting polypeptide) was significantly downregulated, both of which indicated impaired bile acid transport. Studies verified that taurine concentration was increased in the brain of whether aged diabetic rats or db/db mice with cognitive decline or early AD rats [40]. Clinical investigations also suggested that elevated taurine levels may indicate the occurrence of early cognitive impairment, and its level is negatively correlated with the progress of cognitive impairment [40,41]. ...
... Studies verified that taurine concentration was increased in the brain of whether aged diabetic rats or db/db mice with cognitive decline or early AD rats [40]. Clinical investigations also suggested that elevated taurine levels may indicate the occurrence of early cognitive impairment, and its level is negatively correlated with the progress of cognitive impairment [40,41]. Therefore, it is possible that bile acids as a potential link between the gut microbiome and the brain play a critical role in cognitive impairment. ...
Type 2 diabetes mellitus (T2DM) is a complex metabolic disorder frequently accompanied by cognitive impairment. Contributing factors such as modern lifestyle, genetic predisposition, and gene environmental interactions have been postulated, but the pathogenesis remains unclear. In this study, we attempt to investigate the potential mechanisms and interventions underlying T2DM-induced cognitive deficits from the brain–gut axis perspective. A combined analysis of the brain transcriptome, plasma metabolome, and gut microbiota in db/db mice with cognitive decline was conducted. Transcriptome analysis identified 222 upregulated gene sets and 85 downregulated gene sets, mainly related to mitochondrial respiratory, glycolytic, and inflammation. In metabolomic analysis, a total of 75 significantly altered metabolites were identified, correlated with disturbances of glucose, lipid, bile acid, and steroid metabolism under disease state. Gut microbiota analysis suggested that the species abundance and diversity of db/db mice were significantly increased, with 23 significantly altered genus detected. Using the multi-omics integration, significant correlations among key genes (n = 33), metabolites (n = 41), and bacterial genera (n = 21) were identified. Our findings suggest that disturbed circulation and brain energy metabolism, especially mitochondrial-related disturbances, may contribute to cognitive impairment in db/db mice. This study provides novel insights into the functional interactions among the brain, circulating metabolites, and gut microbiota.
... As the downstream metabolite of methionine and cysteine, taurine is widely distributed in all tissues and organs of the human body, with the highest content in the liver. Previous studies showed that taurine exerts many important physiological functions, such as anti-oxidative stress, maintenance of energy metabolism homeostasis, and anti-inflammatory processes [10,11]. A recent study revealed that taurine can inhibit tumor growth, induce tumor cell apoptosis, and mitigate the side effects of cancer chemotherapy [12]. ...
Hepatocellular carcinoma (HCC) is one of the most prevalent subtypes of primary liver cancer, with high mortality and poor prognosis. Immunotherapy has revolutionized treatment strategies for many cancers. However, only a subset of patients with HCC achieve satisfactory benefits from immunotherapy. Therefore, a reliable biomarker that could predict the prognosis and immunotherapy response in patients with HCC is urgently needed. Taurine plays an important role in many physiological processes. However, its participation in the occurrence and progression of liver cancer and regulation of the composition and function of various components of the immune microenvironment remains elusive. In this study, we identified and validated two heterogeneous subtypes of HCC with different taurine metabolic profiles, presenting distinct genomic features, clinicopathological characteristics, and immune landscapes, using multiple bulk transcriptome datasets. Subsequently, we constructed a risk model based on genes related to taurine metabolism to assess the prognosis, immune cell infiltration, immunotherapy response, and drug sensitivity of patients with HCC. The risk model was validated using several independent external cohorts and showed a robust predictive performance. In addition, we evaluated the expression patterns of taurine metabolism-related genes in the tumor microenvironment and the heterogeneity of taurine metabolism among cancer cells using a single-cell transcriptome. In conclusion, our study provides insights into the important role played by taurine metabolism in tumor progression and immune regulation. Furthermore, the risk model can serve as a biomarker to assess patient prognosis and immunotherapy response, potentially helping clinicians make more precise and personalized clinical decisions.
... Body organs development: Insufficient synthesis of taurine in the human fetus results in problems with birth weight since taurine is an important amino acid throughout development. Mice that lack TauT are often smaller and have abnormalities in the growth of the heart and skeletal muscles [29][30][31] Taurine supplementation has an impact on learning ability and low plasma taurine content can harm mental development 32 . These problems may be better studied using different animal models, such as CDO (cysteine dioxygenase) or CSAD (cysteine sulphinic acid dioxygenase). ...
Taurine, a sulfur-containing non-protein amino acid is one of the most prevalent amino acids in all mammalian plasma and tissues. The objective is to identify the therapeutic role of taurine in animal models and human systemic physiology. Various electronic databases, including author, year of publication, country, purpose, data collection, significant findings and research focus/domain were used in search of published material referencing assessment of the physio-pharmacological potentials of taurine. Taurine protects against a wide range of pathophysiological conditions, including neurological abnormalities, mitochondrial malfunction, metabolic disease, reproductive failure and poor fetal development. Taurine was also reviewed to possess antioxidant, reno-protective, hemo-protective, hepato-protective and anti-inflammatory potentials as well as cardio-protective and anti-aging effects. Taurine, found in excitable tissues, protects systemic physiology against maladaptive responses. Further research is needed to determine if taurine insufficiency can monitor maladaptive responses. Although, clinical trials are also needed to determine optimal therapeutic doses.
... La taurina se considera como un aminoácido no esencial en roedores, esencial en gatos y condicionalmente esencial en humanos(Lourenço y Camilo, 2002).Algunos estudios en diferentes modelos animales han demostrado la importancia de la taurina durante el desarrollo y su ausencia se ha relacionado con varios procesos patológicos, retraso mental, miocardiopatía y degeneración de la retina. Además, participa en varios procesos metabólicos como la osmorregulación, la estabilización de la membrana, la modulación del nivel de calcio celular y la desintoxicación(Chen et al., 2019).Se ha observado que modelos murinos deficientes del transportador de taurina presentan deterioro de varias funciones fisiológicas, lo que implica un papel indispensable en la homeostasis celular. Aunque la taurina se ha reportado en múltiples procesos metabólicos, como la osmorregulación, la estabilización de la membrana, la modulación del nivel de calcio extracelular y la desintoxicación. ...
Introduction: Energy drinks are products that are made up of various compounds that could cause adverse effects on human metabolism and affect their health. In recent years, the consumption of these products has increased considerably, mainly in the population of young university students who seek to improve their academic performance, sports performance or for recreational purposes. Objective: In the present study we sought to know the frequency and the main reasons for the consumption of energy drinks and the associated effects in a population of young university students. Methodology. The study was conducted in a population of students from the ETAC Coacalco campus. The work was prepared under a quantitative approach, descriptive, observational and cross-sectional, through the application of surveys, with a confidence level of 95%. Results: Information was obtained from 212 students enrolled in nursing, nutrition, psychology and optometry degrees, who were surveyed through a simple random sampling of which 39.15% mentioned that they consume energy drinks at least once a week. The main brands with the highest preference were: Coffee, Gatorade, Coca-Cola and Pepsi, and less frequently: Powerade, Vive100, Red Bull, among others, the main reason being to improve academic performance. Conclusions: The consumption of energy drinks is high in a population of university students. It is necessary to carry out studies on the effects of these drinks in the long term and finally it is necessary to guide the student population and the general population about the effects that these drinks can have on the health of consumers.
... Taurine is an amino acid that is not considered a neurotransmitter, because a specific receptor has not been identified [54]. However, taurine has inhibitory effects through interactions with GABA, glycine, and NMDA receptors [42,43,51,[54][55][56][57]. ...
Type 2 diabetes mellitus (T2DM) leads to the development of cardiovascular diseases, cognitive impairment, and dementia. There are sex differences in the presentation of T2DM and its associated complications. We sought to determine the impact of sex and T2DM on the brain metabolome to gain insights into the underlying mechanisms of T2DM-associated cognitive complications. Untargeted metabolomic analysis was performed, using liquid chromatography-mass spectrometry, on whole brain tissue from adult male and female db/db mice (a T2DM model) compared to wild-type (WT) C57Bl6/J mice. Regardless of sex, T2DM increased free fatty acids and decreased acylcarnitines in the brain. Sex impacted the number (103 versus 65 in males and females, respectively), and types of metabolites shifted by T2DM. Many choline-containing phospholipids were decreased by T2DM in males. Female-specific T2DM effects included changes in neuromodulatory metabolites (γ-aminobutyric acid, 2-linoleoyl glycerol, N-methylaspartic acid, and taurine). Further, there were more significantly different metabolites between sexes in the T2DM condition as compared to the WT controls (54 vs. 15 in T2DM and WT, respectively). T2DM alters the murine brain metabolome in both sex-independent and sex-dependent manners. This work extends our understanding of brain metabolic sex differences in T2DM, cognitive implications, and potential sex-specific metabolic therapeutic targets.
... This observation aligns with the growing body of literature highlighting the potential role of taurine in neurodevelopmental disorders. Taurine has been shown to have a vital role in various developmental processes, including eye and brain development, as well as reproductive function [17,18]. Moreover, studies on laboratory animals have indicated associations between low taurine levels and pathologies such as cardiomyopathies, retinal degeneration, and growth retardation, particularly during developmental periods [19][20][21]. ...
The objective of this study was to analyze the serum amino acid profile in children diagnosed with autistic spectrum disorder (ASD) in southern Romania. The analysis aimed to provide insights into the underlying metabolic dysregulations associated with ASD. ASD is a neurodevelopmental disorder characterized by impaired social interaction, communication deficits, and restricted repetitive behaviors. Although the exact cause of ASD is largely unknown, recent evidence suggests that abnormalities in amino acid metabolism may contribute to its pathogenesis. Therefore, studying the amino acid profile in children with ASD could offer valuable information for understanding the metabolic disturbances associated with this complex disorder. This single-center study examined serum samples from children diagnosed with ASD, utilizing advanced analytical techniques to quantify the levels of different amino acids, amino acid derivatives, and amino acid-like substances. The results showed a lower level of taurine and a higher level of asparagine and leucine in the ASD group versus the control group. In the ASD group, we observed significant differences in tryptophan and alpha-aminobutyric acid levels based on age, with higher tryptophan levels in children older than 7 years when compared to children younger than 7 years; however, no significant correlations were found with the ASD group older than 7 years old. Additionally, younger children with ASD exhibited higher levels of alpha-aminobutyric acid than older children with ASD. The findings from this study contribute to the growing body of knowledge on the metabolic aspects of ASD, highlighting potential biomarkers and therapeutic targets for improving the management and treatment of ASD in children.
... The contribution of taurine to cognitive impairment has been widely studied. Taurine shows a strong time dependence during the process of cognitive development [35]. It is also abundant in the developmental stage, where it serves as a trophic factor for the brain, promoting the proliferation of cells and protecting them from external damage [36,37]. ...
Stress caused by noise is becoming widespread globally. Noise may lead to deafness, endocrine disorders, neurological diseases, and a decline in mental health. The mechanism behind noise-induced neurodevelopmental abnormalities is unclear, but apoptosis and pro-inflammatory signals may play an important role. In this study, weaned piglets were used as a model to explore noise-induced neurodevelopmental abnormalities. We hypothesized that long-term noise exposure would induce anxiety and cause acute stress, exhibited by alterations in neurotransmission in the amygdala. A total of 72 hybrid piglets (Large White × Duroc × Min Pig) were randomly divided into three groups, including noise (exposed to mechanical noise, 80–85 dB), control (blank, exposed to natural background sound
... In APP/PS1 AD transgenic mice, taurine administration was shown to bind oligomeric Aβ peptides and improve cognition (Jang et al., 2017). Moreover, decreased taurine levels, as detected by ion exchange in the temporal cortices of patients with AD could lead to higher aggregation and more rapid disease progression, highlighting the potential role of taurine as co-adjuvant in the delaying of neurodegenerative processes (Arai et al., 1985;Chen et al., 2019). ...
