ArticleHuman molecular genetics2015
Mitochondrial ATP synthase activity is impaired by suppressed O-GlcNAcylation in Alzheimer's disease.
Article in Human molecular genetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
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Who cites it
55 citing papers in PubMed, 86 citations in OpenAlex.
- O-GlcNAcylation: A molecular switch linking brain health to neurodegeneration.Neural regeneration research · 2026Article
- Mitochondrial Complex V Dysfunction in Neurodegeneration: Secondary Bystander or Primary Driver?Brain sciences · 2026Review
- Brain O-GlcNAcylation in Neurodegenerative Diseases: Context-Dependent Mechanisms and Precision Therapeutic Translation.Brain sciences · 2026Review
- Comprehensive Lipidomic Profiling Reveals Distinct Metabolic Remodeling during Differentiation of Human Monocyte-Derived Macrophages.Journal of proteome research · 2026Article
- The Role of the Ketogenic Diet in Modulating Biochemical Pathophysiology in Psychiatric and Neurodegenerative Disorders.International journal of molecular sciences · 2026Review
- Sex-dependent differences in bioenergetics of young mouse brain microvasculature: implications for oxygen-glucose deprivation and reoxygenation injury.American journal of physiology. Heart and circulatory physiology · 2026Article
- N-acetylcysteine (NAC) ameliorates ethanol-induced oxidative stress, neuroinflammation, and cognitive dysfunction in APP/PS1 mouse model.Translational psychiatry · 2025Article
- Hyaluronidase-1 mediates postprandial suppression of hepatic gluconeogenesis.Life metabolism · 2025Article
- Article
- Paternal DDT exposure induces sex-specific programming of fetal growth, placenta development and offspring's health phenotypes in a mouse model.Scientific reports · 2024Article
- O-GlcNAcylation: a pro-survival response to acute stress in the cardiovascular and central nervous systems.European journal of medical research · 2024Review
- Simple model systems reveal conserved mechanisms of Alzheimer's disease and related tauopathies.Molecular neurodegeneration · 2023Review
- Human Prune Regulates the Metabolism of Mammalian Inorganic Polyphosphate and Bioenergetics.International journal of molecular sciences · 2023Article
- Altered O-GlcNAcylation and mitochondrial dysfunction, a molecular link between brain glucose dysregulation and sporadic Alzheimer's disease.Neural regeneration research · 2023Article
- Electroacupuncture ameliorates surgery-induced spatial memory deficits by promoting mitophagy in rats.Annals of translational medicine · 2023Article
- The sORF-Encoded Peptides, ATP Synthase Subunits, Facilitate WSSV Duplication in Shrimp.Viruses · 2022Article
- SIRT1 deficiency increases O-GlcNAcylation of tau, mediating synaptic tauopathy.Molecular psychiatry · 2022Article
- Short O-GlcNAcase Is Targeted to the Mitochondria and Regulates Mitochondrial Reactive Oxygen Species Level.Cells · 2022Article
- From the Structural and (Dys)Function of ATP Synthase to Deficiency in Age-Related Diseases.Life (Basel, Switzerland) · 2022Review
- Bacterial F-type ATP synthases follow a well-choreographed assembly pathway.Nature communications · 2022Article
Corrections and comments
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Authors and funding
19 authors at 6 institutions in 2 countries.
Funding
Abstract
Glycosylation with O-linked β-N-acetylglucosamine (O-GlcNAc) is one of the protein glycosylations affecting various intracellular events. However, the role of O-GlcNAcylation in neurodegenerative diseases such as Alzheimer's disease (AD) is poorly understood. Mitochondrial adenosine 5'-triphosphate (ATP) synthase is a multiprotein complex that synthesizes ATP from ADP and Pi. Here, we found that ATP synthase subunit α (ATP5A) was O-GlcNAcylated at Thr432 and ATP5A O-GlcNAcylation was decreased in the brains of AD patients and transgenic mouse model, as well as Aβ-treated cells. Indeed, Aβ bound to ATP synthase directly and reduced the O-GlcNAcylation of ATP5A by inhibition of direct interaction between ATP5A and mitochondrial O-GlcNAc transferase, resulting in decreased ATP production and ATPase activity. Furthermore, treatment of O-GlcNAcase inhibitor rescued the Aβ-induced impairment in ATP production and ATPase activity. These results indicate that Aβ-mediated reduction of ATP synthase activity in AD pathology results from direct binding between Aβ and ATP synthase and inhibition of O-GlcNAcylation of Thr432 residue on ATP5A.
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