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Alzheimer's disease, AD, is the most common form of dementia. AD initially targets memory and progressively destroys the mind. The brain atrophies as the neocortex suffers neuronal, synaptic, and dendritic losses, and the hallmark amyloid plaques and neurofibrillary tangles proliferate. Pharmacological management, at best, is palliative and transie...
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Citations
... Furthermore, the negative effects of a diet high in methionine but low in folate and vitamins B6/B12 on brain function in mice were previously reported, demonstrating significant short-term memory loss and increased neuronal degeneration (Nuru et al., 2018). Furthermore, blood vitamin B12 levels may influence memory by influencing plasma levels of choline and betaine (Kidd, 2008;Nurk et al., 2013). Vitamin B12 is involved in pathways that regulate the methylation of genes related to memory and cognitive functions at different stages of brain development (Bekdash, 2019). ...
Background
Transient global amnesia (TGA), which is described as short-term amnesia, may be influenced by some dietary components involved in brain function. The aim of the present study was to assess the connection between TGA and dietary intake of vitamin B12.
Methods
This cross-sectional study was conducted on 258 people with TGA and 520 people without TGA in Sabzevar, Iran. All participants were screened for TGA (ICD-10 code: G45.4). A validated Food Frequency Questionnaire (FFQ) was utilized to estimate the dietary intake of vitamin B12. Different models of logistic regression were used to determine the association between TGA and dietary intake of vitamin B12 after adjusting the confounders.
Results
There was an inverse association between the risk of TGA and the intake of vitamin B12 (OR = 0.94, CI 95%: 0.89–0.99, p = .02, effect size: −0.04). The result did not change after adjustment for age, gender, education, job, and marital status (OR = 0.93, CI 95%: 0.88–0.98, p = .01, effect size: −0.03). The result remained significant after additional adjustments for body mass index (BMI) and physical activity (OR = 0.94, CI 95%: 0.89–0.99, p = .03, effect size: −0.04), and after further adjustments for the underlying diseases, including diabetes, hypertension, and stroke (OR = 0.86, CI 95%: 0.81–0.92, p < .01, effect size: −0.10).
Conclusion
Vitamin B12 deficiency may increase the risk of TGA and should be considered as a potential concern for people at risk for TGA. Further studies are needed to validate these findings and to discover the underlying mechanisms of the effects of vitamin B12 on TGA.
... 14 Timely detection of cognitive decline can facilitate early interventions and support involvement in clinical trials for AD/ADRD. [15][16][17][18] Electronic health records (EHRs), particularly clinical notes, are crucial resources for identifying early indicators of disease, yet traditional diagnostic tools and variability in screening practices complicate detection. [19][20][21][22] NLP provides a promising solution by efficiently analysing large datasets and identifying subtle signs of decline that traditional diagnostics may miss. ...
Background
Large language models (LLMs) have shown promising performance in various healthcare domains, but their effectiveness in identifying specific clinical conditions in real medical records is less explored. This study evaluates LLMs for detecting signs of cognitive decline in real electronic health record (EHR) clinical notes, comparing their error profiles with traditional models. The insights gained will inform strategies for performance enhancement.
Methods
This study, conducted at Mass General Brigham in Boston, MA, analysed clinical notes from the four years prior to a 2019 diagnosis of mild cognitive impairment in patients aged 50 and older. We developed prompts for two LLMs, Llama 2 and GPT-4, on Health Insurance Portability and Accountability Act (HIPAA)-compliant cloud-computing platforms using multiple approaches (e.g., hard prompting, retrieval augmented generation, and error analysis-based instructions) to select the optimal LLM-based method. Baseline models included a hierarchical attention-based neural network and XGBoost. Subsequently, we constructed an ensemble of the three models using a majority vote approach. Confusion-matrix-based scores were used for model evaluation.
