Hippocampal neurogenesis and pro‐neurogenic therapies for Alzheimer's disease

Abstract

Adult hippocampal neurogenesis (AHN) in the hippocampal dentate gyrus (DG) subset enables the neuronal network to encode new information flexibly and update stored content in due time. 1 Though the number of adult-born neurons declines with age, there is increasing evidence of an indispensable role for limited AHN in hippocampusdependent learning, memory and emotional regulation. 2Alzheimer's disease (AD) is the most common cause of dementia in people over age 65. It is characterized by progressive neurodegeneration in the brain, with no treatment to date for halting disease progression. A sea of money has been invested in the development of anti-AD drugs. Two major drug targets include the extracellular amyloid-beta (Aβ) protein and intraneuronal hyperphosphorylated tau. Besides considering the anti-neurodegenerative potential of AHN and other pro-neurogenic treatments, neuroscientists are also trying to develop new drugs to directly facilitate neurogenesis in the AD brain. 3 However, introducing neurogenesis is challenging in AD. The pool of active hippocampal neural stem cells (NSCs) is prone to being progressively depleted due to sustained homeostatic abnormality within the neurogenic niche under AD and accelerated aging. 4 Innate AHN is dysregulated under AD and the underlying mechanisms remain largely unknown, 5 which hinders the development of pro-AHN drugs. Simultaneously, emerging techniques such as cell transplantation and glia-neuron reprogramming also shed new light on the proneurogenic treatment of AD. 3 These strategies may help overcome

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