Nutritional Neuroscience (Nutr Neurosci)

Publisher: Maney Publishing

Journal description

Nutritional Neuroscience is an international, interdisciplinary broad-based journal for reporting both basic and clinical research in the field of nutrition that relates to the central and peripheral nervous system. Studies may include the role of different components of normal diet (protein, carbohydrate, fat, moderate use of alcohol, etc.), dietary supplements (minerals, vitamins, hormones, herbs, etc.), and food additives (artificial flavors, colors, sweeteners, etc.) on neurochemistry, neurobiology, and behavioral biology of all vertebrate and invertebrate organisms. Ideally this journal will serve as a forum for neuroscientists, nutritionists, neurologists, psychiatrists, and those interested in preventive medicine.

Current impact factor: 2.11

Impact Factor Rankings

2015 Impact Factor Available summer 2015
2013 / 2014 Impact Factor 2.114
2012 Impact Factor 1.647
2011 Impact Factor 1.563
2010 Impact Factor 1.301
2009 Impact Factor 1.143
2008 Impact Factor 1.092

Impact factor over time

Impact factor
Year

Additional details

5-year impact 1.83
Cited half-life 7.10
Immediacy index 0.30
Eigenfactor 0.00
Article influence 0.53
Website Nutritional Neuroscience website
Other titles Nutritional neuroscience (Online)
ISSN 1476-8305
OCLC 50166447
Material type Document, Periodical, Internet resource
Document type Internet Resource, Computer File, Journal / Magazine / Newspaper

Publisher details

Maney Publishing

  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author cannot archive a post-print version
  • Restrictions
    • 12 months embargo for STEM (science, technology, engineering and medicine) journals
    • 2 years embargo for HSS (humanities and social science) journals
  • Conditions
    • Authors' pre-print on author's personal website or institutional website, or institutional repository, or subject-based repository
    • Author's post-print on institutional repository, or subject-based repository
    • Must link to publisher version with DOI
    • Publisher copyright and source must be acknowledged with citation
    • On a non-profit server
  • Classification
    ​ yellow