... They administered taurine orally through drinking water to amyloid precursor protein (APP)/PS1 transgenic mice for six weeks. The results of the experiment showed that taurine treatment can improve the cognitive performance of the APP/PS1 mice without affecting their behavior in the Y-maze or passive avoidance test (Chen et al., 2019). In a transgenic AD mouse model, it has been shown that taurine has the ability to improve cognitive abilities. ...
... Taurine, a major constituent of bile, has multiple biological functions, including conjugation of bile acids, antioxidation, osmoregulation, membrane stabilization, and modulation of calcium signaling [42]. Taurine was also found significantly higher in females in several CSF metabolomic analyses, which is in line with our result [42,43]. A Duke CSF metabolomics study found that men had significantly higher levels of cysteine, uric acid, and N-acetyl-serotonin, while women had significantly higher 5-HIAA levels [32]. ...
Background
During biological aging, significant metabolic dysregulation in the central nervous system may lead to cognitive decline and neurodegeneration. However, the metabolomics of the aging process in cerebrospinal fluid (CSF) has not been thoroughly explored.
Methods
In this cohort study of CSF metabolomics using liquid chromatography-mass spectrometry (LC–MS), fasting CSF samples collected from 92 cognitively unimpaired adults aged 20–87 years without obesity or diabetes were analyzed.
Results
We identified 37 metabolites in these CSF samples with significant positive correlations with aging, including cysteine, pantothenic acid, 5-hydroxyindoleacetic acid (5-HIAA), aspartic acid, and glutamate; and two metabolites with negative correlations, asparagine and glycerophosphocholine. The combined alterations of asparagine, cysteine, glycerophosphocholine, pantothenic acid, sucrose, and 5-HIAA showed a superior correlation with aging (AUC = 0.982). These age-correlated changes in CSF metabolites might reflect blood–brain barrier breakdown, neuroinflammation, and mitochondrial dysfunction in the aging brain. We also found sex differences in CSF metabolites with higher levels of taurine and 5-HIAA in women using propensity-matched comparison.
Conclusions
Our LC–MS metabolomics of the aging process in a Taiwanese population revealed several significantly altered CSF metabolites during aging and between the sexes. These metabolic alterations in CSF might provide clues for healthy brain aging and deserve further exploration.
... Besides that, a small amount of taurine can be produced from cysteine and methionine metabolism [54,55]. Taurine is often considered a neurotrophic factor, as it acts in promoting brain cell proliferation and protecting against toxic agent-induced damages [56], possibly by inhibiting excitotoxicity, mitochondrial stress, and apoptosis [54]. This amino acid is also involved in the signaling of multiple neural pathways including GABAergic, dopaminergic, serotonergic, and adrenergic [57], the signaling pathways that play a pivotal role in modulating cognitive functions. ...
Kratom (M. speciosa Korth) is an herbal plant native to Southeast Asia. The leaves have been widely used to alleviate pain and opioid withdrawal symptoms. However, the increasing trend of recreational use of kratom among youth is concerning because substance abuse may render the adolescent brain more susceptible to neuropathological processes, causing dramatic consequences that persist into adulthood. Therefore, the present study aimed to investigate the long-term effects of mitragynine, the main alkaloid and lyophilized kratom decoction (LKD) exposure during adolescence on cognitive behaviours and brain metabolite profiles in adult rats. Adolescent male Sprague-Dawley rats were given mitragynine (3, 10 or 30mg/kg) or LKD orally for 15 consecutive days during postnatal days 31-45 (PND31-45). Behavioural testing was performed during adulthood (PND70-84) and the brains were subjected to metabolomic analysis. The results show that a high dose of mitragynine impaired long-term object recognition memory. Social behaviour and spatial learning were not affected, but both mitragynine and LKD impaired reference memory. Brain metabolomic study revealed several altered metabolic pathways that may be involved in the cognitive behavioural effects of LKD and mitragynine exposure. These pathways include arachidonic acid, taurine and hypotaurine, pantothenate and CoA biosynthesis, and tryptophan metabolism, while the N-isovalerylglycine was identified as the potential biomarker. In summary, adolescent kratom exposure can cause long-lasting cognitive behavioural deficits and alter brain metabolite profiles that are still evident in adulthood. This finding also indicates that the adolescent brain is vulnerable to the impact of early kratom use.
... Game meat is a source of bioactive contents, including conjugated linoleic acid (CLA), as well as different beneficial peptides such as anserine or carnosine [19]. Moreover, the aforementioned peptides and its analogs have been shown to be able to significantly reduce the incidence of heart attack and improve neuronal function [17,[24][25][26][27][28][29]. ...
Game meat contains bioactive compounds that directly influence the formation of a rich reservoir of flavor precursors that produce specific sensory properties. Quality is considered one of the most influential determinants of consumer behavior, but the interpretation of this concept differs between consumers. Although recognized for its quality, its unique sensory characteristics (smell, taste, aroma) may have a major impact on consumer perception. The aim of this review is to describe the consumer behavior regarding game meat through elements of neuroperception, using methods of analysis, observation, and interpretation of scientific information from the literature. Following the analysis of published papers on this topic, it was shown that external factors influencing the biological basis of behavior could provide explanations for the acceptance or rejection of this type of meat and solutions. Neuroperception can explain the mechanism behind consumer decision-making. The influence of extrinsic factors (environment, mood, emotions, stress) shapes the perception of the quality attributes of game meat, the unique sensory characteristics of game meat passing through a primary filter of sensory receptors (eyes, nose, tongue, etc). Game meat is darker and tougher (compared to meat from domestic animals), and the taste and smell have the power to trigger memories and change the mood, influencing consumer behavior. Understanding consumer attitudes towards game meat in relation to quality attributes and the physiology of sensory perception can provide important insights for food industry professionals, processors, sensory evaluators, and researchers.
... As an essential amino acid and pharmacologically speaking, its clinical uses are expanding. The taurine extract, which is colorless, water-soluble, and strongly acidic due to its sulfonate group, has high antioxidant and antibacterial properties, much like whey powder [3][4][5]. ...
In this original research, biodegradable corn starch (CS) and wheat gluten (wg)-based silver nanofilms were synthesized and analyzed by using goji berry extract taurine (ta), garlic extract (GC), whey powder (wh), and montmorillonite clay nanoparticles. Antibacterial-corn-starch-based nano films were analyzed by using the methods of high-performance liquid chromatography (HPLC), Fourier Transform infrared spectroscopy (FTIR-ATR), X-ray diffraction (XRD), dynamic and mechanical (DMA) analysis, and scanning electron microscopy (SEM). In addition, the antibacterial resistances of the corn starch nano films against the bacteria Salmonella and Staphylococcus aureus (S. aureus) and Listeria monocytogenes were examined and the migration assays were carried out. The migration analysis results of CS1, CS2, and CS3 nanocomposite films were found as 0.305, 0.297, and 0.297 mg/dm2, respectively. The inhibition zone of CS1, CS2, and CS3 nanocomposite films were found as 1547, 386, and 1884 mm2 against Salmonella bacteria. The results show that silver nanofilms are suitable as packaging films for the production of packaging in milk and dairy products, liquid foods, and acidic foods.
... A taurine supplementation has been associated with a potential protective activity in aging brains and direct beneficial effects during nervous system toxicity episodes [54][55][56][57], but the EFSA states that a taurine dietary intake does not increase the taurine levels in the brain, ruling out the possibility of a stimulant effect on the CNS [29]. Therefore, a taurine supplementation may not be necessary in healthy consumers. ...
The consumption of energy drinks (EDs) is increasing globally while the evidence and concern about the potential health risks are also growing. Caffeine (generally 32 mg/100 mL) together with a wide variety of other active components such as taurine (usually 4000 mg/L) and D-glucuronolactone (generally 2400 mg/L) are the main ingredients of EDs. This study aims to assess the exposures to caffeine, taurine and D-glucuronolactone from EDs in various consumption scenarios and consumer profiles and to characterize the risks by evaluating caffeine and taurine intakes with their reference values and by calculating the margin of safety (MOS) for D-glucuronolactone. While the exposure assessment results showed that caffeine intakes from EDs ranged from 80 to 160 mg (1.14–4 mg/kg b.w.) for the considered scenarios, the risk characterization estimated some risks that could be managed with consumption recommendations such as limiting EDs in 40, 60 and 80 kg b.w. consumers to 175, 262.5 and 350 mL, respectively, to prevent sleep disturbances and to 375, 562.5 and 750 mL to prevent general caffeine adverse health risks, respectively. Dietary exposure to D-glucuronolactone from EDs ranged from 600 to 1200 mg (7.5–30 mg/kg b.w.). As D-glucuronolactone MOS ≥ 100 is only observed when EDs consumption is limited to 250 mL, for individuals weighing above 60 kg, some risks were observed in some of the studied scenarios. A taurine exposure from EDs varied from 1000 to 2000 mg (12.5–50 mg/kg b.w.) and consumptions over 500 mL were estimated to generate intakes above the reference value. In conclusion, the management of these risks requires a European legal framework for EDs with maximum limits for the active components, volume size limitations and labeling improvements along with the development of education and awareness programs and risk communication actions in collaboration with the industry and society.
... CSAD catalyzes cysteine sulfinic acid to hypotaurine, which is further oxidized to taurine. Taurine is a nutritional factor for the development of the central nervous system [18], and plays an important role in the cardiovascular system [19], the hepatobiliary system [20], and the treatment of diabetes [21]. Since amino acid decarboxylases and their products are involved in many biological processes and are closely related to many diseases, it is of great biological significance to identify the corresponding substrates and products of amino acid decarboxylases. ...
Amino acid decarboxylases convert amino acids into different biogenic amines which regulate diverse biological processes. Therefore, identifying the substrates of amino acid decarboxylases is critical for investigating the function of the decarboxylases, especially for the new genes predicted to be amino acid decarboxylases. In the present work, we have established a simple and efficient method to identify the substrates and enzymatic activity of amino acid decarboxylases based on LC-MS methods. We chose GAD65 and AADC as models to validate our method. GAD65 and AADC were expressed in HEK 293T cells and purified through immunoprecipitation. The purified amino acid decarboxylases were subjected to enzymatic reaction with different substrate mixtures in vitro. LC-MS analysis of the reaction mixture identified depleted or accumulated metabolites, which corresponded to candidate enzyme substrates and products, respectively. Our method successfully identified the substrates and products of known amino acid decarboxylases. In summary, our method can efficiently identify the substrates and products of amino acid decarboxylases, which will facilitate future amino acid decarboxylase studies.
... Exposure to MeHg induced a decrease in taurine levels in the present study. Fluctuations in taurine levels and transporters were associated with cognitive impairments [49]. Many studies have shown the protective effect of taurine supplementation against dementia in animal models, by improving memory impairment, inflammation, and apoptosis [24,[50][51][52][53]. Taurine also plays a critical role in hippocampus maintenance in nutrition, neuronal cell growth, and differentiation [54]. ...
