Abstract
Adult neurogenesis occurs throughout life in restricted brain regions in mammals. However, the number of neural stem cells (NSCs) that generate new neurons steadily decreases with age, resulting in a decrease in neurogenesis. Transplantation of mesenchymal cells or cultured NSCs has been studied as a promising treatment in models of several brain injuries including cerebral infarction and cerebral contusion. Considering the problems of host-versus-graft reactions and the tumorigenicity of transplanted cells, the mobilization of endogenous adult NSCs should be more feasible for the treatment of these brain injuries. However, the number of adult NSCs in the adult brain is limited, and their mitotic potential is low. Here, we outline what we know to date about why the number of NSCs and adult neurogenesis decrease with age. We also discuss issues applicable to regenerative medicine.
Highlights
Origin of adult neural stem cells (NSCs) NSCs are actively self-renewing, allowing the generation of a large number of neurons and glia during central nervous system development [35] and rapid cerebral development during the embryonic stage
Active neurogenesis via transit amplifying progenitor cells (TAPs) generated from slowly dividing NSCs occurs only in the ventricular-subventricular zone (V-SVZ) and subgranular zone (SGZ) [14, 22, 30, 31, 36–38]
What factors contribute to the decrease in adult neurogenesis upon aging? The expression of EGF and FGF, which are well-known mitogens that promote the self-renewal of activated neural stem cells (aNSC) and TAPs, in the brain decreases with age, which may be a cause of the agedependent decline in neurogenesis [32, 33, 42]
Summary
Neural stem cells (NSCs) in the early embryonic period are called neuroepithelial cells. Neuroepithelial cells self-renew symmetrically on the ventricular surface [1, 2] This symmetric division increases the number of neuroepithelial cells lining the ventricular surface and enlarges the ventricular zone (VZ) [3]. The attenuation of neurogenesis in the mouse SGZ has been reported to result in the impairment of new memory formation [7, 18–23]. These new neurons are important for the formation of spatial memories [24–27]. Adult neurogenesis decreases with age, mainly due to a decrease in NSCs and TAPs [14, 30, 31]. We review adult NSCs and neurogenesis and the mechanisms of their age-related declines. We will describe the challenges of NSC activation as a therapeutic strategy
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