ArticleAlzheimer's & dementia : the journal of the Alzheimer's Association2020
Mitophagy alterations in Alzheimer's disease are associated with granulovacuolar degeneration and early tau pathology.
Article in Alzheimer's & dementia : the journal of the Alzheimer's Association, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 3 of them syntheses that pooled it.
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Who cites it
48 citing papers in PubMed, 3 syntheses or guidelines pooled it.
- Mitochondrial quality control in neurodegenerative diseases: from molecular mechanisms to natural product therapies.Frontiers in physiology · 2025Pooled it
- The Emerging Roles of E3 Ligases and DUBs in Neurodegenerative Diseases.Molecular neurobiology · 2023Pooled it
- Deregulated mitochondrial microRNAs in Alzheimer's disease: Focus on synapse and mitochondria.Ageing research reviews · 2022Pooled it
- The role of phospho-ubiquitin in mitochondrial health and diseases.The Journal of biological chemistry · 2026Review
- Association of mitochondrial genetic background with pS65-Ub in Lewy body disease.Acta neuropathologica · 2026Article
- Association between Human Leukocyte Antigen Alleles and Neuropathological Outcomes in Lewy Body Disease.Annals of neurology · 2026Article
- Autophagy and mitophagy at the synapse and beyond: implications for learning, memory and neurological disorders.Autophagy · 2026Review
- Targeting protein aggregate co-pathologies in neurodegeneration: a viable therapeutic strategy?Molecular neurodegeneration advances · 2026Review
- Genetic factors and comorbid pathologies interact to drive regional mitophagy alterations in Lewy body dementia.Acta neuropathologica · 2025Article
- Activation of endogenous PRKN by structural derepression is linked to increased turnover of the E3 ubiquitin ligase.Autophagy · 2025Article
- LRRK2 kinase-mediated accumulation of lysosome-associated phospho-Rabs in tauopathies and synucleinopathies.Acta neuropathologica · 2025Article
- Amyloid-β protein precursor modulates mitophagy and mitochondrial function through its cellular localization.Journal of Alzheimer's disease : JAD · 2025Article
- Mitochondrial complex I deficiency induces Alzheimer's disease-like signatures that are reversible by targeted therapy.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- LRRK2-mediated mitochondrial dysfunction in Parkinson's disease.The Biochemical journal · 2025Review
- Article
- Genome-wide association analysis identifies APOE as a mitophagy modifier in Lewy body disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Hippocampal mitophagy alterations in MAPT-associated frontotemporal dementia with parkinsonism.Acta neuropathologica communications · 2025Article
- Cornuside alleviates cognitive impairments induced by AβAlzheimer's research & therapy · 2025Article
- Tau phosphorylation suppresses oxidative stress-induced mitophagy via FKBP8 receptor modulation.PloS one · 2025Article
- Insights into targeted ferroptosis in mechanisms, biology, and role of Alzheimer's disease: an update.Frontiers in aging neuroscience · 2025Review
Corrections and comments
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Authors and funding
21 authors.
Funding
Abstract
introductionThe cytoprotective PTEN-induced kinase 1 (PINK1)-parkin RBR E3 ubiquitin protein ligase (PRKN) pathway selectively labels damaged mitochondria with phosphorylated ubiquitin (pS65-Ub) for their autophagic removal (mitophagy). Because dysfunctions of mitochondria and degradation pathways are early features of Alzheimer's disease (AD), mitophagy impairments may contribute to the pathogenesis.
methodsMorphology, levels, and distribution of the mitophagy tag pS65-Ub were evaluated by biochemical analyses combined with tissue and single cell imaging in AD autopsy brain and in transgenic mouse models.
resultsAnalyses revealed significant increases of pS65-Ub levels in AD brain, which strongly correlated with granulovacuolar degeneration (GVD) and early phospho-tau deposits, but were independent of amyloid beta pathology. Single cell analyses revealed predominant co-localization of pS65-Ub with mitochondria, GVD bodies, and/or lysosomes depending on the brain region analyzed. DISCUSSION: Our study highlights mitophagy alterations in AD that are associated with early tau pathology, and suggests that distinct mitochondrial, autophagic, and/or lysosomal failure may contribute to the selective vulnerability in disease.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.