Methylmercury (MeHg) is highly toxic to the human brain. Although much is known about MeHg neurotoxic effects, less is known about how chronic MeHg affects hippocampal amino acids and other neurochemical markers in adult mice. In this study, we evaluated the MeHg effects on systemic lipids and inflammation, hippocampal oxidative stress, amino acid levels, neuroinflammation, and behavior in adult male mice. Challenged mice received MeHg in drinking water (2 mg/L) for 30 days. We assessed weight gain, total plasma cholesterol (TC), triglycerides (TG), endotoxin, and TNF levels. Hippocampal myeloperoxidase (MPO), malondialdehyde (MDA), acetylcholinesterase (AChE), amino acid levels, and cytokine transcripts were evaluated. Mice underwent open field, object recognition, Y, and Barnes maze tests. MeHg-intoxicated mice had higher weight gain and increased the TG and TC plasma levels. Elevated circulating TNF and LPS confirmed systemic inflammation. Higher levels of MPO and MDA and a reduction in IL-4 transcripts were found in the hippocampus. MeHg-intoxication led to increased GABA and glycine, reduced hippocampal taurine levels, delayed acquisition in the Barnes maze, and poor locomotor activity. No significant changes were found in AChE activity and object recognition. Altogether, our findings highlight chronic MeHg-induced effects that may have long-term mental health consequences in prolonged exposed human populations.
... The abundances of betaine, creatine, and taurine were all significantly decreased. Betaine has been reported to have anti-inflammatory effects (Chen et al., 2021), while creatine and taurine are thought to provide energy to fuel the normal function of the brain (Chen et al., 2019;Roschel et al., 2021). Combined, these results suggested that the perturbation of amino acid metabolism may contribute to the aging of hippocampus through the modulation of synaptic plasticity, energy metabolism, and neuroinflammation. ...
Aging is an intricate biological event that occurs in both vertebrates and invertebrates. During the aging process, the brain, a vulnerable organ, undergoes structural and functional alterations, resulting in behavioral changes. The hippocampus has long been known to be critically associated with cognitive impairment, dementia, and Alzheimer’s disease during aging; however, the underlying mechanisms remain largely unknown. In this study, we hypothesized that altered metabolic and gene expression profiles promote the aging process in the hippocampus. Behavioral tests showed that exploration, locomotion, learning, and memory activities were reduced in aged mice. Metabolomics analysis identified 69 differentially abundant metabolites and showed that the abundance of amino acids, lipids, and microbiota-derived metabolites (MDMs) was significantly altered in hippocampal tissue of aged animals. Furthermore, transcriptomic analysis identified 376 differentially expressed genes in the aged hippocampus. A total of 35 differentially abundant metabolites and 119 differentially expressed genes, constituting the top 200 correlations, were employed for the co-expression network. The multi-omics analysis showed that pathways related to inflammation, microglial activation, synapse, cell death, cellular/tissue homeostasis, and metabolism were dysregulated in the aging hippocampus. Our data revealed that metabolic perturbations and gene expression alterations in the aged hippocampus were possibly linked to their behavioral changes in aged mice; we also provide evidence that altered MDMs might mediate the interaction between gut and brain during the aging process.
... Taurine, the free amino acid with the highest abundance within the nervous system, has an essential nutritional effect on brain cell proliferation, development, and differentiation [32]. Previous studies have indicated that taurine administration could effectively mitigate neuronal damage severity and white matter injury in TBI and enhance cognitive impairment [33][34][35]. Recently, Daniel's group reported in lampreys that taurine enhances axon growth after complete spinal cord injury (SCI) [36]. ...
Diffuse axonal injury (DAI) represents a frequent traumatic brain injury (TBI) type, significantly contributing to the dismal neurological prognosis and high mortality in TBI patients. The increase in mortality can be associated with delayed and nonspecific initial symptoms in DAI patients. Additionally, the existing approaches for diagnosis and monitoring are either low sensitivity or high cost. Therefore, novel, reliable, and objective diagnostic markers should be developed to diagnose and monitor DAI prognosis. Urine is an optimal sample to detect biomarkers for DAI noninvasively. Therefore, the DAI rat model was established in this work. Meanwhile, the ultraperformance liquid chromatography quadrupole-time-of-flight hybrid mass spectrometry- (UPLC/Q-TOF MS-) untargeted metabolomics approach was utilized to identify the features of urine metabolomics to diagnose DAI. This work included 57 metabolites with significant alterations and 21 abnormal metabolic pathways from the injury groups. Three metabolites, viz., urea, butyric acid, and taurine, were identified as possible biomarkers to diagnose DAI based on the great fold changes (FCs) and biological functions during DAI. The present study detected several novel biomarkers for noninvasively diagnosing and monitoring DAI and helped understand the DAI-associated metabolic events.
... Our metabolomic analysis results showed that levels of hypotaurine and taurine in the serum decreased in mice with viral pneumonia and that XCH intervention could increase these metabolites. Taurine is a sulfur-containing amino acid that is ubiquitous in mammals and has important biological functions such as regulating osmotic pressures, stabilizing cell membranes, and regulating intracellular calcium levels [66]. Recent studies found that taurine has pharmacological effects such as delaying obesity, decreasing blood lipid levels, and improving diabetes as well as having antitumor effects [67][68][69]. ...
Viral pneumonia is widespread, progresses rapidly, and has a high mortality rate. Developing safe and effective therapies to treat viral pneumonia can minimize risks to public health and alleviate pressures on the associated health systems. Xiao-Chai-Hu (XCH) decoction can be used in the treatment of viral pneumonia. However, the mechanisms of XCH on viral pneumonia remain unclear. In this study, poly (I:C) was used to establish a mouse model of viral pneumonia, and the therapeutic effects of XCH on viral pneumonia were assessed. Furthermore, we evaluated the effects of XCH on inflammatory response. Lastly, untargeted metabolomics were used to study the metabolic regulatory mechanisms of XCH on viral pneumonia model mice. Our results showed that XCH treatment decreased the wet/dry ratio in lung tissue, total protein concentration, and total cell count in bronchoalveolar lavage fluid (BALF). H&E staining indicated that XCH treatment alleviated the pathological changes in lung. Moreover, XCH treatment decreased the levels of proinflammatory cytokines (IL-1β, IL-6, and TNF-α) and lowered the ratio of CD86+/CD206+ macrophages and CD11b+LY6G+ neutrophils in BALF. XCH treatment also decreased the myeloperoxidase (MPO) and reduced the phosphorylations of PI3K, AKT, and NF-κB p65 in lung. Serum untargeted metabolomics analysis showed that XCH treatment could affect 18 metabolites in serum such as creatine, hydroxyproline, cortisone, hydrocortisone, corticosterone, hypotaurine, and taurine. These metabolites were associated with arginine and proline metabolism, steroid hormone biosynthesis, and taurine and hypotaurine metabolism processes. In conclusion, our study demonstrated that treatment with XCH can ameliorate viral pneumonia and reduce inflammatory response in viral pneumonia. The mechanism of action of XCH in the treatment of viral pneumonia may be associated with inhibiting the activation of PI3K/AKT/NF-κB signaling pathway in lung and regulating arginine and proline metabolism, steroid hormone biosynthesis, and taurine and hypotaurine metabolism in serum.
... Therefore, upregulated GAT4 might promote Tau level. It has been demonstrated that Tau acts as a partial agonist of the GlyR in vitro and in vivo [36,37], and a proton-dependent taurine transporter (PAT1) can transport other substrates (e.g., glycine) [38]. Therefore, Tau may act as a mediator which could link GAT2 to glycine; however, more experiments are necessary to validate the aforementioned hypothesis. ...
We have previously demonstrated that Slc6a13-deficient (Slc6a13 −/− ; KO) mice are resistant to P. multocida infection, which might be in connection with macrophage-mediated inflammation; however, the specific metabolic mechanism is still enigmatic. Here we reproduce the less sensitive to P. multocida infection in overall survival assays as well as reduced bacterial loads, tissue lesions, and inflammation of lungs in KO mice. The transcriptome sequencing analysis of wild-type (WT) and KO mice shows a large number of differentially expressed genes that are enriched in amino acid metabolism by functional analysis. Of note, glycine levels are substantially increased in the lungs of KO mice with or without P. multocida infection in comparison to the WT controls. Interestingly, exogenous glycine supplementation alleviates P. multocida infection-induced inflammation. Mechanistically, glycine reduces the production of inflammatory cytokines in macrophages by blocking the activation of inflammasome (NALP1, NLRP3, NLRC4, AIM2, and Caspase-1). Together, Slc6a13 deficiency attenuates P. multocida infection through lessening the excessive inflammatory responses of macrophages involving glycine-inflammasome signaling.
... In APP/PS1 AD transgenic mice, taurine administration was shown to bind oligomeric Aβ peptides and improve cognition (Jang et al., 2017). Moreover, decreased taurine levels, as detected by ion exchange in the temporal cortices of patients with AD could lead to higher aggregation and more rapid disease progression, highlighting the potential role of taurine as co-adjuvant in the delaying of neurodegenerative processes (Arai et al., 1985;Chen et al., 2019). ...
Taurine is considered the most abundant free amino acid in the brain. Even though there are endogenous mechanisms for taurine production in neural cells, an exogenous supply of taurine is required to meet physiological needs. Taurine is required for optimal postnatal brain development; however, its brain concentration decreases with age. Synthesis of taurine in the central nervous system (CNS) occurs predominantly in astrocytes. A metabolic coupling between astrocytes and neurons has been reported, in which astrocytes provide neurons with hypotaurine as a substrate for taurine production. Taurine has antioxidative, osmoregulatory, and anti-inflammatory functions, among other cytoprotective properties. Astrocytes release taurine as a gliotransmitter, promoting both extracellular and intracellular effects in neurons. The extracellular effects include binding to neuronal GABAA and glycine receptors, with subsequent cellular hyperpolarization, and attenuation of N-methyl-D-aspartic acid (NMDA)-mediated glutamate excitotoxicity. Taurine intracellular effects are directed toward calcium homeostatic pathway, reducing calcium overload and thus preventing excitotoxicity, mitochondrial stress, and apoptosis. However, several physiological aspects of taurine remain unclear, such as the existence or not of a specific taurine receptor. Therefore, further research is needed not only in astrocytes and neurons, but also in other glial cells in order to fully comprehend taurine metabolism and function in the brain. Nonetheless, astrocyte’s role in taurine-induced neuroprotective functions should be considered as a promising therapeutic target of several neuroinflammatory, neurodegenerative and psychiatric diseases in the near future. This review provides an overview of the significant relationship between taurine and astrocytes, as well as its homeostatic and neuroprotective role in the nervous system.
... Calcium modulation, antioxidation, salt conjugation, inflammation, osmoregulation, and membrane stabilization are numerous physiological functions of taurine (Pandya et al., 2017). As well as has different biological effects on the cardiovascular system, skeletal muscle, retina, liver, kidney, and nervous system (Chen et al., 2019) therefore taurine may have a valuable effect on the treatment of cardiovascular problems (Ibrahim et al., 2020) and liver disease (Makhova et al., 2019) primarily by lessening manufacture of reactive oxygen species (ROS). Taurine is also utilized to recover from exhaustion prior tobeforey (Wang et al., 2020). ...
Taurine, a ubiquitous endogenous sulfur-containing amino acid, possesses numerous pharmacological and physiological actions, including antioxidant activity, modulation of calcium homeostasis, and antiapoptotic effects. There is mounting evidence supporting the utility of taurine as a pharmacological agent against heart disease, including chronic heart failure. This study investigated the potential protective effects of taurine, on behavior and cardiovascular function in the male rat following arrhythmia induced by the social stressor. Here, we studied levels of heart electrical activity following experimental conditions: Cage control, social isolation in standard rat housing for 14 days, and pharmacokinetics effect of intravenous administration of different doses of taurine on arrhythmia induced by social isolation in vivo after. The ECG signals and parameters were recorded and analyzed with the aid of Bio Amp of ADInstruments data acquisition system and LabChart software. The results showed infusion of Taurine 1mg/kg/ hr, 2.5mg/kg/hr and 10mg/kg/hr non significantly change heart rate (BPM), QRS intervals, S amplitude (mV), T amplitude (mV), ST height (mV), JT height (mV), QT intervals (s) and QTc (s)
... 4 Several in vivo studies utilizing different experimental models have demonstrated the significance of taurine during development; its scarcity during various developmental phases has been linked to various pathological issues such as retardation, cardiomyopathy, and retinal degeneration. 5,6 Taurine is involved in a number of metabolic processes, including osmoregulation, membrane stabilization, modulation of cellular calcium level, and detoxification. 7,8 Taurine-transporter-deficient mice are characterized by im- ...