Findings
We used a randomly annotated sample of 4949 note sections from 1969 patients (women: 1046 [53.1%]; age: mean, 76.0 [SD, 13.3] years), filtered with keywords related to cognitive functions, for model development. For testing, a random annotated sample of 1996 note sections from 1161 patients (women: 619 [53.3%]; age: mean, 76.5 [SD, 10.2] years) without keyword filtering was utilised. GPT-4 demonstrated superior accuracy and efficiency compared to Llama 2, but did not outperform traditional models. The ensemble model outperformed the individual models in terms of all evaluation metrics with statistical significance (p < 0.01), achieving a precision of 90.2% [95% CI: 81.9%–96.8%], a recall of 94.2% [95% CI: 87.9%–98.7%], and an F1-score of 92.1% [95% CI: 86.8%–96.4%]. Notably, the ensemble model showed a significant improvement in precision, increasing from a range of 70%–79% to above 90%, compared to the best-performing single model. Error analysis revealed that 63 samples were incorrectly predicted by at least one model; however, only 2 cases (3.2%) were mutual errors across all models, indicating diverse error profiles among them.
Interpretation
LLMs and traditional machine learning models trained using local EHR data exhibited diverse error profiles. The ensemble of these models was found to be complementary, enhancing diagnostic performance. Future research should investigate integrating LLMs with smaller, localised models and incorporating medical data and domain knowledge to enhance performance on specific tasks.
Funding
This research was supported by the National Institute on Aging grants (R44AG081006, R01AG080429) and National Library of Medicine grant (R01LM014239).
... Mild cognitive impairment (MCI), as an early stage of cognitive decline, also increases the number of patients. Although MCI patients can still maintain basic self-care abilities in daily life, they have shown mild cognitive impairment in areas such as memory, attention, and executive function [2]. If effective intervention measures are not taken, MCI patients have a higher risk of progressing to more severe dementia, such as Alzheimer's disease (AD), which not only seriously affects the quality of life of patients, but also brings a heavy burden of care to families and society [3]. ...
This study aims to evaluate the impact of unarmed strength training on the cognitive function of middle-aged and elderly patients with mild cognitive impairment (MCI). The study subjects are 60 elderly male MCI patients from the Community Health Service Center in Hangzhou, with an age range of 66±5 years. The participants were randomly divided into two groups: the control group and the intervention group. The control group did not receive any intervention measures, while the intervention group underwent a 12-week unarmed strength training program. Before and after the study, the Montreal Cognitive Assessment Scale (MoCA) was used to assess the changes in cognitive function of the subjects. The data analysis was conducted using SPSS 23.0 software, and t-tests and chi-square tests were used for inter-group comparisons based on the distribution characteristics of the data. After 12 weeks of unarmed training, the MoCA score of the intervention group at T2 was significantly higher than that of the control group (P<0.05), indicating that the cognitive function of the intervention group had significantly improved. Unarmed strength training has a positive impact on the cognitive function of middle-aged and elderly MCI patients, and a 12-week training program can effectively improve the cognitive ability of this group.
... Alzheimer's disease (AD) and related dementias (ADRD), the sixth leading cause of death in the US, affect 5.7 million Americans, with projections estimating an increase to 13 million by 2060. 1 The progression of AD/ADRD significantly diminishes patient quality of life and places substantial emotional and financial strain on families, communities, and healthcare systems, 2 with care costs anticipated to reach $1.1 trillion by 2050. 3 Existing treatments, which only temporarily alleviate symptoms and decelerate progression, 4 underscore the urgent need for breakthroughs in AD/ADRD therapy. 5 Cognitive decline, characterized by noticeable deficits in cognitive functions beyond what might be expected from normal aging 6 serves as a key early sign of AD/ADRD, 7 emphasizing the necessity of timely detection for slowing disease advancement, facilitating involvement in clinical trials, and initiating early interventions. 8,9 Electronic health records (EHRs) provide comprehensive, both real-time and historical, patient data, making them a critical resource for identifying cognitive decline. ...
... Many existing studies focused on using AI techniques to predict later stage of cognitive decline 7,9,[32][33][34] 36 integrated NLP techniques to identify cognitive decline using both structured and unstructured EHR data, and achieved an AUROC of 0.68 meanwhile ranked important predictors from both structured data and unstructured data. Compared with existing studies, our study achieved state-of-the-art performance (precision 0.90, recall 0.94, and f1 score 0.92) meanwhile identified keywords that were missed by experts and traditional AI models. ...
