Mechanisms of enhanced quiescence in neural stem cell aging.

Mechanisms of enhanced quiescence in neural stem cell aging.
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DOI:
10.1016/j.mad.2020.111323
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发表时间:
2020-10
影响因子:
5.3
通讯作者:
Webb AE
Webb AE
中科院分区:
医学3区
文献类型:
--
作者:
Audesse AJ;Webb AE

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神经干细胞功能的维持对于确保整个成年期的神经发生至关重要。在衰老过程中,成人神经发生显着减少,这与认知功能下降相关。尽管最近的研究揭示了调节成体神经干细胞(NSC)池和谱系进展的新的外在和内在机制,但在衰老背景下驱动成体神经发生失调的精确分子机制才刚刚开始出现。最近的研究揭示了调节成体神经发生的最早步骤(即静态 NSC 的激活)的机制。有趣的是,老年大脑中神经干细胞进入细胞周期的能力显着下降,表明静止状态加深。鉴于成人神经发生对支持人类认知功能的可能贡献,增强神经发生可能是对抗与年龄相关的认知衰退的策略。这篇综述重点介绍了整个成年期调节 NSC 库的机制,并讨论了这些过程的失调如何导致整个衰老过程中神经发生和认知功能的下降。
The maintenance of neural stem cell function is vital to ensure neurogenesis throughout adulthood. During aging, there is a significant reduction in adult neurogenesis that correlates with a decline in cognitive function. Although recent studies have revealed novel extrinsic and intrinsic mechanisms that regulate the adult neural stem cell (NSC) pool and lineage progression, the precise molecular mechanisms that drive dysregulation of adult neurogenesis in the context of aging are only beginning to emerge. Recent studies have shed light on mechanisms that regulate the earliest step of adult neurogenesis, the activation of quiescent NSCs. Interestingly, the ability of NSCs to enter the cell cycle in the aged brain significantly declines suggesting a deepend state of quiescence. Given the likely contribution of adult neurogenesis to supporting cognitive function in humans, enhancing neurogenesis may be a strategy to combat age-related cognitive decline. This review highlights the mechanisms that regulate the NSC pool throughout adulthood and discusses how dysregulation of these processes may contribute to the decline in neurogenesis and cognitive function throughout aging.
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