ArticleCommunications biology2021
Mitochondrial ubiquitin ligase alleviates Alzheimer's disease pathology via blocking the toxic amyloid-β oligomer generation.
Article in Communications biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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Who cites it
21 citing papers in PubMed, 30 citations in OpenAlex.
- Mechanisms and Therapeutic Potential of Targeting Mitophagy in Neurodegenerative Diseases.Molecular neurobiology · 2026Review
- Interplay of oxidative stress and neuroinflammation in alzheimer's: insights into age-driven pathogenesis.Inflammopharmacology · 2026Review
- Article
- Association of Human Gut Microbiota with Alzheimer's Disease Pathogenesis: An Exploratory Clinical Study.Brain sciences · 2026Article
- The emerging role of ubiquitin-proteasome system dysfunction in the pathogenesis of perioperative neurocognitive disorders: a narrative review.Frontiers in behavioral neuroscience · 2026Review
- E3 ubiquitin ligases in neurodegenerative diseases.Military Medical Research · 2026Review
- Dapagliflozin mitigates cognitive deficits in a rat model of chronic restrained stress by addressing insulin resistance and mitochondrial dysfunction.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- March5-mediated Trim28 degradation preserves islet β-cell function in mice.Nature communications · 2025Article
- Review of FUNDC1-mediated mitochondrial autophagy in Alzheimer's disease.Frontiers in aging neuroscience · 2025Review
- New Insights into Mitochondria in Health and Diseases.International journal of molecular sciences · 2024Review
- Mitochondrial E3 ligase MARCH5 is a safeguard against DNA-PKcs-mediated immune signaling in mitochondria-damaged cells.Cell death & disease · 2023Article
- Mitochondria-sequestered Aβ renders synaptic mitochondria vulnerable in the elderly with a risk of Alzheimer disease.JCI insight · 2023Article
- MARCH5-dependent NLRP3 ubiquitination is required for mitochondrial NLRP3-NEK7 complex formation and NLRP3 inflammasome activation.The EMBO journal · 2023Article
- H3K27 acetylation-induced FSTL1 upregulation by P300/RUNX1 co-activation exacerbated autophagy-mediated neuronal damage and NF-κB-stimulated inflammation in Alzheimer's disease.Cytotechnology · 2023Article
- Alzheimer's Progenitor Amyloid-β Targets and Dissolves Microbial Amyloids and Impairs Biofilm Function.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Development of a Mitochondrial Targeting Lipid Nanoparticle Encapsulating Berberine.International journal of molecular sciences · 2023Article
- Natural products regulate mitochondrial function in cognitive dysfunction-A scoping review.Frontiers in pharmacology · 2023Article
- Amyloid Cascade Hypothesis for the Treatment of Alzheimer's Disease: Progress and Challenges.Aging and disease · 2022Article
- Co-expression network analysis of human tau-transgenic mice reveals protein modules associated with tau-induced pathologies.iScience · 2022Article
- Disentangling Mitochondria in Alzheimer's Disease.International journal of molecular sciences · 2021Review
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondrial pathophysiology is implicated in the development of Alzheimer's disease (AD). An integrative database of gene dysregulation suggests that the mitochondrial ubiquitin ligase MITOL/MARCH5, a fine-tuner of mitochondrial dynamics and functions, is downregulated in patients with AD. Here, we report that the perturbation of mitochondrial dynamics by MITOL deletion triggers mitochondrial impairments and exacerbates cognitive decline in a mouse model with AD-related Aβ pathology. Notably, MITOL deletion in the brain enhanced the seeding effect of Aβ fibrils, but not the spontaneous formation of Aβ fibrils and plaques, leading to excessive secondary generation of toxic and dispersible Aβ oligomers. Consistent with this, MITOL-deficient mice with Aβ etiology exhibited worsening cognitive decline depending on Aβ oligomers rather than Aβ plaques themselves. Our findings suggest that alteration in mitochondrial morphology might be a key factor in AD due to directing the production of Aβ form, oligomers or plaques, responsible for disease development.
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Registered trials
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.