Background: Early detection of cognitive decline in elderly individuals facilitates clinical trial enrollment and timely medical interventions. This study aims to apply, evaluate, and compare advanced natural language processing techniques for identifying signs of cognitive decline in clinical notes.
Methods: This study, conducted at Mass General Brigham (MGB), Boston, MA, included clinical notes from the 4 years prior to initial mild cognitive impairment (MCI) diagnosis in 2019 for patients ≥ 50 years. Note sections regarding cognitive decline were labeled manually. A random sample of 4,949 note sections filtered with cognitive functions-related keywords were used for traditional AI model development, and 200 random subset were used for LLM and prompt development; another random sample of 1996 note sections without keyword filtering were used for testing. Prompt templates for large language models (LLM), Llama 2 on Amazon Web Service and GPT-4 on Microsoft Azure, were developed with multiple prompting approaches to select the optimal LLM-based method. Baseline comparisons were made with XGBoost and a hierarchical attention-based deep neural network model. An ensemble of the three models was then constructed using majority vote.
Results: GPT-4 demonstrated superior accuracy and efficiency to Llama 2. The ensemble model outperformed individual models, achieving a precision of 90.3%, recall of 94.2%, and F1-score of 92.2%. Notably, the ensemble model demonstrated a marked improvement in precision (from a 70%-79% range to above 90%) compared to the best performing single model. Error analysis revealed 63 samples were wrongly predicted by at least one model; however, only 2 cases (3.2%) were mutual errors across all models, indicating diverse error profiles among them.
Conclusion: Our findings indicate that LLMs and traditional models exhibit diverse error profiles. The ensemble of LLMs and locally trained machine learning models on EHR data was found to be complementary, enhancing performance and improving diagnostic accuracy.
... The group that participated the least in midand high-intensity exercises was 0.65 times more likely to be at risk of cognitive dysfunction than the group that participated the most [60]. Those who were more active, especially those who exercised more than three times a week, were at a lower risk of developing dementia [61]. ...
Background: The purpose of this study was to investigate the effect of circuit training on β-amyloid, BDNF, and cognitive function in untrained obese elderly Korean women. Methods: The subjects for the study were aged 65–70 years and were each assigned to a circuit training group (EG, n = 12) or a control group (CG, n = 11). The 60 min combined exercise was performed 3 times per week for 16 weeks. The exercise intensity was progressively increased from a 40% heart rate reserve to a 70% heart rate reserve. The test data were analyzed using a paired t-test, an independent t-test, and a two-way repeated measures ANOVA, and an alpha level of 0.05 was set for all tests of significance. Results: Group-by-time interaction effects were observed for β-amyloid (p < 0.05), brain-derived neurotrophic factor (p < 0.01), and cognitive function (p < 0.05). Within the exercise group, significant differences were found in β-amyloid (p < 0.05), brain-derived neurotrophic factor (p < 0.001), and cognitive function (p < 0.05) when comparing across different time points. Additionally, there were statistically significant differences between groups in post-exercise β-amyloid (p < 0.05), change in β-amyloid (p < 0.05), brain-derived neurotrophic factor (p < 0.01), and cognitive function (p < 0.05). Conclusions: Therefore, it is suggested that the circuit training used in this study could be an effective exercise method for improving the risk factors of cognitive impairment in obese elderly Korean women.
... The group that participated the least in mid-and high-intensity exercises was 0.65 times more likely to be at risk of cognitive dysfunction than the group that participated the most [59]. Those who were more active, especially those who exercised more than three times a week, were at a lower risk of developing dementia [60]. ...