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: Objective To determine the association in amount of daily coffee consumption with incidence of stroke in a broad cohort, considering other vascular risk factors. Methods We utilized the Third National Health and Nutrition Examination Survey (1988-1994; NHANES III) data on participants aged ≥17 years old to examine coffee consumption and stroke. Multivariate logistic regression models related the amount of coffee use reported in a food frequency questionnaire with stroke, controlling for other vascular risk factors. Results Of 33 994 NHANES III subjects, coffee consumption and stroke data in adults ≥17 years old were available in 19 994. Daily coffee consumption ranged from 0 to 20 (median 1) cups and 644 (3.2%) participants had a stroke diagnosed by a physician. Coffee intake varied with age, gender, and ethnicity (P < 0.001). Interestingly, heart failure, diabetes, and hypertension were less frequent, and high cholesterol more frequent in those consuming ≥3 cups per day (P < 0.001). Smoking was more frequent in all coffee drinkers (P < 0.0001). Multivariate analyses revealed an independent effect of heavier coffee consumption (≥3 cups/day) on reduced stroke (OR 0.44, 95% CI 0.22-0.87, P < 0.02) in healthy subjects that was attenuated by vascular risk factors (OR 0.78, 95% CI 0.58-1.07, P ≈ 0.12). Conclusion Heavier daily coffee consumption is associated with decreased stroke prevalence, despite smoking tendency in heavy coffee drinkers.
    Nutritional Neuroscience 06/2015; DOI:10.1179/1476830515Y.0000000035
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    ABSTRACT: Western-style diets high in saturated fat and refined carbohydrate have been shown to alter gut microbiota as well as being associated with altered behaviour and learning ability. The objective of this study was to determine the effects of short-term intake of a Western-style diet on intestinal cytokine expression, tryptophan metabolism, and levels of neurotransmitters in the brain. At 7 weeks of age, 129S1/SvImJ mice were placed on a standard chow or Western-style diet (fat 33%, refined carbohydrates 49%) for 3 weeks. Anxiety-like behaviour was assessed by the latency to step-down test and exploration assessed in a Barnes maze. Neurotransmitter levels in forebrains were analysed by high-pressure liquid chromatography. Liver metabolism was examined by (1)H nuclear magnetic resonance (NMR). Cytokine expression in the intestine was measured using MesoScale discovery platform. mRNA levels of tryptophan hydroxylase (Tph) and indoleamine 2,3-dioxygenase (IDO) in the brain and intestine were measured using qPCR. Results showed that mice fed the Western diet displayed reduced exploratory and anxiety-like behaviour. Anxiolytic effects correlated with increased hippocampal brain-derived neurotrophic factor (BDNF) and tryptophan levels. Brain serotonin was not altered. These changes were associated with reduced expression of small intestinal indoleamine 2,3-dioxygenase, a tryptophan-processing enzyme. Western diet-fed mice exhibited low-grade systemic and intestinal inflammation along with altered liver metabolic profiles. In conclusion, diets high in fat and refined sugar are associated with increased levels of brain BDNF and tryptophan and decreased exploratory and anxiety-like behaviour. These behavioural changes correlated with altered intestinal tryptophan metabolism and liver metabolic profiles.
    Nutritional Neuroscience 06/2015; DOI:10.1179/1476830515Y.0000000034
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    ABSTRACT: Objective The consumption of hyperlipidic diets has grown markedly in recent decades, and several studies have linked this consumption with the development of neurodegenerative diseases. Conversely, hyperlipidic diets have been used as an alternative therapy for refractory epilepsy. The purpose of this study was to evaluate the effects of a hyperlipidic diet on brain electrical activity before and during status epilepticus (SE) using computational and mathematical methods. Methods Electrocorticogram (ECoG) was recorded in Wistar rats fed with standard and hyperlipidic diets. Each recording was obtained during 30-minute period (baseline), after this time, the SE was induced by pilocarpine, and recording was continued for another 30 minutes. The ECoG signals were analyzed by the following methods: power spectrum, Lempel-Ziv complexity (LZC), and fractal dimension of the phase space. Results Hyperlipidic diet in normal animals caused a decrease in the theta, alpha, and beta rhythm, and reduced the LZC of the brain electrical activity. However, when the animals were induced to SE, these differences between nutritional groups were not observed. SE caused in both dietary groups increase in theta, alpha, and beta rhythm values, and increase in the complexity of brain electrical activity. Discussion Hyperlipidic diet consumption attenuated the brain's electrical activity, suggesting that healthy individuals who habitually eat a hyperlipidic diet may develop dysfunctions such as cognitive decline and memory impairment. Furthermore, the antagonistic effect between hyperlipidic diet and SE suggests that this diet could protect against seizures.
