Abstract
Although studies show new neurons generated from progenitor cells in a healthy adult neocortex, neurogenic potential derived from stem/progenitor cells in the cortex of Alzheimer's patients still remains unsolved. In this study, we isolated the glial progenitor cells (GPCs) from the cortex of healthy (HC) and Alzheimer's disease (AD). The AD-GPCs displayed reduced capability to renew and decreased production of new neurons. Interestingly, we found significant reduction of [beta]-catenin in AD-GPCs compared to HC while glycogen synthase kinase 3[beta] (GSK-3[beta]) was promoted. Moreover, we found both increased phosphorylation of [beta]-catenin in AD-GPCs and their progeny cells. Amyloid [beta] peptide (A[beta]) treatment results in increase of GSK-3[beta] and a reduction of [beta]-catenin, ultimately impairment of neurogenesis of GPCs. Similar results were observed in GPCs from AD transgenic mice. These results suggest that decreased [beta]-catenin signaling by A[beta] may be one of causes for the lack of neurogenesis in AD-GPCs.
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He, P., Staufenbiel, M. & Shen, Y. Interruption of [beta]-Catenin Signaling Reduces Neurogenesis in Alzheimer's Disease Brains. Nat Prec (2008). https://doi.org/10.1038/npre.2008.2257.1
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DOI: https://doi.org/10.1038/npre.2008.2257.1