The purpose of this study was to investigate the effect of circuit training on β-amyloid, BDNF, and cognitive function in untrained obese elderly Korean women. The subjects for the study were aged 65–70 years, composed of the circuit training group(n=12) and control group(n=11). The 60-minute combined exercise was performed 3 times per week for 16 weeks. Exercise intensity was progressively increased from 40% HRR to 70% HRR. The test data were analyzed by paired t-test, independent t-test, and two-way repeated measures ANOVA, and the alpha level of .05 was set for all tests of significance. The findings of this study were as follows: β-amyloid significantly decreased after the exercise group had compared to before the exercise and BDNF and cognitive function significantly increased after the exercise group had compared to before the exercise. However, there were no significant changes in β-amyloid, BDNF, and cognitive function in the control group Therefore, it is suggested that the circuit training used in this study could be an effective exercise method for improving the risk factors of cognitive impairment in obese elderly Korean women.
... Numerous therapeutics strategies explored under clinical trials for several decades, nonetheless still curative therapies are under development and currently primarily treatment for symptoms available. As per collected data in world, because of modifiable risk factors, around 30% of AzD cases could provide promising and enhancing target using prevention strategies to decline AzD causing cognitive damages [17]. ...
Alzheimer's disease (AzD) is the most common type of dementia among older adults, with a progressive disorder of brain that affect thinking ability, behavior, and memorizing capability. It is the most common cause of dementia in older adults, accounting for approximately 60%–80% of all cases of dementia. The exact cause of AzD is yet not fully understood, however several reports indicate that a combinations of genetic, environmental, and lifestyle factors contribute to the development and progression of AzD. The risk factors associated with AzD are age, family history, head injuries, high blood pressure, and high cholesterol. Moreover, the abnormal deposition of protein (β-amyloid plaques and tau tangles) in brain lead to the mortality of brain cells and gradual decline of cognitive functions. Currently, there is no complete cure for AzD available, however advancement in drug delivery system developed several treatment strategies that can help manage symptoms and slow the progression of the disease. The management strategies include medications to improve cognitive function, behavioral and environmental modifications, and support for caregivers and family members. Recently nanotechnology have gained significant attention among researcher in management of AzD although the drug diffusion to blood brain barriers presents several difficulty. Carrier-based drug delivery presents promising alternative to deliver medicament to the brain. Several carrier-based drug delivery reported such as liposomes, nanocrystals, nanoemulsions, dendrimers, polymer-protein/drug conjugates, nanoparticles, antibody conjugated drugs, nanotubes, nanogels, and micelles are included in this chapter for the management AzD. While the use of nanotechnology in AzD is still in early stages of research, it holds great promise for the fabrication of pharmaceuticals in management of this devastating disease.
... After the publication of this first finding, the term "AD" was described by the German psychiatrist Emil Kraepelin. In this first case of AD, the patient had delusional jealousy about her husband (Kidd, 2008). Then, an impairment has been detected in high brain functions, mainly memory. ...
Alzheimer’s Disease (AD) is an irreversible neurological disease that progresses with disruption in cognitive functions depending on age, decreasing incompetence in performing the basic activities of the daily life and with fluctuations in personality characteristics (Castellani, Rolston, & Smith, 2010). The hypotheses in this con-text are the Amyloid Cascade Hypothesis, Cholinergic Hypothe-sis, and Excitotoxicity Hypothesis. Intracellular neurofibrillary tangle accumulation and extracellular amyloid beta (Aβ) protein accumulation leads to the amyloid cascade hypothesis. Then, the Ca+2 homeostasis disruption causes neuronal damage because of free radical and inflammation formation. In the second hypothesis (the Cholinergic Hypothesis), the nerve stimuli transmission be-comes worse because of acetylcholine reduction that occurs as a result of reduced choline acetyltransferase (ChAT) activity and acetylcholine esterase (AChE) activity that is increased (Parihar & Hemnani, 2004). In the pathogenesis of dementia, cholinergic system dysfunction (cholinergic cell losses in the basal forebrain and