ArticleJournal of Alzheimer's disease : JAD2015
Mitochondrial lysates induce inflammation and Alzheimer's disease-relevant changes in microglial and neuronal cells.
Article in Journal of Alzheimer's disease : JAD, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
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Who cites it
54 citing papers in PubMed, 78 citations in OpenAlex.
- Circulating mitochondrial DNA: New indices of type 2 diabetes-related cognitive impairment in Mexican Americans.PloS one · 2019Trial
- The Crosstalk Between Diabetes and Alzheimer's Disease: A Molecular Perspective.Basic & clinical pharmacology & toxicology · 2026Review
- The role of gut microbiota-mitochondria crosstalk in neurodegeneration: Underlying mechanisms and potential therapies.Neural regeneration research · 2026Article
- Physical Exercise Counteracts Impaired Cognition by Improving Mitochondrial Function.International journal of molecular sciences · 2026Review
- Thioredoxin protects against diabetic hearing loss by regulating TOMM22 mediated mitochondrial autophagy in hair cells and inhibiting microglial M1 polarization.Scientific reports · 2026Article
- Ceramides may Play a Central Role in the Pathogenesis of Alzheimer's Disease: a Review of Evidence and Horizons for Discovery.Molecular neurobiology · 2025Review
- The neuroimmune nexus: unraveling the role of the mtDNA-cGAS-STING signal pathway in Alzheimer's disease.Molecular neurodegeneration · 2025Review
- Mitophagy-associated programmed neuronal death and neuroinflammation.Frontiers in immunology · 2024Review
- Unraveling the intricate link between cell death and neuroinflammation usingFrontiers in cell and developmental biology · 2024Review
- Brain alarm by self-extracellular nucleic acids: from neuroinflammation to neurodegeneration.Journal of biomedical science · 2023Review
- From the Bush to the Brain: Preclinical Stages of Ethnobotanical Anti-Inflammatory and Neuroprotective Drug Discovery-An Australian Example.International journal of molecular sciences · 2023Review
- The Impact of microRNAs on Mitochondrial Function and Immunity: Relevance to Parkinson's Disease.Biomedicines · 2023Review
- Fish Models for Exploring Mitochondrial Dysfunction Affecting Neurodegenerative Disorders.International journal of molecular sciences · 2023Review
- Nano-Brake Halts Mitochondrial Dysfunction Cascade to Alleviate Neuropathology and Rescue Alzheimer's Cognitive Deficits.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Mitochondrial control of inflammation.Nature reviews. Immunology · 2023Review
- Cell type and sex specific mitochondrial phenotypes in iPSC derived models of Alzheimer's disease.Frontiers in molecular neuroscience · 2023Article
- Review
- The Role of Bioenergetics in Neurodegeneration.International journal of molecular sciences · 2022Review
- Pharmacological considerations for treating neuroinflammation with curcumin in Alzheimer's disease.Journal of neural transmission (Vienna, Austria : 1996) · 2022Review
- Molecular regulation of neuroinflammation in glaucoma: Current knowledge and the ongoing search for new treatment targets.Progress in retinal and eye research · 2022Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Neuroinflammation occurs in Alzheimer's disease (AD). While AD genetic studies implicate inflammation-relevant genes and fibrillar amyloid-β protein promotes inflammation, our understanding of AD neuroinflammation nevertheless remains incomplete. In this study we hypothesized damage-associated molecular pattern (DAMP) molecules arising from mitochondria, intracellular organelles that resemble bacteria, could contribute to AD neuroinflammation. To preliminarily test this possibility, we exposed neuronal and microglial cell lines to enriched mitochondrial lysates. BV2 microglial cells treated with mitochondrial lysates showed decreased TREM2 mRNA, increased TNFα mRNA, increased MMP-8 mRNA, increased IL-8 mRNA, redistribution of NFκB to the nucleus, and increased p38 MAPK phosphorylation. SH-SY5Y neuronal cells treated with mitochondrial lysates showed increased TNFα mRNA, increased NFκB protein, decreased IκBα protein, increased AβPP mRNA, and increased AβPP protein. Enriched mitochondrial lysates from SH-SY5Y cells lacking detectable mitochondrial DNA (ρ0 cells) failed to induce any of these changes, while mtDNA obtained directly from mitochondria (but not PCR-amplified mtDNA) increased BV2 cell TNFα mRNA. These results indicate at least one mitochondrial-derived DAMP molecule, mtDNA, can induce inflammatory changes in microglial and neuronal cell lines. Our data are consistent with the hypothesis that a mitochondrial-derived DAMP molecule or molecules could contribute to AD neuroinflammation.
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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.