ArticleAlzheimer's & dementia : the journal of the Alzheimer's Association2024
Inhibiting mtDNA transcript translation alters Alzheimer's disease-associated biology.
Article in Alzheimer's & dementia : the journal of the Alzheimer's Association, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Metabolic breakdown: Linking insulin resistance and mitochondrial dysfunction to neurodegeneration in Alzheimer's disease.Neural regeneration research · 2026Article
- Variecolactone, a Natural PDE4 Inhibitor from Marine-DerivedBiomolecules · 2026Article
- ALKB-1-dependent tRNA methylation is required for efficient paternal mitochondrial elimination.Nature communications · 2026Article
- Advances in research on mitochondrial dysfunction in neurodegenerative diseases.Journal of neurology · 2025Review
- Inhibiting mtDNA transcript translation alters Alzheimer's disease-associated biology.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024Article
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14 authors.
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Abstract
introductionAlzheimer's disease (AD) features changes in mitochondrial structure and function. Investigators debate where to position mitochondrial pathology within the chronology and context of other AD features.
methodsTo address whether mitochondrial dysfunction alters AD-implicated genes and proteins, we treated SH-SY5Y cells and induced pluripotent stem cell (iPSC)-derived neurons with chloramphenicol, an antibiotic that inhibits mtDNA-generated transcript translation. We characterized adaptive, AD-associated gene, and AD-associated protein responses.
resultsSH-SY5Y cells and iPSC neurons responded to mtDNA transcript translation inhibition by increasing mtDNA copy number and transcription. Nuclear-expressed respiratory chain mRNA and protein levels also changed. There were AD-consistent concordant and model-specific changes in amyloid precursor protein, beta amyloid, apolipoprotein E, tau, and α-synuclein biology. DISCUSSION: Primary mitochondrial dysfunction induces compensatory organelle responses, changes nuclear gene expression, and alters the biology of AD-associated genes and proteins in ways that may recapitulate brain aging and AD molecular phenomena. HIGHLIGHTS: In AD, mitochondrial dysfunction could represent a disease cause or consequence. We inhibited mitochondrial translation in human neuronal cells and neurons. Mitochondrial and nuclear gene expression shifted in adaptive-consistent patterns. APP, Aβ, APOE, tau, and α-synuclein biology changed in AD-consistent patterns. Mitochondrial stress creates an environment that promotes AD pathology.
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