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: 2.27

Impact Factor Rankings

2015 Impact Factor Available summer 2016
2014 Impact Factor 2.274
2013 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

Additional details

5-year impact 2.11
Cited half-life 6.70
Immediacy index 0.68
Eigenfactor 0.00
Article influence 0.52
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

Publications in this journal

  • David O Kennedy · Philippa A Jackson · Joanne Forster · Julie Khan · Torsten Grothe · Tania Perrinjaquet-Moccetti · Crystal F Haskell-Ramsay ·
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    ABSTRACT: Objectives A wild green-oats extract (Neuravena(®)) containing a range of potentially bioactive components, including flavonoids and triterpene saponins, has previously been shown to enhance animal stress responses and memory, and improve cognitive performance in humans at a dose of 1600 mg. Methods This double-blind, placebo-controlled, counterbalanced cross-over study assessed the effects of single doses of the green-oat extract (GOE) across a broad range of cognitive domains in healthy adults aged 40-65 years who self-reported that they felt that their memory had declined with age. Participants attended on six occasions, receiving a single dose of either placebo, 800, or 1600 mg GOE on each occasion, with the counterbalanced order of treatments repeated twice for each participant. Cognitive function was assessed with a range of computerized tasks measuring attention, spatial/working/episodic memory, and executive function pre-dose and at 1, 2.5, 4, and 6 hours post-dose. Results The results showed that 800mg GOE increased the speed of performance across post-dose assessments on a global measure including data from all of the timed tasks. It also improved performance of a delayed word recall task in terms of errors and an executive function task (Peg and Ball) in terms of decreased thinking time and overall completion time. Working memory span (Corsi blocks) was also increased, but only on the second occasion that this dose was taken. Discussion These results confirm the acute cognitive effects of GOE seen in previous research, and suggest that the optimal dose lies at or below 800 mg.
    Nutritional Neuroscience 11/2015; DOI:10.1080/1028415X.2015.1101304
  • Amanda N Carey · Marshall G Miller · Derek R Fisher · Donna F Bielinski · Casey K Gilman · Shibu M Poulose · Barbara Shukitt-Hale ·
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    ABSTRACT: Objectives The present study was carried out to determine if lyophilized açaí fruit pulp (genus, Euterpe), rich in polyphenols and other bioactive antioxidant and anti-inflammatory phytochemicals, is efficacious in reversing age-related cognitive deficits in aged rats. Methods The diets of 19-month-old Fischer 344 rats were supplemented for 8 weeks with 2% Euterpe oleracea (EO), Euterpe precatoria (EP), or a control diet. Rats were tested in the Morris water maze and then blood serum from the rats was used to assess inflammatory responses of BV-2 microglial cells. Results After 8 weeks of dietary supplementation with 2% EO or EP, rats demonstrated improved working memory in the Morris water maze, relative to controls; however, only the EO diet improved reference memory. BV-2 microglial cells treated with blood serum collected from EO-fed rats produced less nitric oxide (NO) than control-fed rats. Serum from both EO- and EP-fed rats reduced tumor necrosis factor-alpha (TNF-α). There is a relationship between performance in the water maze and the production of NO and TNF-α by serum-treated BV-2 cells, such that serum from rats with better performance was more protective against inflammatory signaling. Discussion Protection of memory during aging by supplementation of lyophilized açaí fruit pulp added to the diet may result from its ability to influence antioxidant and anti-inflammatory signaling.
    Nutritional Neuroscience 11/2015; DOI:10.1080/1028415X.2015.1115213
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    ABSTRACT: Objectives Depression is one of the most common psychiatric disorders, and the fourth leading cause of long-term disability throughout the world. Despite the availability of different classes of antidepressant drugs, most of them are not completely effective and above all are associated with many serious adverse effects. Recently, accumulating evidence suggests that dietary supplements rich in important phytochemicals possess beneficial therapeutic roles in depression. Methods In this review, we will first consider what is known about the pathogenesis of depression and discuss the need for more safe and efficacious treatment. We will then review the potential clinical relevance of natural plant-derived products based on data derived from pre-clinical animal studies, randomized controlled studies and placebo-controlled trials published on this topic within the last decade. Results Among the natural compounds that show antidepressive-like activity, green tea catechins have been shown to decrease depressive symptoms in experimental animals, possibly in part through the inhibition of monoamine oxidase (MAO). Anthocyanins and their aglycons, responsible for the typical color of berries, inhibit MAO isoforms A or B with IC50 values corresponding to the micromolar range. Other studies suggest that cocoa extracts, whose main components are procyanidins, attenuate depressive symptoms in rats. Resveratrol, one of the most important natural stilbenoid, inhibits noradrenaline and serotonin reuptake in rats, and significantly decreases anxiety/depressive behaviours while increasing hippocampal serotonin and noradrenaline levels. Trans-resveratrol possesses MAO-A inhibitory effects in different brain areas, particularly in the frontal cortex and hippocampus, as already reported for tea catechins. Although these effects have been documented in rodent models, further randomized controlled trials in this area are warranted. However, so far, there is only correlative evidence between certain nutrients, such as omega-3 polyunsaturated fatty acids and B vitamins, and depression in human population studies. Discussion Growing evidence suggests that consumption of these compounds may represent an alternative strategy to delay the onset and progression of depression, and depressive-like symptoms. However, further randomized and placebo-controlled trials are necessary to confirm the potential of these compounds as a possible remedy for this debilitating disorder.
