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Mechanisms of enhanced quiescence in neural stem cell aging

adult neurogenesis aging cognitive decline neural stem cell nsc quiescence

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#1 Engadin

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Posted 08 August 2020 - 07:36 PM


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P A Y W A L L E D    S O U R C E :   Mechanisms of Aging and Development

 

 

 

 

 

 

Highlights
 
 
  •  During aging, there is a significant reduction in adult neurogenesis that correlates with a decline in cognitive function.
 
  •  In humans, there is strong evidence that neurogenesis persists in the dentate gyrus in healthy adults, and declines in aged individuals.
 
  •  Recent evidence suggests that the depth of NSC quiescence increases with age.
 
  •  We discuss cell intrinsic and extrinsic changes that impact NSC quiescence and activation during aging.
 
 
 
 
Abstract
 
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.
 
 
 
Outline
 
1. Introduction
 
2. Intrinsic changes with age: altered metabolism, proteostasis, senescence, and epigenetic states
   
   2.1. Metabolism
   2.2. Proteostasis
   2.3. Senescence
   2.4. Epigenetics
 
3. Extrinsic mechanisms that impact NSC quiescence and activation during aging
 
4. Conclusions
 
 
 
 
 
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Also tagged with one or more of these keywords: adult neurogenesis, aging, cognitive decline, neural stem cell, nsc, quiescence

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