hippocampus included) has an important place (Becker, Giacobini, Elble, McIlhany, & Sherman, 1988; Guo, Shen, Meng, Yang, & Li, 2016). As a result of these basic hypotheses, besides cognitive impairment due to AD, it is thought that possible pe-ripheral pathological involvements also reduce the quality of life and prepare the ground for mortality. The Aβ peptide accumulates to form long, unresolved fibrils in other peripheral tissues (includ-ing the skin and muscle) as well as in the brain. It has been re-ported that the known form of Aβ (Aβ42) found in brains from AD patients is also significantly increased in skeletal muscles of patients (Mukhamedyarov et al., 2014). In AD, it has been con-sidered that the anomalies observed widely in the energy metabo-lism due to dysfunction of mitochondria might be presented as a testable hypothesis as a biological explanation of the disruptions that occur in both muscle and cognitive functions (Burkholder, Fingado, Baron, & Lieber, 1994). The mitochondrial anomalies like the disruptions in the cytochrome C oxidase activity, structur-al defects and mitochondrial DNA deletions were also detected in the muscles of the ICM patients (Horvath et al., 1998; Moslemi, Lindberg, & Oldfors, 1997; Oldfors et al., 2006). Boncompagni et al. conducted a study and showed that there were mitochondrial anomalies by analysing the redox status and the changing tricar-boxylic acid (TCA) cycle activity in the muscles obtained from rats by using electron microscope (Boncompagni et al., 2012). Askanas et al. showed similar mitochondrial anomalies in the normal muscle cells to which βAPP gene transfer was performed in adenoviruses (Askanas et al., 1996). Aβ is a peptide found anywhere in both the brain and the periphery and has been shown to be toxic to a variety of tissues including cellular blood (such as erythrocytes, lymphocytes), fibroblasts, and muscles (Mukhamedyarov et al., 2014). Studies have shown that muscle disorders associated with AD can affect both skeletal and cardiac myocytes (Mukhamediarov et al., 2011; Turdi et al., 2009). It is thought that loss of muscle function besides diminishing cognitive functions makes an important contribution to the inability to per-form the basic activities of daily life in AD. It has been recently considered that muscle disorders may be an internal aspect of AD. Studies on the detection of body mass using brain magnetic reso-nance imaging (MR) and dual-energy X-ray absorptiometry (DEXA) have shown that loss of lean muscle mass is accelerated in patients with AD and is associated with hippocampal atrophy and cognitive impairment (Burns, Johnson, Watts, Swerdlow, & Brooks, 2010).
In a study using conventional electrophysiological techniques to investigate the effects and mechanisms of βAP on the resting membrane of skeletal muscle fibers of the frog, it was shown that βAP disrupted the resting membrane potential of skeletal muscle fibers by leading to a marked depolarization on skeletal muscle plasma membrane and also this was due to both the inhibition of Na+/K+-ATPase and the formation of βAP-pores. The formation of βAP-pores causes increased membrane permeability. It has been reported that βAP-induced depolarization of skeletal muscle plasma membranes can significantly disturb the functioning of skeletal muscles and therefore contribute to motor dysfunction observed in AD and other disorders associated with βAP accu-mulation (Mukhamedyarov, Grishin, Yusupova, Zefirov, & Palotas, 2009). In another study of genetically engineered (trans-genic) AD rats, it has been reported that the electrical activity of diaphragm muscle fibers impairs and these motor impairments may play an important key role in decreased activity of daily life in AD, and that consideration of muscle pathophysiology may improve the quality of life in AD (Mukhamedyarov et al., 2014). Despite the neuropathologic criteria of the AD, its diagnosis is made by investigating other reasons that might cause dementia and secondary reasons. For this reason, specific biomarkers are needed in the AD. In this section, the hypotheses that have been claimed until our present day about the pathology of the AD and the reflection of the AD into the periphery were compared. By doing this, the aim was to attract attention to the importance of the pathological changes in the vascular dementia and pathologic changes in periphery in differential diagnosis and treatment of the AD.
... ALCAR is the short-chain ester of the carnitine L-isomer, which is available in some countries as a registered drug and in others as a nutraceutical [8]. ALCAR can transport fatty acids in the cell's cytoplasm into the mitochondria, providing a substrate for ATP generation [8,31]. In the brain, ALCAR is transported across the blood-brain barrier (BBB), which is significant for the energy balance in the brain [8,31]. ...