Taurine (2-aminoethane sulfonic acid) is a non-essential amino acid mainly obtained through diet in humans. Despite the lack of research on the health effects of taurine in animals and humans, it is widely used as a dietary supplement. Evidence from human and animal studies indicates that taurine is involved in conjugation of bile acids and regulation of blood pressure and has anti-oxidative, anti-inflammatory, and anti-obesogenic properties. Taurine can benefit both human and non-human animal health in multiple ways. However, few interventional and epidemiological studies regarding the beneficial impacts of taurine in humans and other animals have been conducted. Here, we review the evidence from animal and human studies showing that taurine protects against dyslipidemia, obesity, hypertension, and diabetes mellitus.
... At week eight, taurine levels decreased compared to the results observed after five weeks of simultaneous bacteria supplementation and stress but were still higher than those observed in the placebo group. Bacterial supplementation during five weeks of stress influenced taurine level stabilization compared to the baseline result, but progressive stress and aging-related changes could have affected its concentration later in the experiment, as observed in other studies related to brain development [53][54][55][56]. The other metabolites showed no statistically significant differences between the initial results and the results after simultaneous stress and administration of bacteria. ...
The intestinal microbiome composition and dietary supplementation with psychobiotics can result in neurochemical alterations in the brain, which are possible due to the presence of the brain–gut–microbiome axis. In the present study, magnetic resonance spectroscopy (MRS) and behavioural testing were used to evaluate whether treatment with Lacticaseibacillus rhamnosus JB-1 (JB‑1) bacteria alters brain metabolites’ levels and behaviour during continuous exposure to chronic stress. Twenty Wistar rats were subjected to eight weeks of a chronic unpredictable mild stress protocol. Simultaneously, half of them were fed with JB-1 bacteria, and the second half was given a daily placebo. Animals were examined at three-time points: before starting the stress protocol and after five and eight weeks of stress onset. In the elevated plus maze behavioural test the placebo group displayed increased anxiety expressed by almost complete avoidance of exploration, while the JB-1 dietary supplementation mitigated anxiety which resulted in a longer exploration time. Hippocampal MRS measurements demonstrated a significant decrease in glutamine + glutathione concentration in the placebo group compared to the JB-1 bacteria-supplemented group after five weeks of stress. With the progression of stress the decrease of glutamate, glutathione, taurine, and macromolecular concentrations were observed in the placebo group as compared to baseline. The level of brain metabolites in the JB-1-supplemented rats were stable throughout the experiment, with only the taurine level decreasing between weeks five and eight of stress. These data indicated that the JB-1 bacteria diet might stabilize levels of stress-related neurometabolites in rat brain and could prevent the development of anxiety/depressive-like behaviour.
... Therefore, the prevention and remediation of cognitive impairment are extremely crucial. Nutraceuticals such as polyphenols, flavonoids, glycosides, terpenes, vitamins, phosphatidylserine, ω-3 polyunsaturated fatty acids, taurine and creatine have been widely studied and exhibited positive effects on the management of cognitive deficit [13][14][15][16][17]. As a kind of food component, non-starch polysaccharides (NSPs) showed a large number of physiological effects including anti-cancer, anti-virus, anti-inflammation, anti-oxidation, anti-fatigue, anti-hypoxia, anti-hypertensive, hypoglycemic, hypolipidemic, vasodilation, immunomodulation, gastro-protection, hepato-protection, neuro-protection, reno-protection, cardioprotection and gut microbiota modulation [18][19][20][21][22]. Numerous studies have also revealed the preventive and therapeutic effects of NSPs on cognitive deficit. ...
Non-starch polysaccharides (NSPs) are food ingredients proven to be beneficial in a large number of health issues. However, there is no literature systematic review about the effects and corresponding mechanisms of NSPs on the prevention and remediation of cognitive impairment. In this review, studies on prevention and remediation of NSPs for cognitive deficit caused by diseases, menopause, ageing, chronic stress and environmental pollutants were summarized and the corresponding mechanisms were established. The anti-cognitive deficit effects of NSPs were associated with the modulation of amyloid β (Aβ) deposition, p-Tau aggregation, oxidative stress, inflammation, neuron apoptosis, neurogenesis, neurotransmitters, synaptic plasticity, autophagy and gut microbiota. Although the structure-function relationship has not been elucidated, several structural properties of NSPs such as molecular weight, sulfate content, hydroxyl group content, monosaccharide composition and molecular chain linkage might be crucial for the anti-cognitive deficit property. Notably, this review revealed that NSPs had a positive effect on cognitive impairment and proposed the future perspectives for further research on the anti-cognitive dysfunction effects of NSPs.
... Glycerophospholipids and glycerolipid metabolism were involved in aging and age-related changes [17]. AGING Besides, taurine, as one of the intracellular antioxidants, plays an important role in oxidative stress during aging [34]. And the activity of the cytochrome P450 enzyme remains unchanged in the normal aging process, and the genetic effect is more obvious than the age effect. ...
The functions of stem cells decline progressively with aging, and some metabolic changes occur during the process. However, the molecular mechanisms of stem cell aging remain unclear. In this study, the combined application of metabolomics and transcriptomics technologies can effectively describe the possible molecular mechanisms of rat bone marrow mesenchymal stem cell (BMSC) senescence. Metabolomic profiles revealed 23 differential metabolites which were abundant in "glycerophospholipid metabolism", "linoleic acid metabolism" and "biosynthesis of unsaturated fatty acids". In addition, transcriptomics analysis identified 590 genes with enormously differential expressions in young and old BMSCs. KEGG enrichment analyses showed that metabolism-related pathways in BMSC senescence had stronger responses. Furthermore, the integrated analysis of the interactions between the differentially expressed genes (DEGs) and metabolites indicated the differential genes related to lipid metabolism of Scd, Scd2, Dgat2, Fads2, Lpin1, Gpat3, Acaa2, Lpcat3, Pcyt2 and Pla2g4a may be closely associated with the aging of BMSCs. Finally, Scd2 was identified as the most significant DEG, and Scd2 over-expression could alleviate cellular senescence in aged BMSCs. In conclusion, this work provides a validated understanding that the DEGs and metabolites related to lipid metabolism present more apparent changes in the senescence of rat BMSCs.
Taurine (TAU) is a sulfur-containing amino acid abundantly found in the human body. Endogenously, TAU is synthesized from cysteine in the liver. However, newborns rely entirely on TAU's dietary supply (milk). There is no investigation on the effect of long-term TAU administration on next-generation neurological development. The current study evaluated the effect of long-term TAU supplementation during the maternal gestational and litter weaning time on several neurological parameters in mice offspring. Moreover, the effects of TAU on mitochondrial function and oxidative stress biomarkers as plausible mechanisms of its action in the whole brain and hippocampus have been evaluated. TAU (0.5% and 1% w/v) was dissolved in the drinking water of pregnant mice (Day one of pregnancy), and amino acid supplementation was continued during the weaning time (post-natal day; PND = 21) until litters maturity (PND = 65). It was found that TAU significantly improved cognitive function, memory performance, reflexive motor activity, and emotional behaviors in F1-mice generation. TAU measurement in the brain and hippocampus revealed higher levels of this amino acid. TAU and ATP levels were also significantly higher in the mitochondria isolated from the whole brain and hippocampus. Based on these data, TAU could be suggested as a supplement during pregnancy or in pediatric formula. The effects of TAU on cellular mitochondrial function and energy metabolism might play a fundamental role in the positive effects of this amino acid observed in this investigation.
Brain health is largely dependent on the metabolic regulation of amino acids. Brain injuries, diseases, and disorders can be detected through alterations in free amino acid (FAA) concentrations; and thus, mapping the changes has high diagnostic potential. Common methods focus on optimizing neurotransmitter quantification; however, recent focus has expanded to investigate the roles of molecular precursors in brain metabolism. An isocratic method using high performance liquid chromatography with electrochemical cell detection was developed to quantify a wide range of molecular precursors and neurotransmitters: alanine, arginine, aspartate, serine, taurine, threonine, tyrosine, glycine, glutamate, glutamine, and γ-Aminobutyric acid (GABA) following traumatic brain injury. First, baseline concentrations were determined in the serum, cerebrospinal fluid, hippocampus, cortex, and cerebellum of naïve male Sprague Dawley rats. A subsequent study was performed investigating acute changes in FAA concentrations following blast-induced traumatic brain injury (bTBI). Molecular precursor associated FAAs decreased in concentration at 4hours after injury in both the cortex and hippocampus while those serving as neurotransmitters remained unchanged. In particular, the influence of oxidative stress on the observed changes within alanine and arginine pathways following bTBI should be further investigated to elucidate the full therapeutic potential of these molecular precursors at acute time points.
Background:
Researches on diagnosis and treatment of Alzheimer's disease, the most common type of dementia, are still ongoing. Taurine is frequently used in Alzheimer's disease models due to its protective effects. Metal cation dyshomeostasis is an important etiological factor for Alzheimer's disease. Transthyretin protein is thought to act as a transporter for the Aβ protein that accumulates in the brain and is eliminated in the liver and kidneys via the LRP-1 receptor. However, the effect of taurine on this mechanisms is not fully known.
Methods:
30 male rats, aged 28 ± 4 months, were divided into 5 groups (n = 6) as follows: control group, sham group, Aβ 1-42 group, taurine group and taurine+Aβ 1-42 group. Oral taurine pre-supplementation was given as 1000 mg/kg-body weight/day for 6 weeks to taurine and taurine+Aβ 1-42 groups.
Results:
Plasma copper, heart transthyretin and Aβ 1-42, brain and kidney LRP-1 levels were found to be decreased in the Aβ 1-42 group. Brain transthyretin was higher in taurine+Aβ 1-42 group and brain Aβ 1-42 was higher in Aβ 1-42 and taurine+Aβ 1-42 groups.
Conclusion:
Taurine pre-supplementation maintained cardiac transthyretin levels, decreased cardiac Aβ 1-42 levels and increased brain and kidney LRP-1 levels. Taurine may have a potential to be used as a protective agent for aged people at high risk for Alzheimer's disease.
Diquat (DQ) has been confirmed to be toxic to humans and responsible for severe health impairment. While to date, very little is known about the toxicological mechanisms of DQ. Thus, investigations to discover the toxic targets and potential biomarkers of DQ poisoning are urgently needed. In this study, a metabolic profiling analysis was conducted to reveal the changes of metabolites of plasma and find out the potential biomarkers of DQ intoxication by GC-MS. First, multivariate statistical analysis demonstrated that acute DQ poisoning can lead to metabolomic changes in human plasma. Then, metabolomics studies showed that 31 of the identified metabolites were significantly altered by DQ. Pathway analysis indicated that three primarily metabolic pathways including phenylalanine, tyrosine and tryptophan biosynthesis, taurine and hypotaurine metabolism, and phenylalanine metabolism were affected by DQ, resulting in the perturbations of phenylalanine, tyrosine, taurine, and cysteine. Finally, the results of receiver operating characteristic analysis showed the above four metabolites could be used as reliable tools for the diagnosis and severity assessments of DQ intoxication. These data provided the theoretical basis for basic research to understand the potential mechanisms of DQ poisoning, and also identified the desirable biomarkers with great potential for clinical applications.
