Neurogenesis and Aging and Disease
Circa 2010
This review examines the evidence for a reduction of neurogenesis as underlying aging-related cognition deficits and impairments associated with disorders like Alzheimer’s Disease (AD). We discuss the molecular changes and cellular changes associated with impaired brain neurogenesis as we age. The impairment of neurogenesis in AD is likely due to dysfunction of presenilin-1 and misprocessing of the amyloid precursor proteins, as well as toxic effects from hyperphosphorylated tau or b-amyloid. Exercise, enrichment, and dietary energy restrictions can enhance neurogenesis and protect against age related cognitive decline and AD. Understanding the neurogenic signaling pathway could lead to new therapeutic strategies that preserve brain function. The manipulation of neural stem cells, and stem cell therapy, either as a stand-alone treatment or an adjunct, seems promising.
The regenerative ability of many organs decreases as we age. This leads to a decline in function and a poorer response to injury or disease. It was once believed that stem cells were only found in tissues with high turnover, like the intestinal lining and bone marrow. However, it appears that they are present in most tissues. These cells contribute to tissue integrity all through life. The stem cell number decreases with age in many cases. This suggests that stem cell aging could be fundamental to the biology and aging process. [1]). Understanding the regulation of stem cells maintenance or activation will help us to understand the age-related decline of tissue integrity, function and regenerative response.
The adult brain contains neural progenitor (NPC) cells that are partially lineage-committed. They self-renew and proliferate. After several cycles of proliferation, NPC differentiates into new neurons or glia. NSCs have been increasingly recognized as having a functional importance and containing the potential to repair a diseased or damaged brain. It is believed that the dramatic decline in neurogenesis as we age may be responsible for learning and memory impairments, at least partially. Alzheimer’s (AD), a neurodegenerative disorder characterized by progressive memory loss and cognitive decline, is most likely to be caused by aging. Animal models of AD have described extensive changes in neurogenesis, and it has been shown that key proteins involved with AD pathogenesis regulate neurogenesis.
Source:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2981641/
