ArticleMolecular neurobiology2025
UQCRC1 is a Key Pathogenic Determinant and Potential Therapeutic Target for Cognitive Impairment in Alzheimer's Disease.
Article in Molecular neurobiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Characterization of aMolecular genetics and metabolism reports · 2026Article
- Aging-related gene signatures as potential biomarkers in ischemic stroke: an integrated bioinformatics and machine learning study.BMC neurology · 2026Article
- Synaptic mitochondrial dysfunction and Alzheimer's disease: from molecular mechanisms to therapeutic strategies.Frontiers in pharmacology · 2026Review
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Authors and funding
6 authors.
Funding
Abstract
Alzheimer's disease (AD) is a chronic neurodegenerative disorder and the most prevalent cause of dementia, yet it remains incurable. Ubiquinol-cytochrome c reductase core protein 1 (UQCRC1), a pivotal subunit of mitochondrial complex III, has been implicated in Alzheimer's disease pathogenesis, though its precise mechanistic contributions remain undefined. In this study, we systematically investigated the mechanistic involvement of UQCRC1 in AD pathogenesis. Our findings reveal significant downregulation of UQCRC1 expression in hippocampal tissues from both AD patients and APP/PS1 transgenic mice. Conditional UQCRC1 knockdown in AD model mice exacerbated cognitive deficits while transmission electron microscopy analysis demonstrated that UQCRC1 deficiency induces pathological lysosomal enlargement, lipofuscin accumulation, and increased neuronal apoptosis in hippocampal neurons. Mechanistic interrogation revealed that UQCRC1 depletion triggers lysosomal Ca
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Registered trials
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