    Nutritional Neuroscience 11/2015; DOI:10.1080/1028415X.2015.1103461
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    ABSTRACT: Objectives Long-term d-galactose injection induces accelerated aging in experimental rodent models. The aim of this study was to determine the effects of dietary fructo-oligosaccharide (FO) on the brain β-amyloid (Aβ), amyloid-associated enzymes, cognitive function, and plasma antioxidant levels in d-galactose-treated Balb/c mice. Methods The subcutaneous (s.c.) injection and the dietary treatment were conducted simultaneously for 49 days. Mice (12 weeks of age) were divided into five groups (n = 14/group): control (s.c. saline, control diet) serving as a young control, DG (s.c. 1.2 g d-galactose/kg body weight, control diet), DG + LFO (2.5% w/w FO, low-dose FO diet), DG + HFO (5% w/w FO, high-dose FO diet), and DG + E (α-tocopherol 0.2% w/w, vitamin E diet) as an antioxidant reference group. Another group of older mice (64 weeks of age) without any injection served as a natural aging (NA) group. Results The DG and NA groups had greater Aβ levels in the cortex, hippocampus, and the whole brain. High-dose FO, similar to α-tocopherol, attenuated the d-galactose-induced Aβ density in the cortex and hippocampus. In addition, FO attenuated the d-galactose-induced protein expression of Aβ and beta-site amyloid precursor cleaving enzyme of the whole brain in a dose-response manner. Either dose of FO supplementation, similar to α-tocopherol, attenuated the d-galactose-induced cognitive dysfunction. In addition, FO improved the plasma ascorbic acid level in a dose-response manner. Conclusion Dietary FO (2.5-5% w/w diet) could attenuate the development of Alzheimer's disease, which was likely to be associated with its systematic antioxidant effects.
    Nutritional Neuroscience 11/2015; DOI:10.1080/1028415X.2015.1110952
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    ABSTRACT: Objectives Vitamin B12 is essential for the integrity of the central nervous system. However, performances in different cognitive domains relevant to vitamin B12 deficiency remain to be detailed. To date, there have been limited studies that examined the relationships between cognitions and structural neuroimaging in a single cohort of low-vitamin B12 status. The present study aimed to depict psychometrics and magnetic resonance imaging (MRI) morphometrics among patients with vitamin B12 deficiency, and to examine their inter-relations. Methods We compared 34 consecutive patients with vitamin B12 deficiency (serum level ≤250 pg/ml) to 34 demographically matched controls by their cognitive performances and morphometric indices of brain MRI. The correlations between psychometrics and morphometrics were analyzed. Results The vitamin B12 deficiency group had lower scores than the controls on total scores of Mini-Mental Status Examination (MMSE) and Cognitive Abilities Screening Instrument (CASI) (both P < 0.05), language (P < 0.01), orientation (P < 0.01), and mental manipulation (P < 0.05). The patients also showed a greater frontal horn ratio than the controls (P < 0.05). Bicaudate ratio, fronto-occipital ratio, uncotemporal index, and normalized interuncal distance all showed a strong correlation with the total score of MMSE and CASI (all P < 0.01). Among these psychometric and morphometric indices, pronounced correlations between bicaudate ratio and long-term memory, mental manipulation, orientation, language, and verbal fluency were noted (all P < 0.01). Discussion Vitamin B12 deficiency is associated with a global cognition decline with language, orientation, and mental manipulation selectively impaired. Preferential atrophy in frontal regions is the main neuroimaging feature. Although the frontal ratio highlights the relevant atrophy among patients, the bicaudate ratio might be the best index on the basis of its strong association with global cognition and related cognitive domains, implying dysfunction of fronto-subcortical circuits as the fundamental pathogenesis related to vitamin B12 deficiency.
    Nutritional Neuroscience 09/2015; DOI:10.1179/1476830515Y.0000000045
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    ABSTRACT: Objectives To observe the expression of brain-derived neurotrophic factor (BDNF) in hypothalamic and adipose tissue in mice with monosodium glutamate (MSG)-induced obesity. Methods The effects of hypothalamic lesions, specifically arcuate nucleus (ARC) lesions, induced by MSG injection were studied in male ICR mice at the neonatal stage. The following parameters were compared: body weight, body length, Lee's index, food intake, body temperature, fat weight, and levels of total cholesterol (CHOL), triglyceride (TG), low-density lipoprotein (LDL), high-density lipoprotein (HDL), and blood glucose (GLU). The BDNF expression levels in hypothalamic and adipose tissue were measured using western blotting. Results Compared with the control group, the model group body had significantly higher weight, Lee's index, food intake, fat weight, CHOL, TG, LDL, HDL, and GLU levels. BDNF expression levels in hypothalamic and adipose tissue were markedly down-regulated in the model group. Discussion BDNF may be closely associated with MSG-induced hypothalamic obesity.