    Nutritional Neuroscience 06/2015; DOI:10.1179/1476830515Y.0000000033
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    ABSTRACT: Objectives Adequate choline supply during the perinatal period is critical for proper brain formation, when robust neurogenesis and neuronal maturation occur. Therefore, the objective of this study was to examine the impact of perinatal choline status on neurodevelopment. Methods Sows were fed a choline-deficient (CD) or choline-sufficient (CS) diet during the last half of the gestational period. At 2 days of age, piglets from sows within each prenatal treatment group were further stratified into postnatal treatment groups and provided either a CD or CS milk replacer, resulting in four treatment groups. At 30 days of age, piglets underwent magnetic resonance imaging (MRI) procedures to analyze structural and metabolite differences. Results Single-voxel spectroscopy (SVS) analysis revealed postnatally CS piglets had higher (P < 0.001) concentrations of glycerophosphocholine-phosphocholine than postnatally CD piglets. Volumetric analysis indicated smaller (P < 0.006) total brain volumes in prenatally CD piglets compared with prenatally CS piglets. Differences (P < 0.05) in the corpus callosum, pons, midbrain, thalamus, and right hippocampus, were observed as larger region-specific volumes proportional to total brain size in prenatally CD piglets compared with CS piglets. Diffusion tensor imaging (DTI) suggested interactions (P < 0.05) between prenatal and postnatal choline status in fractional anisotropy values of the thalamus and right hippocampus. Prenatally CS piglets had lower cerebellar radial diffusivity (P = 0.045) compared with prenatally CD piglets. Discussion This study demonstrates that prenatal choline deficiency has profound effects by delaying neurodevelopment as evidenced by structural and metabolic MRI assessments.
    Nutritional Neuroscience 06/2015; DOI:10.1179/1476830515Y.0000000031
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    ABSTRACT: Background and objectives Studies in humans and animal models have established a close relationship between early environment insult and subsequent risk of development of non-communicable diseases, including the cardiovascular. Whereas experimental evidences highlight the early undernutrition and the late cardiovascular disease relation, the central mechanisms linking the two remain unknown. Owing to the oxidative balance influence in several pathologies, the aim of the present study was to evaluate the effects of maternal undernutrition (i.e. a low-protein (LP) diet) on oxidative balance in the brainstem. Methods and results Male rats from mothers fed with an LP diet (8% casein) throughout the perinatal period (i.e. gestation and lactation) showed 10× higher lipid peroxidation levels than animals treated with normoprotein (17% casein) at 100 days of age. In addition, we observed the following reductions in enzymatic activities: superoxide dismutase, 16%; catalase, 30%; glutathione peroxidase, 34%; glutathione-S-transferase, 51%; glutathione reductase, 23%; glucose-6-phosphate dehydrogenase, 31%; and in non-enzymatic glutathione system, 46%. Discussion This study is the first to focus on the role of maternal LP nutrition in oxidative balance in a central nervous system structure responsible for cardiovascular control in adult rats. Our data observed changes in oxidative balance in the offspring, therefore, bring a new concept related to early undernutrition and can help in the development of a new clinical strategy to combat the effects of nutritional insult. Wherein the central oxidative imbalance is a feasible mechanism underlying the hypertension risk in adulthood triggered by maternal LP diet.
    Nutritional Neuroscience 06/2015; DOI:10.1179/1476830515Y.0000000030
