ArticleMolecular psychiatry2025
Mitochondrial DNA abundance in blood is associated with Alzheimer's disease- and dementia-risk.
Article in Molecular psychiatry, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed.
- Lower mitochondrial DNA copy number in ATTRV50M Swedish carriers.Orphanet journal of rare diseases · 2026Article
- Preliminary insights into whole-blood mitochondrial DNA copy number and telomere length in Parkinson's disease and multiple system atrophy.Journal of neurology · 2026Article
- Photobiomodulation with 808 nm Laser Light Repairs Mitochondrial Integrity and Normalizes ROS, ATP, and Membrane Depolarization in Aβ-Exposed Primary Neurons in Alzheimer's Disease Model.International journal of molecular sciences · 2026Article
- Mitochondrial Dysfunction: From Molecular Mechanisms to Modern Approaches for Basic and Clinical Research.Biomedicines · 2026Review
- Reduced Mitochondrial DNA Copy Number and Telomere Length in Essential Tremor Patients: Evidence from an Age- and Sex-Adjusted Cross-Sectional Case-Control Study.International journal of molecular sciences · 2026Article
- Potential diagnostic markers in Alzheimer's disease: current perspectives and future directions.Neurodegenerative disease management · 2026Review
- 3-Hydroxybutyrate, a metabolite in sustaining neuronal cell vitality: a mendelian randomization and in vitro experimentation.Nutrition & metabolism · 2025Article
- Reflections on "mitochondrial DNA abundance in blood is associated with Alzheimer's disease- and dementia-risk".Molecular psychiatry · 2025Article
- The role of mitochondrial dysfunction in the pathogenesis of Alzheimer's disease and future strategies for targeted therapy.European journal of medical research · 2025Review
- Association of Nonmodifiable Risk Factors With Alzheimer Disease Blood Biomarkers in Community-Dwelling Adults in the ESTHER Study.Neurology · 2025Article
- Mitochondrial dysfunction in Alzheimer's disease: Guiding the path to targeted therapies.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Review
- Elevated mitochondrial DNA copy number in euthyroid individuals with impaired peripheral sensitivity to thyroid hormones.Frontiers in endocrinology · 2025Article
- Cell-Free DNA, a Noninvasive Biomarker for Prediction and Detection of Neurodegenerative Diseases, New Insights, and Perspectives.CNS & neurological disorders drug targets · 2025Review
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13 authors.
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Abstract
The mitochondrial cascade hypothesis of Alzheimer's disease (AD) has been portrayed through molecular, cellular, and animal studies; however large epidemiological studies are lacking. This study aimed to explore the association of mitochondrial DNA copy number (mtDNAcn), a marker representative of mtDNA abundance per cell, with risk of incident all-cause dementia, AD, and vascular dementia diagnosis within 17 years and dementia-related blood biomarkers (P-tau181, GFAP, and NfL). Additionally, sex-stratified analyses were completed. In this German population-based cohort study (ESTHER), 9940 participants aged 50-75 years were enrolled by general practitioners and followed for 17 years. Participants were included in this study if information on dementia status and blood-based mtDNAcn measured via real-time polymerase chain reaction were available. In a nested case-control approach, a subsample of participants additionally had measurements of P-tau181, GFAP, and NfL in blood samples taken at baseline. Of 4913 participants eligible for analyses, 386 were diagnosed with incident all-cause dementia, including 130 AD and 143 vascular dementia cases, while 4527 participants remained without dementia diagnosis within 17 years. Participants with low mtDNAcn (lowest 10%) experienced 45% and 65% percent increased risk of incident all-cause dementia and AD after adjusting for age and sex (all-cause dementia: HRadj, 95%CI:1.45, 1.08-1.94; AD: HRadj, 95%CI: 1.65, 1.01-2.68). MtDNAcn was not associated to vascular dementia diagnosis and was more strongly associated with all-cause dementia among women. In the nested case-control study (n = 790), mtDNAcn was not significantly associated with the dementia-related blood biomarkers (P-tau181, GFAP, and NfL) levels in blood from baseline before dementia diagnosis. This study provides novel epidemiological evidence connecting mtDNA abundance, measured via mtDNAcn, to incident dementia and AD at the population-based level. Reduced mitochondrial abundance may play a role in pathogenesis, especially among women.
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