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The role of nutrition in health and disease has been appreciated from time immemorial. Around 400 B.C., Hippocrates wrote “Let food by thy medicine and medicine be thy food.” In the 12th century, the great philosopher and physician Moses Maimonides wrote “any disease that can be treated by diet should be treated by no other means.” Now, in the 21st century, we are bombarded by claims in the media of “superfoods,” wondrous nutritional supplements, and special diets that promise to cure or prevent disease, improve health and restore functioning. Much of the focus has been on neurological disease, brain health and psychological functioning (behavior, cognition, and emotion). The hyperbole aside, there has been considerable progress in the past decade in our understanding of the contribution of specific nutrients and dietary patterns to brain development, physiology, and functioning. This Special Issue of Brain Sciences is devoted to the latest research on the role of nutritional deficiencies and excesses in the genesis of brain dysfunction, and use of diet for the prevention and treatment of brain and mental disorders. Basic laboratory and clinical research studies of the immature, adult, and aged nervous system are all welcome.
epilepsy --- glioblastoma multiforme --- ADHD --- n/a --- prefrontal cortex --- regainers --- functional neuroimaging --- malignant glioma --- nutrients --- caffeine --- children --- inflammation --- working memory --- cytokines --- modified Atkins diet --- fish intake --- insulin resistance --- transpulmonary administration --- obesity --- maintainers --- electroencephalography --- Alzheimer’s disease --- omega-3 fatty acids --- diet-deficient --- weight loss maintenance --- neural processing --- hippocampal neurogenesis --- Brain --- Diseases --- Diet therapy. --- Cerebrum --- Mind --- Central nervous system --- Head --- Alzheimer's disease
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During aging, reductions in hippocampal neurogenesis are associated with memory decline indicating a causal relationship. Indeed, insulin-like growth factor-1 (IGF-1), a major activator of the extracellular receptor kinase pathway that is central in learning and memory processes, is also a key modulator of hippocampal neurogenesis. Previously, we showed that age-related declines in spatial memory tasks can be improved by antioxidant-rich diets containing blueberries. In this study, to begin to understand the mechanisms responsible for the beneficial effects of blueberries, we assessed changes in hippocampal plasticity parameters such as hippocampal neurogenesis, extracellular receptor kinase activation, and IGF-1 and IGF-1R levels in blueberry-supplemented aged animals. Our results show that all these parameters of hippocampal neuronal plasticity are increased in supplemented animals and aspects such as proliferation, extracellular receptor kinase activation and IGF-1 and IGF-1R levels correlate with improvements in spatial memory. Therefore, cognitive improvements afforded by polyphenolic-rich fruits such as blueberries appear, in part, to be mediated by their effects on hippocampal plasticity
Activation. --- Adult dentate gyrus. --- Aged rats. --- Aging. --- Alzheimers-disease. --- Animal. --- Animals. --- Antioxidants. --- Behavior. --- Cognition. --- Diet. --- Dietary supplementation. --- Environmental enrichment. --- Erk. --- Growth-factor-i. --- Growth. --- Hippocampal neurogenesis. --- Hippocampal. --- Human. --- Igf-1. --- Learning and memory. --- Learning. --- Level. --- Mechanisms. --- Medial prefrontal cortex. --- Memory. --- Modulation. --- Neurogenesis. --- Neuronal signal-transduction. --- Neuronal. --- Parameters. --- Plasticity. --- Rat. --- Rats. --- Receptor. --- Reduction. --- Spatial memory. --- Spatial. --- Task. --- Tasks. --- Time. --- Vitamin-e. --- Water maze.
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Although thousands of new neurons are continuously produced in the dentate gyrus of rodents each day, the function of these newborn cells remains unclear. An increasing number of reports have provided correlational evidence that adult hippocampal neurogenesis is involved in learning and memory. Exposure of animals to an enriched environment leads to improvement of performance in several learning tasks and enhances neurogenesis specifically in the hippocampus. These data raise the question of whether new neurons participate in memory improvement induced by enrichment. To address this issue, we have examined whether the increase in the number of surviving adult-generated cells following environmental enrichment contributes to improved memory function. To this end, neurogenesis was substantially reduced throughout the environmental enrichment period using the antimitotic agent methylazoxymethanol acetate (MAM). Recognition memory performance of MAM-treated enriched rats was evaluated in a novel object recognition task and compared with that of naive and nontreated enriched rats. Injections of 5-bromo-2'-deoxyuridine were used to label dividing cells, together with double immunofluorescent labelling using glial or neuronal cell-specific markers. We found that enrichment led to improved long-term recognition memory and increased hippocampal neurogenesis, and that MAM treatment during environmental enrichment completely prevented both the increase in neurogenesis and enrichment-induced long-term memory improvement. These results establish that newborn cells in the dentate gyrus contribute to the expression of the promnesic effects of behavioural enrichment, and they provide further support for the idea that adult-generated neurons participate in modulating memory function
Adult-rat brain. --- Adult. --- Animal. --- Animals. --- Axonal projections. --- Consolidation. --- Dentate gyrus. --- Enriched environment. --- Enriched. --- Enrichment. --- Environment. --- Environmental enrichment. --- Exposure. --- Expression. --- Function. --- Generated granule cells. --- Hippocampal neurogenesis. --- Hippocampal. --- Hippocampus. --- Increase. --- Injections. --- Learning and memory. --- Learning. --- Long-term. --- Memory. --- Methylazoxymethanol acetate. --- Mice. --- Neurogenesis. --- Neuronal plasticity. --- Neuronal. --- Neurons. --- Object recognition. --- Object-recognition memory. --- Object. --- Olfactory-bulb. --- Performance. --- Rat. --- Rats. --- Recognition. --- Rodent. --- Rodents. --- Spatial memory. --- Synaptic plasticity. --- Task. --- Tasks. --- Time. --- Trace memories. --- Treatment.
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