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Molecular mechanisms of regeneration in Alzheimer's disease brain
Author(s) -
Uchida Yoko
Publication year - 2010
Publication title -
geriatrics and gerontology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.823
H-Index - 57
eISSN - 1447-0594
pISSN - 1444-1586
DOI - 10.1111/j.1447-0594.2010.00607.x
Subject(s) - neuroscience , downregulation and upregulation , neurite , progenitor cell , programmed cell death , regeneration (biology) , medicine , amyloid beta , alzheimer's disease , microbiology and biotechnology , disease , biology , stem cell , pathology , apoptosis , biochemistry , in vitro , gene
Regenerative responses, including re‐expression of developmentally regulated proteins, occur in Alzheimer's disease (AD) brain and in β‐amyloid (Aβ)‐treated neuronal cultures. Brain microenvironment might also be altered by Aβ or by unknown materials in AD brain to make neurons or progenitor cells regenerative. However, these responses and alterations might not be sufficient to replace neuronal loss, but rather might act as an effecter of cell death. For instance, downregulation of growth inhibitory factor/metallothionein‐III and upregulation of MAP1B result in both neurite sprouting and neuronal death. The deteriorative regulation of Mash1 and Olig2 by Aβ also leads to differentiation and death of progenitor cells. Clarifying the cell death mechanism accompanied with regenerative responses might be necessary for repairing the nervous system or slowing disease progression in AD. Geriatr Gerontol Int 2010; 10 (Suppl. 1): S158–S168.