Cognitive impairment is the main central nervous system complication of diabetes, affecting the quality of life of patients. Herba Cistanche is a homologous plant widely used as a health food and therapeutic drug. Verbascoside, a signature component of Herba Cistanche, has anti-diabetic and neuroprotective effects. However, it is quickly metabolized by the gut microbiota, and the mechanism of its neuroprotection and improvement of learning and memory remains unclear. We investigated the effectiveness and potential mechanisms of verbascoside on cognitive dysfunction in db/db mice using a 16S rRNA microbiome and serum metabolomics approach. We found that 12-week treatment with verbascoside significantly inhibited insulin resistance, reduced blood glucose and lipids, and improved cognitive deficits. In addition, verbascoside increased the gut microbiota diversity, improved intestinal dysbiosis, attenuated intestinal barrier disruption, reduced the levels of inflammatory factors, regulated the expression of the metabolites associated with cognitive function, and enhanced the central insulin sensitivity and hippocampal synaptogenesis signaling. We revealed that verbascoside induced the enrichment of Alistipes, Roseburia, and Intestinimonas in the gut, suppressed the abundance of Escherichia-Shigella, increased the serum levels of gamma-aminobutyric acid, L-glutamic acid, and L-lysine, and decreased taurine expression. Finally, a strong association between gut microbes, serum metabolites, and cognitive performance affected by verbascoside was observed. Our research suggests that alterations in gut microbes/metabolites are involved in the development of diabetic cognitive dysfunction, which is alleviated by verbascoside in the db/db mice through restructuring the gut microbiota composition, ameliorating diabetic metabolic disorders, and attenuating pathological brain damage.
As known, the chitosan is a biodegradable biopolymer with antibacterial properties, therefore it is used in the fields of pharmacy, medical, wastewater treatment, biotechnology, cosmetics, textiles, and agriculture. Apart from these, the chitosan has an important place in the food industry with its widespread use. In this research article, the chitosan were encapsulated with the taurine and garlic extracts by the spray dryer. The CSA and CSB compounds synthesized as final products were analyzed by Fourier transformed infrared spectroscopy (FTIR) and High Performance Liquid Chromatography (HPLC). The effect of the encapsulation process on the molecular weight of the polymer structure was investigated using the cryoscopy method. The compound CSA represents 1/2 encapsulation of chitosan with taurine and increased garlic extracts, respectively, while CSB represents 1/1 encapsulation of chitosan with increased taurine and fixed garlic extracts. The % antioxidant activity of the final products was determined by DDPH method. The inhibition zone and surface activity proporties of the CSA and CSB were carried out against Listeria monocytogenes, Staphylococcus aureus, E. coli, and Salmonella bacteria. The results obtained as a result of the analyzes were evaluated, and optimum values were determined for use in food packaging.
Taurine, or 2-aminoethanesulfonic acid, is one of the most abundant sulfur-containing amino acids in the human body. It is found in the heart, brain, retina, and skeletal muscles, and is synthesized in the pancreas. Studies have revealed that taurine is of high physiological importance: it protects against pathologies associated with mitochondrial diseases, and linked processes like aging, metabolic syndrome, cancer, cardiovascular diseases, and neurological disorders. It is also used as a nutritional supplement. Taurine and the Mitochondrion: Applications in the Pharmacotherapy of Human Diseases explores the significance of taurine in the biology of mitochondria. It also explains its role as a pharmacological agent for treating different diseases. Readers will gain an insight into the crucial role it plays in human physiology and the benefits of taurine supplements. Topics covered in this reference include - Synthesis of taurine and its dietary sources - The Role of taurine in mitochondrial health - Taurine as a neurotransmitter - Beneficial effects of taurine in physiological systems such as the reproductive system, renal system, and the gastrointestinal tract - Hepatoprotective and anti-inflammatory properties of taurine - The anti-aging promise of taurine supplementation - Role of taurine supplementation in obesity
Taurine (TAU) reaches a high concentration in the central nervous system (CNS). The physiological role of TAU in the CNS is the subject of many investigations. It has been suggested that this amino acid could act as a membrane stabilizer, a modulator of calcium signaling, a trophic factor for neuronal development, and even be proposed as a neurotransmitter in the CNS. Besides, several investigations revealed the neuroprotective properties of TAU in various experimental models. Multiple mechanisms, including the inhibition of the excitotoxic response, the blockade of cytoplasmic calcium overload, regulation of oxidative stress, and the positive effects of TAU on mitochondrial parameters, have been proposed for the neuroprotective properties of this amino acid. Today, it has been well-known that mitochondrial function and energy metabolism play a pivotal role in the pathogenesis of various neurodegenerative disorders and xenobiotics-induced neurotoxicity. Hence, targeting mitochondria with safe and clinically applicable agents is a viable therapeutic option in various neurodegenerative disorders. In the current chapter, the effects of TAU on the CNS will be highlighted, focusing on the positive effects of this amino acid on mitochondrial parameters. The data could help the development of safe therapeutic agents against CNS complications.
Ochratoxin A (OTA) is one of the most harmful mycotoxins, which can cause multiple toxicological effects, especially nephrotoxicity in animals and humans. Taurine is an essential amino acid with various biological functions such as anti‐inflammatory and anti‐oxidation. However, the protective effect of taurine on OTA‐induced nephrotoxicity and pyroptosis had not been reported. Our results showed that OTA exposure induced cytotoxicity and oxidative stress in PK‐15 cells, including reactive oxygen species (ROS) accumulation, increased mRNA levels of inducible nitric oxide synthase (iNOS) and cyclooxygenase 2 (COX‐2), and decreased mRNA levels of catalase (CAT), glutathione peroxidase 1 (GPx1), and glutathione peroxidase 4 (GPx4). In addition, OTA treatment induced pyroptosis by increasing the expressions of pyroptosis‐related proteins NLRP3, GSDMD, Caspase‐1 P20, ASC, Pro‐caspase‐1, and IL‐1β. Meanwhile, taurine could alleviate OTA‐induced pyroptosis and cytotoxicity, as well as reduce ROS level, COX‐2, and iNOS mRNA levels, and increase the mRNA levels of the antioxidant enzyme in PK‐15 cells. Taken together, taurine alleviated OTA‐induced pyroptosis in PK‐15 cells by inhibiting ROS generation and altering the activity of antioxidant enzymes, thereby attenuating its nephrotoxicity. Schematic depicting role of taurine in OTA‐induced nephrotoxicity. OTA exposure activates NLRP3 inflammasome‐mediated pyroptosis and oxidative stress in PK‐15 cells. Taurine attenuates OTA‐induced cytotoxicity by inhibiting the accumulation of ROS, reducing the mRNA expressions of COX‐2, and iNOS, and increasing the mRNA expressions of GPx1, GPx4, and CAT in PK‐15 cells.
Diabetes mellitus can result in severe complications, such as neurodegenerative diseases including cognitive impairment and dementia. The glucagon-like peptide-1 (GLP-1) receptor agonist, liraglutide, is a novel antidiabetic drug with neuroprotective effects against neurodegenerative diseases. In this study, we explored the protective effect of liraglutide on SH-SY5Y cells exposed to methylglyoxal (MG), a byproduct of glucose metabolism that plays a key role in the development of diabetic encephalopathy. We found that liraglutide reduced the MG-induced oxidative stress, increased the activity of superoxide dismutase (SOD) and expression levels of P22phox, Gp91phox, and Xdh genes, and reduced reactive oxygen species (ROS) content. Metabolomics analysis based on ¹H nuclear magnetic resonance showed that liraglutide induced alterations in metabolites involved in energy metabolism，including promotion of gluconeogenesis. Moreover, we found that liraglutide promoted oxidative phosphorylation and inhibited glycolysis in SH-SY5Y cells. This study revealed that liraglutide improved diabetes-related neuropathy damage by reducing the level of oxidative stress and maintaining the balance of energy metabolism, thus offering new insights into the potential mechanism of liraglutide in neuronal protection.
Taurine, acting as a free amino acid, is widely distributed and plays multiple functions, including its regulating effect on estrogen synthesis in ovary. However, the mechanisms of taurine regulating estrogen synthesis in granulosa cells are not well understood. In this study, we identify whether microRNA-7a2 (miR-7a2) is involved in the signaling of taurine regulating estrogen synthesis in mouse granulosa cells for the first time. The results demonstrated that taurine transporter (TauT) co-localized with miR-7a in mouse ovarian granulose cells. Further, taurine treatment markedly enhanced the expression of miR-7a and Cyp19a1 in mouse ovaries and increased serum 17β-estradiol (E2) concentration. Meanwhile, miR-7a2 knockout reversed the effect of taurine on E2. In addition, Golgi apparatus protein 1 (Glg1), a downstream target gene of miR-7a2, was significantly down-regulated by taurine, while Glg1 knockdown markedly increased the Cyp19a1 expression and E2 synthesis. Moreover, taurine affected miR-7a expression via activating p38 signaling. These results suggest that taurine promotes E2 synthesis through p38/miR-7a/Glg1/Cyp19a1 signaling pathway, which is crucial to understand the function and mechanism of taurine on estrogen synthesis.
Researchers have begun to direct their research to focus on the use of taurine as a psychopharmacotherapeutic compound to treat a wide range of health- related conditions as well as neuropathological diseases. Moreover, taurine has been shown to improve emotional and cognitive declines associated with senescence in neurotypical animal models. However, despite these advances in the field of taurine therapeutics, much less is known regarding the effects of sex and taurine on neurotypical animal models that are then manipulated, modified, and/or mutated to study human diseases. The present study sought to investigate this matter in a Long Evans Hooded rat model of mature age (i.e., postnatal day 60–90) in an active avoidance test (AAT). Rats were trained for 20 trials, given a 1 h. test break, retrained for another 20 trials, and then tested at 24 h, 48 h, and 1 week for learning and memory retention. An N = 63 rats were randomly assigned to three groups: (1) Control (n = 22), (2) Taurine Pre-Train (n = 19), and (3) Taurine Post-Train (n = 20). The aim of the present study was to determine the effects of taurine given 15 min before training when compared to being given after training but 15 min before testing at 24 h on learning and memory consolidation of the AAT. The results showed in Control rats that females had shorter latencies to cross in the shuttle box, increased rates of correct learning by the % Avoids/Escapes, and decreased rates of learning errors by the % Shocks. In Taurine Post-Train male rats, taurine treatment decreased their latency to cross in the shuttle box and their rate of learning errors by the % Shocks at 24 h and 48 h Testing, but it had no effect on their rate of correct learning by the % Avoids/Escapes when compared to Control and Taurine Pre-Train male rats. In contrast, Taurine Post-Train female rats increased their latency to cross in the shuttle box during Training, 24 h and 48 h Testing, when compared to the Control and Taurine Pre-Train female rats. Further, Taurine Post-Train female rats decreased their rate of learning % Avoids/Escapes and increased the rate of learning errors % Shocks when compared to Control female rats during Training and 24 h Testing but decreased their rate of learning % Avoids/Escapes and increased the rate of learning errors % Shocks when compared to Taurine Pre-Train female rats across all test conditions. These findings suggest that neurotypical female rats may be more sensitive to the aversive stimuli (i.e., foot shocks) used in the AAT as a motivating factor for learning that may cause paradoxical behavioral learning and memory patterns. This phenomenon raises an important concern for researchers to consider when studying learning and behavioral tests in rodents that use aversive and non-aversive stimuli or a combination of both such as in the AAT. Taurine, albeit neuroprotective, may not have as much benefit in a neurotypical animal model and may increase the susceptibility for anxiogenic behaviors and interfere with cognitive learning and memory behaviors. Therefore, the mechanistic way(s) in which taurine can treat, recovery, ameliorate, and forestall other neuropathological diseases in animal models may have different psychopharmacodynamics and psychopharmacokinetics in a neurotypical animal model and should be studied with caution. This does not preclude the continued investigation of taurine psychopharmacotherapies for neuropathological diseases but encourages the careful investigation of taurine supplementation and treatment in neurotypical animals as paradoxical behavioral and cognitive outcomes have been observed herein.