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    ABSTRACT: Background Among various types of polyunsaturated fatty acid (PUFA), omega-3 fatty acids play a crucial role in development and function of the brain. This study was undertaken to investigate the possible neuroprotective efficacy of omega-3 fatty acid on lead-induced neurotoxicity in rats. Material and methods The experiment was carried out on 32 male Wistar rats divided into four groups. The first group (control) was treated with distilled water and second group with lead acetate at the doses of 3 mg/kg b.wt. (body weight)/oral, whereas third and fourth groups were simultaneously treated with lead acetate (3 mg/kg b.wt.) plus omega-3 fatty acid (300 mg/kg b.wt./oral) and lead acetate (3 mg/kg b.wt.) plus vitamin E (100 mg/kg b.wt./oral), respectively, for a period of 90 days. Their biochemical and histopathological investigations have been carried out. Results The level of lead was markedly elevated in brain (4.71-fold) and blood (5.65-fold), also increased levels of ROS, GSH, LPO with concomitant reduction in the activities of delta-ALAD, CAT, SOD, and GPx. In addition, lead-induced brain damage was indicated by histopathological changes. Omega-3 fatty acid resulted in marked improvement in most of the biochemical parameters as well as histopathological changes in rats. The results obtained were compared with vitamin E as the standard antioxidant agents. Discussion Omega-3 fatty acid significantly (P < 0.05) decreased the effect of lead-induced brain damage as well as biochemical changes similar to that of standard drug, vitamin E. So, our result suggested that omega-3 fatty acid may play a protective role in lead-induced neurotoxicity and associated human health risk.
    Nutritional Neuroscience 05/2015; DOI:10.1179/1476830515Y.0000000028
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    ABSTRACT: Objectives Resveratrol appears to have neuroprotective potential in various animal models of brain disorders including cerebral ischemia and neurodegenerative diseases. Chronic cerebral hypoperfusion is a well-known pathological condition contributing to the neurodegenerative diseases such as vascular dementia. Purpose of the present study is to evaluate the possible therapeutic potential of resveratrol in a model of vascular dementia of ovariectomized female rats. Assessment of the potential was based on the determination of brain oxidative status, caspase-3 level, glial fibrillary acidic protein (GFAP), and neuronal damage on hippocampus and cerebral cortex. Methods For creating the model of chronic cerebral hypoperfusion, ovariectomized female Wistar rats were subjected to the modified two vessel occlusion method, with the right common carotid artery being occluded first and the left one a week later. Results At the 15th day following the ligation, neuronal damage was accompanied by the increased immunoreactivities of both GFAP and caspase-3, and significant neurodegeneration was evident in the hippocampus and cortex, all of which were significantly alleviated with resveratrol treatment (10 mg/kg). Biochemical analysis revealed that the resveratrol treatment decreased lipid peroxidation and restored reduced glutathione level as well. Discussion The collected data of the present study suggest that the administration of resveratrol may provide a remarkable therapeutic benefit for vascular dementia, which is most likely related to the prevention of both apoptotic cell death and oxidative stress. We believe that therapeutic efficacy of resveratrol deserves to be tested for potential clinical application in postmenopausal elderly women suffering from vascular dementia.
    Nutritional Neuroscience 05/2015; DOI:10.1179/1476830515Y.0000000027
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    ABSTRACT: Objectives The aim of this study was to investigate the neuroprotective ability of partridgeberry polyphenols in rat primary cortical neurons against oxygen-glucose deprivation/reperfusion (OGD/R) injury in vitro and explore the underlying therapeutic mechanism(s). Methods The OGD/R injury was induced in rat primary cortical neurons by incubation with deoxygenated glucose-free medium in a hypoxia chamber. Results The strongest activity in this regard was exhibited by partridgeberry-derived PPF2 and PPF3, i.e. the flavan-3-ol- and flavonol-rich polyphenol fractions of partridgeberry (P ≤ 0.05). Moreover, partridgeberry polyphenol pre-treatment reduced the membrane damage in primary neurons, as measured by the LDH release assay (P ≤ 0.05). Furthermore, PPF2 and PPF3 pre-treatment (100 µg ml(-1)) for 24 hours, before OGD/R, resulted in the strongest suppression of IL-6 and TNF-α induction by OGD/R injury, compared with the control group (P ≤ 0.05). Additionally, the protein levels of HIF-1α and PPARγ, quantified by ELISA presented a significant modulation following PPFs treatment (100 µg ml(-1)), favorably toward neuroprotection, compared with the respective controls after OGD/R injury in vitro (P ≤ 0.05). Conclusion In summary, partridgeberry polyphenols at concentrations of 1-100 µg ml(-1), significantly induced a decline in OGD/R injury-triggered apoptosis in vitro, suppressed the inflammatory biomarkers in primary neurons, and modulated the activity of HIF-1α and PPARγ following hypoxic injury.
