Mitochondrial DNA abundance in blood is associated with Alzheimer’s disease- and dementia-risk
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 m...
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| Hauptverfasser: | , , , , , , , , , , , , |
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| Dokumenttyp: | Article (Journal) |
| Sprache: | Englisch |
| Veröffentlicht: |
January 2025
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| In: |
Molecular psychiatry
Year: 2025, Jahrgang: 30, Heft: 1, Pages: 131-139 |
| ISSN: | 1476-5578 |
| DOI: | 10.1038/s41380-024-02670-x |
| Online-Zugang: | Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1038/s41380-024-02670-x Verlag, lizenzpflichtig, Volltext: https://www.nature.com/articles/s41380-024-02670-x 
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| Verfasserangaben: | Hannah Stocker, Manuel Gentiluomo, Kira Trares, Léon Beyer, Joshua Stevenson-Hoare, Dan Rujescu, Bernd Holleczek, Konrad Beyreuther, Klaus Gerwert, Ben Schöttker, Daniele Campa, Federico Canzian and Hermann Brenner |
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| 245 | 1 | 0 | |a Mitochondrial DNA abundance in blood is associated with Alzheimer’s disease- and dementia-risk |c Hannah Stocker, Manuel Gentiluomo, Kira Trares, Léon Beyer, Joshua Stevenson-Hoare, Dan Rujescu, Bernd Holleczek, Konrad Beyreuther, Klaus Gerwert, Ben Schöttker, Daniele Campa, Federico Canzian and Hermann Brenner |
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| 520 | |a 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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