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Abstract
Mitochondrial pathophysiology is implicated in Alzheimer's disease (AD). This study finds that MITOL/MARCH5, a mitochondrial ubiquitin ligase regulating mitochondrial dynamics, is downregulated in AD patients. MITOL deletion in an AD mouse model exacerbated cognitive decline and mitochondrial impairments. This was linked to increased production of toxic Aβ oligomers due to enhanced seeding by Aβ fibrils, rather than increased Aβ plaque formation. The findings suggest that mitochondrial morphology alterations direct Aβ aggregation towards oligomers, a key factor in AD pathogenesis.
Publisher
Communications Biology
Published On
Feb 12, 2021
Authors
Keisuke Takeda, Aoi Uda, Mikihiro Mitsubori, Shun Nagashima, Hiroko Iwasaki, Naoki Ito, Isshin Shiiba, Satoshi Ishido, Masaaki Matsuoka, Ryoko Inatome, Shigeru Yanagi
Tags
Alzheimer's disease
mitochondrial dynamics
MITOL/MARCH5
cognitive decline
Aβ oligomers
pathogenesis
neurodegeneration
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