ArticleNature communications2016
Deregulation of mitochondrial F1FO-ATP synthase via OSCP in Alzheimer's disease.
Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 125 papers, 1 of them a synthesis that pooled it.
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Who cites it
125 citing papers in PubMed, 1 synthesis or guideline pooled it, 169 citations in OpenAlex.
- Hippocampal transcriptome-wide association study and pathway analysis of mitochondrial solute carriers in Alzheimer's disease.Translational psychiatry · 2024Pooled it
- Combined metabolic activators improve cognitive functions in Alzheimer's disease patients: a randomised, double-blinded, placebo-controlled phase-II trial.Translational neurodegeneration · 2023Trial
- Microglia-targetedMaterials today. Bio · 2026Article
- Mitochondrial Complex V Dysfunction in Neurodegeneration: Secondary Bystander or Primary Driver?Brain sciences · 2026Review
- Mitochondrial quality control in health and disease: mechanisms and therapeutic targets.Signal transduction and targeted therapy · 2026Review
- Mitochondrial Dysfunction in Alzheimer's Disease and Mitochondria-Targeted Therapeutics.Cells · 2026Review
- Loss of ovarian function and estrogen therapy remodel the brain's synaptic and metabolic proteome.American journal of physiology. Regulatory, integrative and comparative physiology · 2026Article
- The multifaceted role of mitochondrial dysfunction in Alzheimer's disease pathogenesis.Metabolic brain disease · 2026Review
- Requirement for oxidation of neuronal ketone bodies in aging and neurodegeneration.bioRxiv : the preprint server for biology · 2026Article
- Reversible dissociation of mitochondrial Complex V balances anabolic and energy-generating needs in cancer.iScience · 2026Article
- Glutaredoxin 2 is essential for AML survival through mitochondrial permeability transition pore regulation.Blood · 2026Article
- Article
- Astrocytic KFrontiers in aging neuroscience · 2026Review
- The Vitamin D Receptor Ortholog Hr96 Modulates Neuronal and Mitochondrial Dynamics in a Drosophila Model of Alzheimer's Disease.Molecular neurobiology · 2025Article
- Loss of ovarian function and estrogen therapy remodel the brain's synaptic and metabolic proteome.bioRxiv : the preprint server for biology · 2025Article
- CRISPR-Enhanced Colorimetric Aptasensor for Adenosine Triphosphate Detection Based on MoSBiosensors · 2025Article
- Cannabidiol alleviates methamphetamine addictionActa pharmaceutica Sinica. B · 2025Article
- Differential effects of age and sex on tau pathology propagation in the htau mouse model: A neuropathological and proteomic study.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Vulnerability of mitochondrial OXPHOS complexes in the arcuate nucleus of the hypothalamus of Alzheimer's disease.Journal of Alzheimer's disease : JAD · 2025Article
- Role of mitochondria in physiological activities, diseases, and therapy.Molecular biomedicine · 2025Review
65 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
Abstract
F1FO-ATP synthase is critical for mitochondrial functions. The deregulation of this enzyme results in dampened mitochondrial oxidative phosphorylation (OXPHOS) and activated mitochondrial permeability transition (mPT), defects which accompany Alzheimer's disease (AD). However, the molecular mechanisms that connect F1FO-ATP synthase dysfunction and AD remain unclear. Here, we observe selective loss of the oligomycin sensitivity conferring protein (OSCP) subunit of the F1FO-ATP synthase and the physical interaction of OSCP with amyloid beta (Aβ) in the brains of AD individuals and in an AD mouse model. Changes in OSCP levels are more pronounced in neuronal mitochondria. OSCP loss and its interplay with Aβ disrupt F1FO-ATP synthase, leading to reduced ATP production, elevated oxidative stress and activated mPT. The restoration of OSCP ameliorates Aβ-mediated mouse and human neuronal mitochondrial impairments and the resultant synaptic injury. Therefore, mitochondrial F1FO-ATP synthase dysfunction associated with AD progression could potentially be prevented by OSCP stabilization.
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