当神经发生遇到衰老和疾病。
When neurogenesis encounters aging and disease.
机构信息
Department of Anatomy and Cell Biology, University of Illinois at Chicago, Chicago, IL, USA.
出版信息
Trends Neurosci. 2010 Dec;33(12):569-79. doi: 10.1016/j.tins.2010.09.003. Epub 2010 Oct 18.
Abstract
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 β-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.
摘要
在这篇综述中，我们考虑了神经发生减少是如何导致与衰老相关的认知缺陷和阿尔茨海默病（AD）等疾病的损伤的证据。讨论了与衰老大脑中神经发生受损相关的分子和细胞改变。早老素-1功能障碍、淀粉样前体蛋白错误处理以及过度磷酸化的tau 和 β-淀粉样蛋白的毒性作用可能导致 AD 中的神经发生受损。由于运动、环境丰富和饮食能量限制等因素可以增强神经发生，并且可以预防与年龄相关的认知能力下降和 AD，因此对潜在的神经发生信号通路的了解可能会导致新的治疗策略，以保护大脑功能。此外，作为独立或辅助治疗的内源性神经干细胞的操作和干细胞移植似乎很有希望。
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