VDAC1-Targeted NHK1 Peptide Recovers Mitochondrial Dysfunction Counteracting Amyloid-β Oligomers Toxicity in Alzheimer's Disease.

ABSTRACT: Mitochondrial dysfunction has been implicated in a broad range of age-related pathologies and has been proposed as a causative factor in Alzheimer's disease (AD). Analysis of post-mortem brains from AD patients showed increased levels of Voltage-dependent anion-selective channel 1 (VDAC1) in the dystrophic neurites surrounding amyloid-β (Aβ) deposits, suggesting a direct association between VDAC1 and mitochondrial toxicity. VDAC1 is the most abundant pore-forming protein of the outer mitochondrial membrane and, as a channel, it plays a pivotal role in regulating cellular bioenergetics, allowing the continuous exchange of ions and metabolites (ATP/ADP, Krebs cycle intermediates) between cytosol and mitochondria. In light of this evidence, we looked into the effects of Aβ oligomers on VDAC1

SUBMITTER: Cavallaro F 

PROVIDER: S-EPMC12266788 | biostudies-literature | 2025 Jul

REPOSITORIES: biostudies-literature