    Nutritional Neuroscience 05/2015; DOI:10.1179/1476830515Y.0000000026
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    ABSTRACT: Objectives The aim of this study was to investigate the neuroprotective ability of partridgeberry polyphenols in rat primary cortical neurons against oxygen-glucose deprivation/reperfusion (OGD/R) injury in vitro and explore the underlying therapeutic mechanism(s). Methods The OGD/R injury was induced in rat primary cortical neurons by incubation with deoxygenated glucose-free medium in a hypoxia chamber. Results The strongest activity in this regard was exhibited by partridgeberry-derived PPF2 and PPF3, i.e. the flavan-3-ol- and flavonol-rich polyphenol fractions of partridgeberry (P ≤ 0.05). Moreover, partridgeberry polyphenol pre-treatment reduced the membrane damage in primary neurons, as measured by the LDH release assay (P ≤ 0.05). Furthermore, PPF2 and PPF3 pre-treatment (100 µg ml−1) for 24 hours, before OGD/R, resulted in the strongest suppression of IL-6 and TNF-α induction by OGD/R injury, compared with the control group (P ≤ 0.05). Additionally, the protein levels of HIF-1α and PPARγ, quantified by ELISA presented a significant modulation following PPFs treatment (100 µg ml−1), favorably toward neuroprotection, compared with the respective controls after OGD/R injury in vitro (P ≤ 0.05). Conclusion In summary, partridgeberry polyphenols at concentrations of 1–100 µg ml−1, significantly induced a decline in OGD/R injury-triggered apoptosis in vitro, suppressed the inflammatory biomarkers in primary neurons, and modulated the activity of HIF-1α and PPARγ following hypoxic injury.
    Nutritional Neuroscience 05/2015;
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    ABSTRACT: Objectives This study aimed to investigate the beneficial effects of Cheonggukjang (CGK) manufactured by mixed culture of Bacillus subtilis MC31 and Lactobacillus sakei 383 on neurotoxic damages. Methods The specific aspects of brain functions were measured in ICR mice that had been pretreated for 4 weeks with three difference doses of CGK before trimethyltin (TMT) treatment. Results The short- and long-term memory loss induced by TMT treatment was significantly improved in the CGK-pretreated group in a dose-dependent manner. The number of dead cells in the granule cell layer of the dentate gyrus was decreased in the TMT/CGK-cotreated group relative to the TMT/vehicle-treated group, whereas significant suppression of acetylcholinesterase (AChE) activity was observed in the same group. Additionally, a dose-dependent increase in nerve growth factor (NGF) concentration, activation of the NGF receptor signaling pathway including the TrkA high affinity receptor and p75(NTR) low affinity receptor, and decline in Bax/Bcl-2 level was measured in all TMT/CGK-treated groups, although a decrease in the active form of caspase-3 was observed in the TMT/H-CGK-treated group. Furthermore, superoxide dismutase (SOD) activity was enhanced in the TMT/CGK-treated group, whereas the level of malondialdehyde (MDA), a marker of lipid peroxidation, was 43-58% lower in the TMT/CGK-treated group than the TMT/vehicle-treated group. Discussion These results demonstrate that CGK fermented by mixed culture of B. subtilis and L. sakei could exert a wide range of beneficial activities for neurodegenerative diseases, including Alzheimer, Parkinson, and Huntington disease.
    Nutritional Neuroscience 04/2015; DOI:10.1179/1476830515Y.0000000025
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    ABSTRACT: Hypophosphatemia (HP) with or without intracellular depletion of inorganic phosphate (Pi) and adenosine triphosphate has been associated with central and peripheral nervous system complications and can be observed in various diseases and conditions related to respiratory alkalosis, alcoholism (alcohol withdrawal), diabetic ketoacidosis, malnutrition, obesity, and parenteral and enteral nutrition. In addition, HP may explain serious muscular, neurological, and haematological disorders and may cause peripheral neuropathy with paresthesias and metabolic encephalopathy, resulting in confusion and seizures. The neuropathy may be improved quickly after proper phosphate replacement. Phosphate depletion has been corrected using potassium-phosphate infusion, a treatment that can restore consciousness. In severe ataxia and tetra paresis, complete recovery can occur after adequate replacement of phosphate. Patients with multiple risk factors, often with a chronic disease and severe HP that contribute to phosphate depletion, are at risk for neurologic alterations. To predict both risk and optimal phosphate replenishment requires assessing the nutritional status and risk for re-feeding hypophosphatemia. The strategy for correcting HP depends on the severity of the underlying disease and the goal for re-establishing a phosphate balance to limit the consequences of phosphate depletion.