Meat constitutes one the main protein sources worldwide. However, ethical and health concerns have limited its consumption over the last years. To overcome this negative impact, new ingredients from natural sources are being applied to meat products to obtain healthier proteinaceous meat products. Algae is a good source of unsaturated fatty acids, proteins, essential amino acids, and vitamins, which can nutritionally enrich several foods. On this basis, algae have been applied to meat products as a functional ingredient to obtain healthier meat-based products. This paper mainly reviews the bioactive compounds in algae and their application in meat products. The bioactive ingredients present in algae can give meat products functional properties such as antioxidant, neuroprotective, antigenotoxic, resulting in healthier foods. At the same time, algae
addition to foods can also contribute to delay microbial spoilage extending shelf-life. Additionally, other algae-based applications such as for packaging materials for meat products are being explored. However, consumers’ acceptance for new products (particularly in Western countries), namely those containing algae, not only depends on their knowledge, but also on their eating habits. Therefore, it is necessary to further explore the nutritional properties of algae-containing meat products to overcome the gap between new meat products and traditional products, so that healthier algae-containing meat can occupy a significant place in the market.
Wild game meat can be a healthier, safer, and more environmentally friendly alternative to meat from farm animals. The aims of this study were to know the preferences and opinions of Polish consumers regarding game meat and its use in their diet, and to identify consumer segments based on differences in individual game meat choices, concerns, and eating habits related to game meat. The survey was conducted using the platform for online surveys among 1261 adult Poles. Six clusters characterizing the behavior of game consumers were identified (casual consumers, occasional game gourmets, indifferent consumers, occasional consumers, accidental consumers, wild game lovers) and four clusters among those who do not eat game (uninterested, restricted, dislikers, fearful). It has been found that wild game is more often eaten by hunters and their family or friends. The most common reasons for not consuming game are high prices, low availability, no family tradition, and unacceptable taste. Many positive respondents eat game because of its nutritional value but are concerned about the potential health risks and lack of cooking skills. The results of this study indicate the need for information programs for consumers about this meat. They will provide guidance to meat companies about consumer preferences for game and allow them to develop appropriate marketing strategies.
Intestinal microbiota and metabonomic were integrated to investigate the efficiency of non-saponification or saponification astaxanthin (N-Asta or S-Asta) derived from Penaeus sinensis by-products on alleviating paracetamol (PCM)-induced oxidative stress. Pre-treated...
Panax Ginseng (PG) has been used to strengthen memory and physique for thousands of years, because its main components ginsenosides (GS) and ginseng polysaccharides (GP) play a major role, but its mechanism is not clear. In this study, a rat model of dementia with vital energy deficiency (DED) was established through intraperitoneal injection with D-galactose and AlCl3 and combined with exhaustive swimming. Pharmacological studies and the urine metabolomics based on ultra-high-performance liquid chromatography-quadrupole time-of-flight mass spectrometry (UPLC-Q-TOF-MS) were employed for evaluation the efficacy of PG and exploring this treatment mechanism. Through urine metabolic profiling, it can be seen that DED rats after PG administration are close to normal group (NG) rats, and PG can regulate the in vivo status of DED rats which tend to NG. The results of behavioral, biochemical indicators and immunohistochemistry further verified the above results, and the mechanism of action of each component is refined. Ultimately, we believe that the mechanism of PG in the treatment of DED is that ginsenosides (GS) intervenes in phenylalanine tryptophan and tyrosine metabolism, stimulates dopamine production, inhibits Aβ deposition and neuroinflammation; and that ginseng polysaccharides (GP) provides energy to strengthen the TCA cycle and improve immune capacity.
Purpose
A mouse model of Alzheimer’s disease demonstrates reduced beta-amyloid levels in the whole brain, associated with a gain of hippocampal memory, after drinking taurine-enriched water; this suggests that a taurine supplement could be a promising treatment for cognitive deficit. The objective of this study is to establish a methodology for quantifying taurine in the whole brain, taking advantage of the rapid development of non-invasive imaging techniques such as magnetic resonance imaging and magnetic resonance spectroscopy (MRS).
Procedures
Single-voxel proton MRS was used to obtain quantifiable taurine peaks at 3.25 and 3.43 ppm. Quantitative MRS results were obtained in C57BL/6 mice of various age groups: 4, 11, 18, and 27 months old.
Results
Compared with the 4-month-old group, taurine levels dropped significantly only at 27 months of age (p = 0.03). However, a significant decrease of N-acetyl-aspartate (NAA) in the brain was observed at both 18 and 27 months (p = 0.03 and p = 0.02). In addition, MRS-measured taurine level is highly correlated with hippocampal volume (r = 0.95).
Conclusions
These results suggest that decreased taurine levels in the brain could be used as biomarkers for hippocampal changes and are fully translatable into putative cognitive loss in both animal models and human studies without the ex vivo approach.
Purpose of review:
The aims of this meta-analysis were to investigate the effects of orally administered isolated taurine on resting systolic blood pressure (SBP) and diastolic blood pressure (DBP) in humans.
Recent findings:
There is growing evidence that taurine deficiency is associated with hypertension and that oral supplementation can have antihypertensive effects in humans. However, these investigations have been conducted across a number of decades and populations and have not been collectively reviewed. A search was performed using various databases in May 2018 and later screened using search criteria for eligibility. There were seven peer-reviewed studies meeting the inclusion criteria, encompassing 103 participants of varying age and health statuses. Taurine ingestion reduced SBP (Hedges' g = - 0.70, 95% CI - 0.98 to - 0.41, P < 0.0001) and DBP (Hedges' g = - 0.62, 95% CI - 0.91 to - 0.34, P < 0.0001). These results translated to mean ~ 3 mmHg reductions in both SBP (range = 0-15 mmHg) and DBP (range = 0-7 mmHg) following a range of doses (1 to 6 g/day) and supplementation periods (1 day to 12 weeks), with no adverse events reported. These preliminary findings suggest that ingestion of taurine at the stated doses and supplementation periods can reduce blood pressure to a clinically relevant magnitude, without any adverse side effects. Future studies are needed to establish the effects of oral taurine supplementation on targeted pathologies and the optimal supplementation doses and periods.
Huntington's disease (HD) is a neurodegenerative disorder causing cognitive and motor impairments, evolving to death within 15-20 years after symptom onset. We previously established a mouse model with the entire human HD gene containing 128 CAG repeats (YAC128) which accurately recapitulates the natural history of the human disease. Defined time points in this natural history enable the understanding of longitudinal trajectories from the neurochemical and structural points of view using non-invasive high-resolution multimodal imaging. Accordingly, we designed a longitudinal structural imaging (MRI and DTI) and spectroscopy (1H MRS) study in YAC128, at three, six, nine and twelve months of age, at 9.4 T. Structural analysis (MRI/DTI), confirmed that the striatum is the earliest affected brain region, but other regions were also identified through connectivity analysis (pre-frontal cortex, hippocampus, globus pallidus and thalamus), suggesting a striking homology with the human disease. Importantly, we found for the first time, a negative correlation between striatal and hippocampal changes only in YAC128. In fact, the striatum showed accelerated volumetric decay in HD, as opposed to the hippocampus. Neurochemical analysis of the HD striatum suggested early neurometabolic alterations in neurotransmission and metabolism, with a significant increase in striatal GABA levels, and specifically anticorrelated levels of N-acetyl aspartate and taurine, suggesting that the later is homeostatically adjusted for neuroprotection, as neural loss, indicated by the former, is progressing. These results provide novel insights into the natural history of HD and prove a valuable role for longitudinal multimodal panels of structural and metabolite/neurotransmission in the YAC128 model.
Angelman syndrome (AS, MIM 105830) is a rare neurodevelopmental disorder affecting 1:10-20,000 children. Patients show moderate to severe intellectual disability, ataxia and absence of speech. Studies on both post-mortem AS human brains and mouse models revealed dysfunctions in the extra synaptic gamma-aminobutyric acid (GABA) receptors implicated in the pathogenesis. Taurine is a free intracellular sulfur-containing amino acid, abundant in brain, considered an inhibiting neurotransmitter with neuroprotective properties. As taurine acts as an agonist of GABA-A receptors, we aimed at investigating whether it might ameliorate AS symptoms. Since mice weaning, we orally administered 1 g/kg/day taurine in water to Ube3a-deficient mice. To test the improvement of motor and cognitive skills, Rotarod, Novel Object Recognition and Open Field tests were assayed at 7, 14, 21 and 30 weeks, while biochemical tests and amino acid dosages were carried out, respectively, by Western-blot and high-performance liquid chromatography (HPLC) on frozen whole brains. Treatment of Ube3a m−/p+ mice with taurine significantly improved motor and learning skills and restored the levels of the post-synaptic PSD-95 and pERK1/2-ERK1/2 ratio to wild type values. No side effects of taurine were observed. Our study indicates taurine administration as a potential therapy to ameliorate motor deficits and learning difficulties in AS.
Immunosenescence contribute to increase the blood-brain barrier (BBB) permeability, leading cognitive impairment and neurodegeneration. Thus, we investigated the anti-inflammatory effect of exercise and taurine supplementation on peripheral markers of blood-brain barrier, inflammation, and cognition of elderly women. Forty-eight elderly women (83.58±6.9 years) participated in the study, and were allocated into combined exercise training (CET: n=13), taurine supplementation (TAU: n=12), exercise training associated with taurine (CET+TAU: n=11), or control group (CG: n=12). Exercise was applied twice a week (multi-modal exercise). Taurine ingestion was 1.5g., once a day. Participants were evaluated before and after 14-weeks of intervention. Plasma levels of IL-1β, IL-1ra, IL-6, IL-10, IL-17, TNF-α, and serum concentration of S100β and neuron specific enolase (NSE) were determined. The mini mental state examination (MMSE) was also applied. Concentrations of S100β were maintained in all intervention groups, while a subtle increase in the CG was found. NSE levels increased only in TAU group (p<0.05). CET reduced TNF-α, IL-6, and IL-1β/IL-1ra, IL-6/IL10, TNF-α/IL-10 ratios (p<0.05). TAU decreased the IL-1β/IL-1ra ratio (p<0.05). MMSE score increased only in CET+TAU group (p<0.05). Multiple regression analysis showed that there was a trend for changes in IL-1β and CCI to be independently associated with changes in S100β. Exercise and taurine decreased inflammation, and maintained the BBB integrity in elderly women. Exercise emerged as an important tool to improve brain health even when started at advanced ages.
Minimal hepatic encephalopathy (MHE) is highly prevalent, observed in up to 80% of patients with liver dysfunction. Minimal hepatic encephalopathy is defined as hepatic encephalopathy with cognitive deficits and no grossly evident neurologic abnormalities. Clinical management may be delayed due to the lack of in vivo quantitative methods needed to reveal changes in brain neurobiochemical biomarkers. To gain insight into the development of alcoholic liver disease-induced neurological dysfunction (NDF), a mouse model of late-stage alcoholic liver fibrosis (LALF) was used to investigate changes in neurochemical levels in the thalamus and hippocampus that relate to behavioral changes. Proton magnetic resonance spectroscopy of the brain and behavioral testing were performed to determine neurochemical alterations and their relationships to behavioral changes in LALF. Glutamine levels were higher in both the thalamus and hippocampus of alcohol-treated mice than in controls. Thalamic levels of taurine and creatine were significantly diminished and strongly correlated with alcohol-induced behavioral changes. Chronic long-term alcohol consumption gives rise to advanced liver fibrosis, neurochemical changes in the nuclei, and behavioral changes which may be linked to NDF. Magnetic resonance spectroscopy represents a sensitive and noninvasive measurement of pathological alterations in the brain, which may provide insight into the pathogenesis underlying the development of MHE.
