ArticleActa neuropathologica communications2020
Associations of mitochondrial genomic variation with corticobasal degeneration, progressive supranuclear palsy, and neuropathological tau measures.
Article in Acta neuropathologica communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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9 citing papers in PubMed, 13 citations in OpenAlex.
- Association of mitochondrial genetic background with pS65-Ub in Lewy body disease.Acta neuropathologica · 2026Article
- Neuronal Vulnerability to Degeneration in Parkinson's Disease and Therapeutic Approaches.CNS & neurological disorders drug targets · 2024Review
- Why Therapeutic Trials Fail in Primary Tauopathies.Movement disorders : official journal of the Movement Disorder Society · 2023Article
- Mitochondrial genomic variation in dementia with Lewy bodies: association with disease risk and neuropathological measures.Acta neuropathologica communications · 2022Article
- Tauopathies: new perspectives and challenges.Molecular neurodegeneration · 2022Review
- Deep learning-based model for diagnosing Alzheimer's disease and tauopathies.Neuropathology and applied neurobiology · 2022Article
- Article
- MAPT subhaplotypes in corticobasal degeneration: assessing associations with disease risk, severity of tau pathology, and clinical features.Acta neuropathologica communications · 2020Article
- Association of mitochondrial genomic background with risk of Multiple System Atrophy.Parkinsonism & related disorders · 2020Article
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11 authors at 3 institutions in 1 country.
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Abstract
Mitochondrial health is important in ageing and dysfunctional oxidative phosphorylation (OXPHOS) accelerates ageing and influences neurodegeneration. Mitochondrial DNA (mtDNA) codes for vital OXPHOS subunits and mtDNA background has been associated with neurodegeneration; however, no study has characterised mtDNA variation in Progressive supranuclear palsy (PSP) or Corticobasal degeneration (CBD) risk or pathogenesis. In this case-control study, 910 (42.6% male) neurologically-healthy controls, 1042 (54.1% male) pathologically-confirmed PSP cases, and 171 (52.0% male) pathologically-confirmed CBD cases were assessed to determine how stable mtDNA polymorphisms, in the form of mtDNA haplogroups, were associated with risk of PSP, risk of CBD, age of PSP onset, PSP disease duration, and neuropathological tau pathology measures for neurofibrillary tangles (NFT), neuropil threads (NT), tufted astrocytes (TA), astrocytic plaques (AP), and oligodendroglial coiled bodies (CB). 764 PSP cases and 150 CBD cases had quantitative tau pathology scores. mtDNA was genotyped for 39 unique SNPs using Agena Bioscience iPlex technologies and mitochondrial haplogroups were defined to mitochondrial phylogeny. After adjustment for multiple testing, we observed an association with risk of CBD for mtDNA sub-haplogroup H4 (OR = 4.51, P = 0.001) and the HV/HV0a haplogroup was associated with a decreased severity of NT tau pathology in PSP cases (P = 0.0023). Our study reports that mitochondrial genomic background may be associated with risk of CBD and may be influencing tau pathology measures in PSP. Replication of these findings will be important.
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