... ALCAR can transport fatty acids in the cell's cytoplasm into the mitochondria, providing a substrate for ATP generation [8,31]. In the brain, ALCAR is transported across the blood-brain barrier (BBB), which is significant for the energy balance in the brain [8,31]. There are several studies on the effects of ALCAR on neurons. ...
Peripheral neuropathies caused by the peripheral nervous system (PNS) damage can occur due to trauma and other disorders. They present as altered sensation, weakness, autonomic symptoms, and debilitating pain syndrome with a wide range of clinical signs. Acetyl-L-Carnitine (ALCAR) is a biological compound with essential roles in mitochondrial oxidative metabolism and anti-oxidant effects that protects mitochondria from oxidative damage and inhibits apoptosis caused by mitochondrial damage. This study is a systematic review and meta-analysis of the effects of ALCAR on peripheral nerve injuries. This review examines studies on treating traumatic peripheral neuropathies in which ALCAR is administered to rats with sciatic nerve injury with an appropriate control group. The articles were divided based on the mode of ALCAR administration. If one method was used in more than one article, their results were entered in the "Revman5.4" software and were meta-analyzed. Studies were selected from 1994 to 2018 on rats with varying physical injuries to their sciatic nerves. In one study, ALCAR was provided to rats in their drinking water, while in other studies, ALCAR was injected intra-peritoneally. Different mechanisms of ALCAR actions have been suggested in this study, but the underpinnings of the neuroprotective effects of ALCAR are still unclear. Further studies are mandatory to clarify the actual mechanisms of the neuroprotective activity of ALCAR. Based on the results of existing studies, ALCAR effectively increases the tolerance threshold of thermal and mechanical stimuli, reduces latency, and reduces apoptosis; finally, adjusting the dose and duration of administration may increase the dose and duration axon diameter.
... Dementia relates to loss of memory and some other intellectual capacity that affects daily tasks. The frequency of dementia is growing globally, and it has become a serious societal concern as the older population has grown [3]. ...
Materials and methods:
Oral acute toxicity studies were performed to evaluate the toxicological effects of europinidin in animals. In this study, four different animal groups (n = 6) were used. Group I was the normal control, group II was the STZ-induced diabetes control, group III was STZ + europinidin-treated (10 mg/kg), and group IV was STZ + europinidin-treated (10 mg/kg). The efficacy of europinidin at a dose of 10 mg/kg and 20 mg/kg was studied with single-dose administration of streptozotocin, which experimentally induced memory impairments in Wistar male rats for 38 days. The mean body weight and blood glucose levels were recorded at the initial and end of the study. The two behavioural paradigms (Y-maze and Morris water maze) were performed to evaluate spatial and working memory in rats. The biochemical parameters such as acetylcholinesterase, choline acetyltransferase, superoxide dismutase, glutathione transferase, malonaldehyde, catalase, and nitric oxide level as hallmarks of oxidative stress were measured. Additionally, the proinflammatory parameters were also determined to evaluate the neuroinflammatory responses associated with streptozotocin such as tumor necrosis factor-alpha (TNF-α) interleukin-1β (IL-1β), interleukin (IL-6), nuclear factor-kappa B (NF-ƙB), interleukin (IL-10), and nuclear factor-erythroid factor 2-related factor 2 (Nrf2) in the perfused brain.
Results:
The rats in the europinidin-treated group exhibited a significant restoration of body weight and blood glucose level as compared with the streptozotocin control group. Furthermore, europinidin significantly modulated the spatial and working memory in rats, when assessed through behavioural paradigms. Streptozotocin caused a significant alteration in biochemical, neuronal enzymatic, and neuroinflammatory parameters, which were significantly restored to normal levels by europinidin.
Conclusion:
The present study attributed the neuroprotective efficacy of europinidin in experimental animal models by subsiding the several biomarkers of oxidative stress, neuroinflammation, and neuronal enzymatic activities.
