Modifiers of Neural Stem Cells and Aging: Pulling the Trigger of a Neurogenic Decline

Abstract

The adult mammalian central nervous system contains resident neural stem cells able to self-renew and to generate new neurons throughout life, as well as other neural cell types. Progressive changes in adult neural stem cells accompany the aging process, which may contribute to a progressive decline in regenerative capacities, tissue degeneration, and functional impairments. For example, accelerated and pathological declines in neural stem cell functions have been associated with age-related brain diseases. Therefore, identifying and better understanding the age-associated molecular events involved in the deterioration of adult neural stem cell homeostasis is of high interest. To date, several intrinsic and extrinsic factors have been identified as putative drivers for age-related dysfunctions in brain stem cell niches. This review aims to provide a concise overview of the age-associated changes that have been reported in mammalian adult neural stem cells as well as the underlying events able to trigger those changes.

Curcumin Alleviates the Senescence of Canine Bone Marrow Mesenchymal Stem Cells during In Vitro Expansion by Activating the Autophagy Pathway

“…As a type of adult stem cells with the capacity for self-renewal, immunosuppression, differentiation, and migration, mesenchymal stem cells (MSCs) extensively reside within various tissues and organs, such as bone marrow, adipose tissue, amniotic fluid, placenta, umbilical cord, and muscle [ 1 , 2 ], and play an essential role in maintaining tissue homeostasis throughout the lifespan of an organism [ 3 , 4 ]. Accumulating evidence has revealed that biological aging and the development of many degenerative diseases can attribute to MSC senescence [ 5 , 6 ]. In addition, MSCs are promising sources of cell-based regenerative therapy, but usually need to be expanded in vitro to achieve the minimum transplantation number of MSCs (20–100 million) for treatments [ 7 ].…”