PUBLICATION

The effects of aging on Amyloid-?42-induced neurodegeneration and regeneration in adult zebrafish brain

Authors
Bhattarai, P., Thomas, A.K., Zhang, Y., Kizil, C.
ID
ZDB-PUB-170629-9
Date
2017
Source
Neurogenesis (Austin, Tex.)   4: e1322666 (Journal)
Registered Authors
Bhattarai, Prabesh, Kizil, Caghan
Keywords
Alzheimer disease, A?42, aging, amyloid-? 42, inflammation, microglia, neural stem progenitor cell, neurodegeneration, neurogenesis, regeneration, zebrafish
MeSH Terms
none
PubMed
28656156 Full text @ Neurogenesis (Austin)
Abstract
Alzheimer disease is the most prevalent neurodegenerative disease and is associated with aggregation of Amyloid-?42 peptides. In mammals, Amyloid-?42 causes impaired neural stem/progenitor cell (NSPC) proliferation and neurogenesis, which exacerbate with aging. The molecular programs necessary to enhance NSPC proliferation and neurogenesis in our brains to mount successful regeneration are largely unknown. Therefore, to identify the molecular basis of effective brain regeneration, we previously established an Amyloid-?42 model in adult zebrafish that displayed Alzheimer-like phenotypes reminiscent of humans. Interestingly, zebrafish exhibited enhanced NSPC proliferation and neurogenesis after microinjection of Amyloid-?42 peptide. Here, we compare old and young fish to address the effects of aging on regenerative ability after Amyloid-?42 deposition. We found that aging does not affect the rate of NSPC proliferation but reduces the neurogenic response and microglia/macrophage activation after microinjection of Amyloid-?42 in zebrafish, suggesting an important link between aging, neuroinflammation, regenerative neurogenesis and neural stem cell plasticity.
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