Intermittent metabolic switching, neuroplasticity and brain health

被引：390

作者：

Mattson, Mark P. ^{[1
,2
]}

Moehl, Keelin ^{[1
]}

Ghena, Nathaniel ^{[1
]}

Schmaedick, Maggie ^{[1
]}

Cheng, Aiwu ^{[1
]}

机构：

[1] NIA, Lab Neurosci, Intramural Res Program, Baltimore, MD 21224 USA

[2] Johns Hopkins Univ, Sch Med, Dept Neurosci, Baltimore, MD 21205 USA

来源：

NATURE REVIEWS NEUROSCIENCE | 2018年 / 19卷 / 02期

关键词：

GROWTH-FACTOR-I; LONG-TERM POTENTIATION; CHRONIC CALORIC RESTRICTION; DISEASE RISK MARKERS; DIETARY RESTRICTION; NEUROTROPHIC FACTOR; MOUSE MODEL; HIPPOCAMPAL NEUROGENESIS; SYNAPTIC PLASTICITY; OXIDATIVE STRESS;

D O I：

10.1038/nrn.2017.156

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

During evolution, individuals whose brains and bodies functioned well in a fasted state were successful in acquiring food, enabling their survival and reproduction. With fasting and extended exercise, liver glycogen stores are depleted and ketones are produced from adipose-cell-derived fatty acids. This metabolic switch in cellular fuel source is accompanied by cellular and molecular adaptations of neural networks in the brain that enhance their functionality and bolster their resistance to stress, injury and disease. Here, we consider how intermittent metabolic switching, repeating cycles of a metabolic challenge that induces ketosis (fasting and/or exercise) followed by a recovery period (eating, resting and sleeping), may optimize brain function and resilience throughout the lifespan, with a focus on the neuronal circuits involved in cognition and mood. Such metabolic switching impacts multiple signalling pathways that promote neuroplasticity and resistance of the brain to injury and disease.

引用

页码：81 / 94

页数：14

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