    Nutritional Neuroscience 07/2015; DOI:10.1179/1476830515Y.0000000039
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    ABSTRACT: Objectives Alzheimer's disease (AD) is a neurodegenerative disorder characterized by intracellular accumulations of phosphorylated forms of the microtubule binding protein tau. This study aimed to explore a novel mechanism for enhancing the clearance of these pathological tau species using the green tea flavonoid epigallocatechin-3-gallate (EGCG). EGCG is a potent antioxidant and an activator of the Nrf2 transcriptional pathway. Nrf2 activators including EGCG have shown promise in mitigating amyloid pathology in vitro and in vivo. This study assessed whether EGCG could also alter tau clearance. Methods Rat primary cortical neuron cultures were treated on day 8 in vitro 8 with EGCG and analyzed for changes in gene and protein expression using luciferase assay, q-PCR, and western blotting. Results EGCG treatment led to a significant decrease in the protein levels of three AD-relevant phospho-tau epitopes. Unexpectedly, EGCG does not appear to be facilitating this effect through the Nrf2 pathway or by increasing autophagy in general. However, EGCG did significantly increase mRNA expression of the key autophagy adaptor proteins NDP52 and p62. Discussion In this study, we show that EGCG enhances the clearance of AD-relevant phosphorylated tau species in primary neurons. Interestingly, this result appears to be independent of both Nrf2 activation and enhanced autophagy - two previously reported mechanisms of phytochemical-induced tau clearance. EGCG did significantly increase expression of two autophagy adaptor proteins. Taken together, these results demonstrate that EGCG has the ability to clear phosphorylated tau species in a highly specific manner, likely through increasing adaptor protein expression.
    Nutritional Neuroscience 07/2015; DOI:10.1179/1476830515Y.0000000038
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    ABSTRACT: Objectives Ketogenic diet (KD) is an important therapy used in the control of drug-refractory seizures. The major goal of this review is to update the knowledge about the adverse effects of KD on lipoproteins, lipid profile, and cardiometabolic risk. Methods Articles on the effect of the KD on plasma lipoproteins of children and adolescents with refractory epilepsy, which were published in the past 15 years and indexed in the PubMed and MedLine databases, were included. Results Dyslipidemia was recurrent in children, and adolescents treated with KD. Evidence suggests that hypercholesterolemia promotes structural modifications in low-density lipoprotein particles. Such modifications possibly favor oxidative processes and contribute to changes in the size of lipoproteins, particularly related to small and denser LDL. However, oxidative modifications in LDL of children on KD are not described in the literature. Discussion The positive effects of KD on the health of children and adolescents with refractory epilepsy are unquestionable. Conversely, this positive role is associated with significant and negative changes in lipid metabolism. Moreover, the positive effects are possibly related to oxidative reactions and unbalance of antioxidants that can contribute to an increased cardiometabolic risk. Therefore, this review invites clinicians and researchers to investigate the lipid and oxidative metabolism in their clinical practice and trials, respectively.
    Nutritional Neuroscience 07/2015; DOI:10.1179/1476830515Y.0000000036
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    ABSTRACT: Objectives Anemia caused by nutritional deficiencies, such as iron and copper deficiencies, is a global health problem. Iron and copper deficiencies have their most profound effect on the developing fetus/infant, leading to brain development deficits and poor cognitive outcomes. Tissue iron depletion or chronic anemia can induce cellular hypoxic signaling. In mice, chronic hypoxia induces a compensatory increase in brain blood vessel outgrowth. We hypothesized that developmental anemia, due to iron or copper deficiencies, induces angiogenesis/vasculogenesis in the neonatal brain. Methods To test our hypothesis, three independent experiments were performed where pregnant rats were fed iron- or copper-deficient diets from gestational day 2 through mid-lactation. Effects on the neonatal brain vasculature were determined using quantitative real-time polymerase chain reaction to assess mRNA levels of angiogenesis/vasculogenesis-associated genes and GLUT1 immunohistochemistry to assess brain blood vessel density and complexity. Results Iron deficiency, but not copper deficiency, increased mRNA expression of brain endothelial cell- and angiogenesis/vasculogenesis-associated genes (i.e. Glut1, Vwf, Vegfa, Ang2, Cxcl12, and Flk1) in the neonatal brain, suggesting increased cerebrovascular density. Iron deficiency also increased hippocampal and cerebral cortical blood vessel branching by 62 and 78%, respectively. Discussion This study demonstrates increased blood vessel complexity in the neonatal iron-deficient brain, which is likely due to elevated angiogenic/vasculogenic signaling. At least initially, this is probably an adaptive response to maintain metabolic substrate homeostasis in the developing iron-deficient brain. However, this may also contribute to long-term neurodevelopmental deficits.
    Nutritional Neuroscience 07/2015; DOI:10.1179/1476830515Y.0000000037
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    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: 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: 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