    Nutritional Neuroscience 04/2015; DOI:10.1179/1476830515Y.0000000024
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    ABSTRACT: Objectives Dietary supplementation of fruits and vegetables has been the main stay for nutritional benefit and overall well-being. GrandFusion(®) is a nutritional supplement that contains the natural nutrients from whole fruits and vegetables that include complex nutrients and phytonutrients that contain anti-oxidant, anti-inflammatory, and neuroprotective properties. Methods In this study, C57BL/6 mice were fed a diet supplemented with GrandFusion(®) for 2 months prior to 1 hour of ischemia induced by occlusion of the middle cerebral artery (MCAo) followed by various times of reperfusion. Mice were subjected to MCAo for 1 hour and then at various times following reperfusion, animals were assessed for behavioral outcomes (open field testing, rotarod, and adhesive test removal), and infarct volumes (cresyl violet and triphenyltetrazolium chloride). In addition, to determine the potential mechanisms associated with treatment, the brain tissue was examined for changes in oxidative stress and inflammatory markers. Results The GrandFusion(®) diet was able to show a significant protection from infarct damage in the brain and an improvement in neurological outcomes. The diet did not alter heart rate, blood pressure, pO2, pCO2, or pH. In addition, the diet mitigated inflammation by reducing microglial and astrocytic activation following ischemia and reperfusion and limiting oxidative stress. Discussion The study demonstrates the neuroprotective effect of a diet rich in fruits and vegetables that contain anti-oxidant and anti-inflammatory against the impact of cerebral ischemia and reperfusion injury.
    Nutritional Neuroscience 04/2015; DOI:10.1179/1476830515Y.0000000021
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    ABSTRACT: Objective The aim of this study was to determine effects of probiotic yogurt and multispecies probiotic capsule supplementation on mental health and hypothalamic-pituitary-adrenal axis in petrochemical workers. Methods The present randomized double-blind, placebo-controlled trial was conducted on 70 petrochemical workers. Subjects were randomly divided into three groups to receive 100 g/day probiotic yogurt + one placebo capsule (n = 25) or one probiotic capsule daily + 100 g/day conventional yogurt (n = 25) or 100 g/day conventional yogurt + one placebo capsule (n = 20) for 6 weeks. Mental health parameters including general health questionnaire (GHQ) and depression anxiety and stress scale (DASS) scores were measured. Fasting blood samples were obtained at the beginning and 6 weeks after the intervention to quantify hypothalamic-pituitary-adrenal axis. Results After 6 weeks of intervention, a significant improvement of GHQ was observed in the probiotic yogurt (18.0 ± 1.5 vs. 13.5 ± 1.9, P = 0.007) and in the probiotic capsule group (16.9 ± 1.8 vs. 9.8 ± 1.9, P = 0.001), as well as a significant improvement in DASS scores in the probiotic yogurt (23.3 ± 3.7 vs. 13.0 ± 3.7, P = 0.02) and the probiotic capsule group (18.9 ± 3.2 vs. 9.4 ± 4.0, P = 0.006). However, there was no significant improvement in the conventional yogurt group (P = 0.05 for GHQ and P = 0.08 for DASS). Discussion The consumption of probiotic yogurt or a multispecies probiotic capsule had beneficial effects on mental health parameters in petrochemical workers.
    Nutritional Neuroscience 04/2015; DOI:10.1179/1476830515Y.0000000023
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    ABSTRACT: Objectives The polyphenol resveratrol has shown regulatory effects on hippocampal neurogenesis, which according to the neurovascular niche hypothesis, likely to involve stimulation of angiogenesis. In rodents, global cerebral ischemia leads to selective CA1 neuronal damage, spatial memory impairments, lasting changes in corticosterone (CORT) secretion, and increased neurogenesis. This study examined dose-related effects of 21-day RSV treatment on markers associated with neurogenesis (DCX, PSA-NCAM) and angiogenesis (CD31) in the hippocampus at short (7-day) and long-term (85-day) intervals following global ischemia. In parallel, post-ischemic and stress-induced CORT levels and spatial memory in the Morris water maze were determined. Methods Five groups of male Wistar rats were included: sham/saline, ischemia/saline, ischemia/1 mg/kg RSV, ischemia/10 mg/kg RSV, and sham/10 mg/kg RSV. Changes in expression of plasticity markers were paralleled by assessment of basal- and stress-induced CORT secretions, and spatial memory performance. Results Our findings revealed a significant attenuation of ischemia-induced DCX/PSA-NCAM expression in RSV-treated rats, whereas RSV treatment increased angiogenesis in the injured CA1 region. RSV attenuated CORT levels 3 days post-ischemia and a trend toward attenuating CORT secretion in response to 15 minutes restraint stress. Increased swimming latencies in the target quadrant during the MWM probe trial in RSV-treated ischemic rats support beneficial effects of on spatial memory retention. Discussion Our findings uncover time- and dose-related effects of RSV and global ischemia on the regulation of hippocampal plasticity. Changes in neuro- and angiogenesis are consistent with RSV neuroprotective effects, but appear independent of RSV regulatory effects on corticosterone secretion.
    Nutritional Neuroscience 04/2015; DOI:10.1179/1476830515Y.0000000020
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    ABSTRACT: Objective Coffee is one of the most widely consumed beverages worldwide. Aim of this study was to investigate short-term effects of espresso coffee on heart rate variability (HRV), a marker of vagal activity, in healthy habitual and non-habitual coffee consumers. Methods Seventy-seven healthy subjects (38 habitual and 39 non-habitual coffee consumers, 74% women, mean age 26.97 ± 6.88 years) took part in three laboratory sessions in a randomized order. In condition 1, subjects consumed espresso; in condition 2, subjects consumed decaffeinated espresso; and in condition 3, subjects consumed warm water. HRV and blood pressure were assessed at rest before and after ingestion of the respective beverage. Results HRV was significantly increased after consumption of caffeinated espresso, decaffeinated espresso, or water, indicating increased vagal activity in the course of the experiments. In the habitual coffee consumers, the increase in vagally mediated HRV was significantly lower after consumption of decaffeinated espresso compared to caffeinated espresso. Increases of systolic blood pressure were only found in the non-habitual consumers. Conclusion We found no evidence for specific short-term effects of caffeinated espresso on vagal activity in healthy subjects. Instead, consumption of decaffeinated espresso inhibited vagal activity in habitual consumers. This may be explained by an attempt of the organism to establish a sympathovagal equilibrium comparable to that after caffeine consumption. In the absence of caffeine-induced sympathetic activation, this may have been achieved by relative vagal withdrawal.
    Nutritional Neuroscience 04/2015; DOI:10.1179/1476830515Y.0000000018
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    ABSTRACT: Background/aims Emblica officinalis is mentioned as a maharasayana in many Ayurvedic texts and promotes intelligence, memory, freedom from disease, longevity, and strength of the senses. The present study has been designed to explore the memory-enhancing effect of the tannoid principles of E. officinalis (EoT) at the biochemical, anatomical, behavioral, and molecular levels against aluminum chloride (AlCl3) induced Alzheimer's disease (AD) in rats. Aluminum is reported to have an important role in the etiology, pathogenesis, and development of AD. Methods Male Wistar rats were divided into control, AlCl3 treated, AlCl3 and EoT (50, 100, and 200 mg/kg bw) co-treated, and EoT (200 mg/kg bw) alone treated groups. In control and experimental rats, behavior tests including water maze and open field test, estimation of aluminum, assay of acetylcholinesterase (AChE) activity, and expression of amyloidogenic proteins were performed. Results Intraperitonial injection of AlCl3 (100 mg/kg bw) for 60 days significantly elevated the concentration of aluminum (Al), activity of AChE and protein expressions of amyloid precursor protein, A-beta1-42, beta-, and gamma-secretases as compared to control group in hippocampus and cortex. Co-administration of EoT orally to AlCl3 rats for 60 days significantly revert back the Al concentration, AChE activity, and A-beta synthesis-related molecules in the studied brain regions. The spatial learning, memory, and locomotor impairments observed in AlCl3 treated rats were significantly attenuated by EoT. Conclusion Therefore, EoT may be a promising therapy in ameliorating neurotoxicity of aluminum, however further studies are warranted to elucidate the exact mechanism of action of EoT.
    Nutritional Neuroscience 04/2015; DOI:10.1179/1476830515Y.0000000016