Molecular changes associated with neuronal aging lead to a decrease in cognitive capacity. Here we discuss these alterations at the level of brain regions, brain cells, and brain membrane and cytoskeletal proteins with an special focus in NMDA molecular changes through aging and its effect in cognitive decline and Alzheimer disease. Here, we propose that some neurodegenerative disorders, like Alzheimer's disease (AD), are characterized by an increase and acceleration of some of these changes. © 2017 Avila, Llorens-Martín,Pallas-Bazarra, Bolós, Perea, Rodríguez-Matellán and Hernández.
There is increasing evidence linking neuroinflammation to many neurological disorders including Alzheimer's disease ( AD ); however, its exact contribution to disease manifestation and/or progression is poorly understood. Therefore, there is a need to investigate neuroinflammation in both health and disease. Here, we investigate cognitive decline, neuroinflammatory and other pathophysiological changes in the APP swe × PS 1 Δe9 transgenic mouse model of AD . Transgenic ( TG ) mice were compared to C57 BL /6 wild type ( WT ) mice at 6, 12 and 18 months of age. Neuroinflammation was investigated by [ ¹⁸ F] DPA ‐714 positron emission tomography and myo ‐inositol levels using ¹ H magnetic resonance spectroscopy ( MRS ) in vivo . Neuronal and cellular dysfunction was investigated by looking at N‐acetylaspartate ( NAA ), choline‐containing compounds, taurine and glutamate also using MRS . Cognitive decline was first observed at 12 m of age in the TG mice as assessed by working memory tests . A significant increase in [ ¹⁸ F] DPA ‐714 uptake was seen in the hippocampus and cortex of 18 m‐old TG mice when compared to age‐matched WT mice and 6 m‐old TG mice. No overall effect of gene was seen on metabolite levels; however, a significant reduction in NAA was observed in 18 m‐old TG mice when compared to WT . In addition, age resulted in a decrease in glutamate and an increase in choline levels. Therefore, we can conclude that increased neuroinflammation and cognitive decline are observed in TG animals, whereas NAA alterations occurring with age are exacerbated in the TG mice. These results support the role of neuroinflammation and metabolite alteration in AD and in ageing.
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A variety of experimental studies demonstrated that neurotransmitters are an important factor for the development of the central nervous system, affecting neurodevelopmental events like neurogenesis, neuronal migration, programmed cell death, and differentiation. While the role of the classical neurotransmitters glutamate and gamma-aminobutyric acid (GABA) on neuronal development is well established, the aminosulfonic acid taurine has also been considered as possible neuromodulator during early neuronal development. The purpose of the present review article is to summarize the properties of taurine as neuromodulator in detail, focusing on the direct involvement of taurine on various neurodevelopmental events and the regulation of neuronal activity during early developmental epochs. The current knowledge is that taurine lacks a synaptic release mechanism but is released by volume-sensitive organic anion channels and/or a reversal of the taurine transporter. Extracellular taurine affects neurons and neuronal progenitor cells mainly via glycine, GABA(A), and GABA(B) receptors with considerable receptor and subtype-specific affinities. Taurine has been shown to directly influence neurogenesis in vitro as well as neuronal migration in vitro and in vivo. It provides a depolarizing signal for a variety of neuronal population in the immature central nervous system, thereby directly influencing neuronal activity. While in the neocortex, taurine probably enhance neuronal activity, in the immature hippocampus, a tonic taurinergic tone might be necessary to attenuate activity. In summary, taurine must be considered as an essential modulator of neurodevelopmental events, and possible adverse consequences on fetal and/or early postnatal development should be evaluated for pharmacological therapies affecting taurinergic functions.
Substantial evidence has shown that elevated circulating corticosteroids or chronic stress contributes to neuronal cell death, cognitive and mental disorders. However, the underlying mechanism is still unclear. Taurine is considered to protect neuronal cells from apoptotic cell death in neurodegenerative diseases and neuropsychiatric disorders. In the present study, the protective effects of taurine against corticosterone (CORT)-induced oxidative damage in SK-N-SH neuronal cells were investigated. The results showed that CORT significantly induced cell death, which was blocked by pretreatment with taurine. Similarly, pretreatment with taurine suppressed CORT-induced apoptotic cell death decreasing the levels of intracellular reactive oxygen species and improving mitochondrial function. Pretreatment with taurine increased the expression of phosphorylated extracellular regulated protein kinases (ERK) as well as the nuclear translocation of nuclear factor (erythroid 2-derived)-like 2 (Nrf2) in the CORT rich environment. Furthermore, administration of the ERK inhibitor U0126 or transient (siRNA) silencing of Nrf2 blocked the protective effects of taurine on cell viability and expression levels of Nrf2 and heme oxygenase-1 (HO-1) in the CORT model of neuronal damage. These results suggest that the Nrf2 signaling pathway may play a role in the protection mechanism of taurine against CORT-induced neuronal oxidative damage.
Diabetes is a chronic metabolic disease associated with oxidative stress, damage to biomolecules such as DNA, and neuroinflammation. Taurine, a sulfur-containing amino acid widespread in the brain, has neuroprotective properties that might prevent tissue injury and DNA damage induced by chronic hyperglycemia. We evaluated the effects of chronic taurine treatment on oxidative stress parameters, DNA damage and inflammatory markers in the frontal cortex, and hippocampus of streptozotocin-induced diabetic rats. Diabetic rats displayed increased levels of reactive oxygen species (ROS) and DNA damage in both areas, evidencing the pro-oxidant effects of diabetes in the brain. Moreover, this condition increased levels of several inflammatory mediators, such as IL-6, IL-12, TNF-γ, and IFN-α, more pronouncedly in the hippocampus. Supporting our hypothesis, taurine treatment reduced ROS, DNA damage, and inflammatory cytokine levels, providing evidence of its beneficial effects against genotoxicity and neuroinflammation associated with diabetes. Our data endorse the necessary clinical trials to evaluate the efficacy and safety of taurine supplementation in the prevention and treatment of neurochemical and metabolic alterations related to diabetes.
Lead (Pb2+) is a historically well-documented environmental neurotoxin that produces developmental cognitive learning and memory impairments. These early neurodevelopmental impairments cause increased brain excitability via disruption of Ca2+ mediated signaling during critical periods of synaptogenesis inducing competition with Ica2+ through NMDARs resulting in altered brain development and functioning across the lifespan. Interestingly, Pb2+ has been shown to decrease GABA transport and uptake, decrease spontaneous and depolarization-evoked GABA neurotransmission and lower the expression of glutamic acid decarboxylase (GAD); thereby, limiting excitatory GABAergic influences that regulate early developmental brain excitability and reducing inhibition across mature GABAergic networks. Taurine has been shown to regulate brain excitability in the mature brain through GABAAR mediated inhibition, thereby attenuating improper brain excitability. Mechanistically, taurine is developmentally a potent neuromodulator that acts as a GABAAR agonist and more recently has been reported as a partial agonist for NMDARs through glycine sites. We investigated the effects of developmental Pb2+ exposure on the rat’s mature inhibitory cognitive control abilities pharmacologically through anxiety and emotional learning-related behaviors and whether taurine could recover Pb2+ induced neurodevelopmental behavioral deficits later in life. Results showed that Pb2+ increased anxiety symptoms in the open field and hole board test, increased sensitivity to context fear training with cognitive deficits in both acquisition and extinction learning while producing learning deficits and inabilities in acquiring inhibitory learned associations through the acoustic startle response and pre-pulse inhibition (ASR-PPI) test. Interestingly, taurine recovered Pb2+ developmentally induced behavioral deficits in the open field and hole board test evidenced by decreased freezing and increased exploration behaviors and facilitated inhibitory dependent ASR-PPI learning to levels higher than controls. In contrast, Baclofen, a GABABR agonist, dose dependently showed no interaction with Pb2+ effects on ASR-PPI learning. Thus, taurine may work as an important neuromodulator at both GABAARs and NMDARs glycine sites, thereby increasing inhibition, enhancing Ca2+-mediated signaling, and decreasing the altered brain excitability, which impedes learning and memory from early Pb2+ exposure. Taken together our data suggests that GABAAR dependent inhibitory learning is altered by early Pb2+ exposure and taurine was able to recover these Pb2+ induced deficits through neuromodulation of GABAARs and potentially NMDARs later in life. These findings may pave the way for further exploration of taurine as a pharmacotherapy for neurodevelopmental lead poisoning in both animal and clinical models.
Alzheimer’s disease (AD) is the most common cause of dementia leading to severe cognitive decline. During the progression of AD, amyloid-β (Aβ) monomers aggregate into neurotoxic soluble oligomeric Aβ that causes cognitive impairments. Our previous study indicates that oral supplementation of taurine at 1000 mg/kg/day significantly ameliorates hippocampal-dependent cognitive deficits in APP/PS1 transgenic AD mouse model. However, Aβ plaques and oligomeric Aβ levels are not affected after administration of taurine and the oral dosage of taurine was relatively high. Thus, in this study, we focused on direct correlation between taurine and oligomeric Aβ, causing memory deficits in a lower oral dosage of taurine, 250 mg/kg/day. We induced AD-like cognitive impairments to adult normal mice and orally administered taurine via drinking water for 10 days. We confirmed that taurine administration improved cognitive deficits in oligomeric Aβ-infusion mice in Y-maze and passive avoidance tests without activity alteration of mice. In addition, we found that taurine directly bound to oligomeric Aβ in surface plasmon resonance analyses. Our results propose that taurine can ameliorate cognitive impairment by directly binding to oligomeric Aβ in oral administration of 250 mg/kg/day for 10 days.
Depression, a psychiatric and dysthymic disorder, severely affects the learning, work and life quality. The main pathogenesis of depression is associated with central nervous system (CNS) dysfunction. Taurine has been demonstrated to exert protective effects on the brain development and can improve learning ability and memory. Our study investigated the antidepressant-like effects of taurine pre-treatment by examining the changes in depression-like behavior, hormones, neurotransmitters, inflammatory factors and neurotrophic factors in the hippocampus of a chronic unpredictable mild stress (CUMS)-induced depressive rat model. Taurine was found to inhibit the decrease of sucrose consumption and prevent the deficiency of spatial memory and anxiety in rats exposed to CUMS, suggesting a preventive effect of taurine on depression-like behavior. Furthermore, the decreased levels of 5-hydroxytryptamine, dopamine, noradrenaline; the increased levels of glutamate, corticosterone; and the decreased expressions of fibroblast growth factor-2, vascular endothelial growth factor and brain derived neurotrophic factor in depressive rats were hindered by taurine pre-administration. However, tumor necrosis factor-α and interleukin-1β levels were not significantly changed by taurine. The results demonstrated that the anti-depressive effect of taurine may be involved in the regulation of hypothalamic-pituitary-adrenal (HPA) axis and the promotion of neurogenesis, neuronal survival and growth in the hippocampus.
As it was established that aging is not associated with massive neuronal loss, as was believed in the mid-20th Century, scientific interest has addressed the influence of aging on particular neuronal subpopulations and their synaptic contacts, which constitute the substrate for neural plasticity. Inhibitory neurons represent the most complex and diverse group of neurons, showing distinct molecular and physiological characteristics and possessing a compelling ability to control the physiology of neural circuits. This review focuses on the aging of GABAergic neurons and synapses. Understanding how aging affects synapses of particular neuronal subpopulations may help explain the heterogeneity of aging-related effects. We reviewed the literature concerning the effects of aging on the numbers of GABAergic neurons and synapses as well as aging-related alterations in their presynaptic and postsynaptic components. Finally, we discussed the influence of those changes on the plasticity of the GABAergic system, highlighting our results concerning aging in mouse somatosensory cortex and linking them to plasticity impairments and brain disorders. We posit that aging-induced impairments of the GABAergic system lead to an inhibitory/excitatory imbalance, thereby decreasing neuron's ability to respond with plastic changes to environmental and cellular challenges, leaving the brain more vulnerable to cognitive decline and damage by synaptopathic diseases.
