Disrupted energy metabolism and neuronal circuit dysfunction in cognitive impairment and Alzheimer's disease

被引：21

作者：

Kapogiannis, Dimitrios ^{[2
]}

Mattson, Mark P. ^{[1
]}

机构：

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

[2] NIA, Clin Res Branch, Intramural Res Program, Baltimore, MD 21224 USA

来源：

LANCET NEUROLOGY | 2011年 / 10卷 / 02期

基金：

美国国家卫生研究院;

关键词：

AMYLOID-BETA-PEPTIDE; TRANSGENIC MOUSE MODEL; A-BETA; NEUROTROPHIC FACTOR; SYNAPTIC PLASTICITY; DIETARY RESTRICTION; IMPROVES COGNITION; PHYSICAL-ACTIVITY; FUNCTIONAL CONNECTIVITY; HIPPOCAMPAL FUNCTION;

D O I：

暂无

中图分类号：

R74 [神经病学与精神病学];

学科分类号：

摘要：

Epidemiological, neuropathological, and functional neuroimaging evidence implicates global and regional disruptions in brain metabolism and energetics in the pathogenesis of cognitive impairment. Nerve cell microcircuits are modified by excitatory and inhibitory synaptic activity and neurotrophic factors. Ageing and Alzheimer's disease cause perturbations in cellular energy metabolism, level of excitation or inhibition, and neurotrophic factor release, which overwhelm compensatory mechanisms and result in dysfunction of neuronal microcircuits and brain networks. A prolonged positive energy balance impairs the ability of neurons to adapt to oxidative and metabolic stress. Results from experimental studies in animals show how disruptions caused by chronic positive energy balance, such as diabetes, lead to accelerated cognitive ageing and Alzheimer's disease. Therapeutic interventions to allay cognitive dysfunction that target energy metabolism and adaptive stress responses (such as neurotrophin signalling) have been effective in animal models and in preliminary studies in humans.

引用

页码：187 / 198

页数：12

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