When neurogenesis encounters aging and disease

被引:321
作者
Lazarov, Orly [1 ]
Mattson, Mark P. [2 ]
Peterson, Daniel A. [3 ,4 ]
Pimplikar, Sanjay W. [5 ]
van Praag, Henriette [2 ]
机构
[1] Univ Illinois, Dept Anat & Cell Biol, Chicago, IL 60607 USA
[2] NIA, Neurosci Lab, Intramural Res Program, Baltimore, MD USA
[3] Rosalind Franklin Univ Med & Sci, Ctr Stem Cell & Regenerat Med, N Chicago, IL USA
[4] Rosalind Franklin Univ Med & Sci, Dept Neurosci, N Chicago, IL USA
[5] Cleveland Clin, Lerner Res Inst, Dept Neurosci, Cleveland, OH 44106 USA
基金
美国国家卫生研究院;
关键词
NEURAL STEM-CELLS; ADULT HIPPOCAMPAL NEUROGENESIS; FAMILIAL ALZHEIMERS-DISEASE; MOUSE DENTATE GYRUS; SPATIAL-PATTERN SEPARATION; GENERATED GRANULE CELLS; TRANSGENIC MICE; OLFACTORY-BULB; SYNAPTIC PLASTICITY; SUBVENTRICULAR ZONE;
D O I
10.1016/j.tins.2010.09.003
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
In this review, we consider the evidence that a reduction in neurogenesis underlies aging-related cognitive deficits and impairments in disorders such as Alzheimer's disease (AD). The molecular and cellular alterations associated with impaired neurogenesis in the aging brain are discussed. Dysfunction of presenilin-1, misprocessing of amyloid precursor protein and toxic effects of hyperphosphorylated tau and beta-amyloid probably contribute to impaired neurogenesis in AD. Because factors such as exercise, environmental enrichment and dietary energy restriction enhance neurogenesis, and protect against age-related cognitive decline and AD, knowledge of the underlying neurogenic signaling pathways could lead to novel therapeutic strategies for preserving brain function. In addition, manipulation of endogenous neural stem cells and stem cell transplantation, as stand-alone or adjunct treatments, seems promising.
引用
收藏
页码:569 / 579
页数:11
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