Diabetes mellitus (DM) can result in cognitive dysfunction, but its potential metabolic mechanisms remain unclear. In the present study, we analyzed the metabolite profiling in eight different brain regions of the normal rats and the streptozotocin (STZ)-induced diabetic rats accompanied by cognitive dysfunction using a (1)H NMR-based metabolomic approach. A mixed linear model analysis was performed to assess the effects of DM, brain region and their interaction on metabolic changes. We found that different brain regions in rats displayed significant metabolic differences. In addition, the hippocampus was more susceptible to DM compared with other brain regions in rats. More interestingly, significant interaction effects of DM and brain region were observed on alanine, creatine/creatine-phosphate, lactate, succinate, aspartate, glutamate, glutamine, γ-aminobutyric acid, glycine, choline, N-acetylaspartate, myo-inositol and taurine. Based on metabolic pathway analysis, we speculate that cognitive dysfunction in the STZ-induced diabetic rats may be associated with brain region-specific metabolic alterations involving energy metabolism, neurotransmitters, membrane metabolism and osmoregulation.
Substantial evidence has shown that the oxidative damage of hippocampal neurons is associated with the cognitive impairment induced by adverse stimuli during gestation named prenatal stress (PS). Taurine, a conditionally essential amino acid, possesses multiple roles in the brain as a neuromodulator or antioxidant. In this study, to explore the roles of taurine in PS-induced learning and memory impairment, prenatal restraint stress was set up and Morris water maze (MWM) was employed for testing the cognitive function in the one-month-old rat offspring. The mitochondrial reactive oxygen species (ROS) level，mitochondrial membrane potential (MMP), ATP and cytochrome c oxidase (CcO) activity and apoptosis-related proteins in the hippocampus were detected. The activity of the Akt-cyclic AMP response element-binding protein (CREB)-peroxisome proliferator-activated receptor –γ coactivator-1α (PGC1α) pathway in the hippocampus was measured. The results showed that high dosage of taurine administration in the early postnatal period attenuated impairment of spatial learning and memory induced by PS. Meanwhile, taurine administration diminished the increase of mitochondrial ROS, reduction of MMP, ATP level and the activities of CcO, superoxide dismutase 2 (SOD2) and catalase induced by PS in the hippocampus. In addition, taurine administration recovered PS-suppressed SOD2 expression level. Taurine administration blocked PS-induced decrease of the ratio of Bcl-2/Bax and increase of the ratio of cleaved caspase-3/full-length caspase-3. Notably, taurine inhibited PS-decreased phosphorylation of Akt (pAkt) and phosphorylation of CREB (pCREB), which consequently enhanced the mRNA and protein levels of PGC1α. Taken together, these results suggest that high dosage of taurine administration during the early postnatal period can significantly improve the cognitive function in prenatally stressed juvenile rats via activating the Akt-CREB-PGC1α pathway. Therefore, taurine has therapeutic potential for prenatal stressed offspring rats in future.
Purpose:
Taurine depletion is known to induce photoreceptor degeneration and was recently found to also trigger retinal ganglion cell (RGC) loss similar to the retinal toxicity of vigabatrin. Our objective was to study the topographical loss of RGCs and cone photoreceptors, with a distinction between the two cone types (S- and L- cones) in an animal model of induced taurine depletion.
Methods:
We used the taurine transporter (Tau-T) inhibitor, guanidoethane sulfonate (GES), to induce taurine depletion at a concentration of 1% in the drinking water. Spectral-domain optical coherence tomography (SD-OCT) and electroretinograms (ERG) were performed on animals after 2 months of GES treatment administered through the drinking water. Retinas were dissected as wholemounts and immunodetection of Brn3a (RGC), S-opsin (S-cones), and L-opsin (L-cones) was performed. The number of Brn3a+ RGCs, and L- and S-opsin+ cones was automatically quantified and their retinal distribution studied using isodensity maps.
Results:
The treatment resulted in a significant reduction in plasma taurine levels and a profound dysfunction of visual performance as shown by ERG recordings. Optical coherence tomography analysis revealed that the retina was thinner in the taurine-depleted group. S-opsin+cones were more affected (36%) than L-opsin+cones (27%) with greater cone cell loss in the dorsal area whereas RGC loss (12%) was uniformly distributed.
Conclusions:
This study confirms that taurine depletion causes RGC and cone loss. Electroretinograms results show that taurine depletion induces retinal dysfunction in photoreceptors and in the inner retina. It establishes a gradient of cell loss depending on the cell type from S-opsin+cones, L-opsin+cones, to RGCs. The greater cell loss in the dorsal retina and of the S-cone population may underline different cellular mechanisms of cellular degeneration and suggests that S-cones may be more sensitive to light-induced retinal toxicity enhanced by the taurine depletion.
Both type 1 (T1DM) and type 2 diabetes mellitus (T2DM) have been associated with reduced performance on multiple domains of cognitive function and with evidence of abnormal structural and functional brain magnetic resonance imaging (MRI). Cognitive deficits may occur at the very earliest stages of diabetes and are further exacerbated by the metabolic syndrome. The duration of diabetes and glycemic control may have an impact on the type and severity of cognitive impairment, but as yet we cannot predict who is at greatest risk of developing cognitive impairment. The pathophysiology of cognitive impairment is multifactorial, although dysfunction in each interconnecting pathway ultimately leads to discordance in metabolic signaling. The pathophysiology includes defects in insulin signaling, autonomic function, neuroinflammatory pathways, mitochondrial (Mt) metabolism, the sirtuin-peroxisome proliferator-activated receptor-gamma co-activator 1α (SIRT-PGC-1α) axis, and Tau signaling. Several promising therapies have been identified in pre-clinical studies, but remain to be validated in clinical trials.
Taurine is especially abundant in rodent brain where it appears to be involved in osmoregulation and synaptic plasticity mechanisms. The demonstration of a physiological role for taurine has been hampered by the difficulty in modifying taurine levels in most tissues, including the brain. We used an experimental strategy to reduce taurine levels, involving treatment with guanidinoethyl sulfonate (GES), a structural analogue of taurine that, among other properties, acts as a competitive inhibitor of taurine transport. GES delivered in the drinking water of rats for 1 month effectively reduced taurine levels in brain structures (hippocampus, cerebellum and cortex) and outside the brain (heart, muscle, kidney, liver and plasma) by between 50 and 80 %, depending on the tissue. This partial taurine depletion did not affect either basal synaptic transmission or the late phase of long-term potentiation (late-LTP) in hippocampal slices. In vivo microdialysis studies in the hippocampus revealed that GES treatment reduced extracellular taurine levels and the magnitude of taurine released in response to the application of either N-methyl-d-aspartate (NMDA) or a hypoosmotic solution, without affecting release mechanisms. Finally, we demonstrated in hippocampal slices that a brief GES application can mimic taurine action on the conversion of a decremental LTP into a perdurable late-LTP, concluding that GES might replace taurine function in some mechanisms such as those implicated in synaptic plasticity.
Isoflurane, a commonly used inhalation anesthetic, may induce neurocognitive deficits, especially in elderly patients after surgery. Recent study demonstrated that isoflurane caused endoplasmic reticulum (ER) stress and subsequent neuronal apoptosis in the brain, contributing to cognitive deficits. Taurine, a major intracellular free amino acid, has been shown to inhibit ER stress and neuronal apoptosis in several neurological disorders. Here, we examined whether taurine can prevent isoflurane-induced ER stress and cognitive impairment in aged rats. Thirty minutes prior to a 4-h 1.3 % isoflurane exposure, aged rats were treated with vehicle or taurine at low, middle and high doses. Aged rats without any treatment served as control. The brains were harvested 6 h after isoflurane exposure for molecular measurements, and behavioral study was performed 2 weeks later. Compared with control, isoflurane increased expression of hippocampal ER stress biomarkers including glucose-regulated protein 78, phosphorylated (P-) inositol-requiring enzyme 1, P-eukaryotic initiation factor 2-α (EIF2α), activating transcription factor 4 (ATF-4), cleaved ATF-6 and C/EBP homologous protein, along with activation of apoptosis pathways as indicated by decreased B cell lymphoma 2 (BCL-2)/BCL2-associated X protein, increased expressions of cytochrome-c and cleaved caspase-3. Taurine pretreatment dose-dependently inhibited isoflurane-induced increase in expression of ER stress biomarkers except for P-EIF2α and ATF-4, and reversed isoflurane-induced changes in apoptosis-related proteins. Moreover, isoflurane caused spatial working memory deficits in aged rats, which were prevented by taurine pretreatment. The results indicate that taurine pretreatment prevents anesthetic isoflurane-induced cognitive impairment by inhibiting ER stress-mediated activation of apoptosis pathways in the hippocampus in aged rats.
Saliva is a biofluid that is sensitive to metabolic changes and is straightforward to collect in a non-invasive manner, but it is seldom used for metabolite analysis when studying neurodegenerative disorders. We present a procedure for both an untargeted and targeted analysis of the saliva metabolome in which nuclear magnetic resonance (NMR) spectroscopy is used in combination with multivariate data analysis. The applicability of this approach is demonstrated on saliva samples selected from the 25-year prospective Betula study, including samples from dementia subjects with either Alzheimer's disease (AD) or vascular dementia at the time of sampling or who developed it by the next sampling/assessment occasion five years later, and age-, gender-, and education-matched control individuals without dementia. Statistically significant multivariate models were obtained that separated the patients with dementia from controls and revealed seven discriminatory metabolites. Dementia patients showed significantly increased concentrations of acetic acid (fold change (fc)=1.25, p=2[times]10-5), histamine (fc=1.26, p=0.019), and propionate (fc=1.35, p=0.002), while significantly decreased levels were observed for dimethyl sulfone (fc=0.81, p=0.005), glycerol (fc=0.79, p=0.04), taurine (fc=0.70, p=0.007), and succinate (fc=0.62, p=0.008). Histamine, succinate, and taurine are known to be important in AD, and acetic acid and glycerol are involved in related pathways. Dimethyl sulfone and propionate originate from the diet and bacterial flora and might reflect poorer periodontal status in the dementia patients. For these seven metabolites, a weak but statistically significant pre-diagnostic value was observed. Taken together, we present a robust and general NMR analysis approach for studying the saliva metabolome that has potential use for screening and early detection of dementia.
A reduction in taurine content accompanies the ageing process in many tissues. In fact, the decline of brain taurine levels has been associated with cognitive deficits whereas chronic administration of taurine seems to ameliorate age-related deficits such as memory acquisition and retention. In the present study, using rats of three age groups (young, adult and aged) we determined whether the content of taurine and other amino acids (glutamate, serine, glutamine, glycine, alanine and GABA) was altered during ageing in different brain areas (cerebellum, cortex and hippocampus) as well non-brain tissues (heart, kidney, liver and plasma). Moreover, using hippocampal slices we tested whether ageing affects synaptic function and plasticity. These parameters were also determined in aged rats fed with either taurine-devoid or taurine-supplemented diets. With age, we found heterogeneous changes in amino acid content depending on the amino acid type and the tissue. In the case of taurine, its content was reduced in the cerebellum of adult and aged rats, but it remained unchanged in the hippocampus, cortex, heart and liver. The synaptic response amplitude decreased in aged rats, although the late phase of long-term synaptic potentiation (late-LTP), a taurine-dependent process, was not altered. Our study highlights the stability of taurine content in the hippocampus during ageing regardless of whether taurine was present in the diet, which is consistent with the lack of changes detected in late-LTP. These results indicate that the beneficial effects of taurine supplementation might be independent of the replenishment of taurine stores.