%0 Journal Article
%T The effects of aging on Amyloid-¦Â42-induced neurodegeneration and regeneration in adult zebrafish brain
%A Alvin Kuriakose Thomas
%A Caghan Kizil
%A Prabesh Bhattarai
%A Yixin Zhang
%J Archive of "Neurogenesis".
%D 2017
%R 10.1080/23262133.2017.1322666
%X Alzheimer disease is the most prevalent neurodegenerative disease and is associated with aggregation of Amyloid-¦Â42 peptides. In mammals, Amyloid-¦Â42 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-¦Â42 model in adult zebrafish that displayed Alzheimer-like phenotypes reminiscent of humans. Interestingly, zebrafish exhibited enhanced NSPC proliferation and neurogenesis after microinjection of Amyloid-¦Â42 peptide. Here, we compare old and young fish to address the effects of aging on regenerative ability after Amyloid-¦Â42 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-¦Â42 in zebrafish, suggesting an important link between aging, neuroinflammation, regenerative neurogenesis and neural stem cell plasticity
%K Alzheimer disease
%K amyloid-¦Â 42
%K A¦Â42
%K aging
%K inflammation
%K neurodegeneration
%K neural stem progenitor cell
%K neurogenesis
%K regeneration
%K microglia
%K zebrafish
%U https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5477701/