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p62 improves AD-like pathology by increasing autophagy
A Caccamo1, E Ferreira1, C Branca1
1The Arizona State University-Banner Neurodegenerative Disease Research Center, Biodesign Institute at Arizona State University, Tempe, AZ, USA.
Molecular Psychiatry
|August 31, 2016
Summary
Increasing brain p62 protein levels improved cognitive function in Alzheimer
Area of Science:
- Neuroscience
- Molecular Biology
- Genetics
Background:
- p62 protein is linked to neurodegenerative diseases like Alzheimer's disease (AD).
- p62 is involved in tau degradation in AD, but its role in amyloid-beta (Aβ) aggregation and clearance is unclear.
Purpose of the Study:
- To investigate the role of p62 in regulating amyloid-beta (Aβ) aggregation and degradation in Alzheimer's disease (AD).
Main Methods:
- Gene therapy to increase p62 expression in APP/PS1 mice (an AD model).
- Assessed cognitive function, Aβ levels, and plaque load.
- Utilized genetic and pharmacological approaches to investigate the role of autophagy and the LC3-interacting region of p62.
Main Results:
- Increased brain p62 expression rescued cognitive deficits in AD mice.
- This cognitive improvement correlated with reduced Aβ levels and plaque burden.
- p62-mediated Aβ reduction was dependent on enhanced autophagy.
Conclusions:
- p62 plays a direct role in regulating amyloid-beta (Aβ) turnover in vivo.
- Enhancing p62 expression and autophagy may represent a therapeutic strategy for Alzheimer's disease (AD).
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