ArticleParkinsonism & related disorders2020
Association of mitochondrial genomic background with risk of Multiple System Atrophy.
Article in Parkinsonism & related disorders, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed, 7 citations in OpenAlex.
- Coenzyme Q10: A Biomarker in the Differential Diagnosis of Parkinsonian Syndromes.Antioxidants (Basel, Switzerland) · 2023Article
- Cell-Type-Specific Mitochondrial Quality Control in the Brain: A Plausible Mechanism of Neurodegeneration.International journal of molecular sciences · 2023Review
- Mitochondrial genomic variation in dementia with Lewy bodies: association with disease risk and neuropathological measures.Acta neuropathologica communications · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
introductionMultiple system atrophy (MSA) is a rare, sporadic, and progressive neurodegenerative disease which is characterized neuropathologically by alpha-synuclein aggregates in oligodendroglia, and clinically by parkinsonism, ataxia, and autonomic dysfunction. Mitochondrial health influences neurodegeneration and defects in mitochondria, particularly in oxidative phosphorylation, are reported in MSA. Mitochondrial DNA (mtDNA) codes for 13 critical OXPHOS proteins, however no study has investigated if mtDNA variation, in the form of mitochondrial haplogroups, influences MSA risk. Therefore, in this study we investigated the association of mtDNA haplogroups with MSA risk in a case-control manner.
methods176 pathologically confirmed MSA cases and 910 neurologically healthy controls from Mayo Clinic Jacksonville were genotyped for 39 unique mtDNA variants using Agena Biosciences MassARRAY iPlex technology. Mitochondrial haplogroups were assigned to mitochondrial phylogeny, and logistic regression models that were adjusted for age and sex were used to assess associations between mitochondrial haplogroups and risk of MSA.
resultsAfter adjusting for multiple testing (P<0.0019 considered significant), no mitochondrial haplogroups were significantly associated with MSA risk. However, several nominally significant (P<0.05) associations were observed; haplogroup I was associated with a decreased risk of MSA (OR=0.09, P=0.021), while an increased risk of MSA was observed for haplogroups H3 (OR=2.43, P=0.017) and T1 and T2 (OR=2.04, P=0.007).
conclusionThis study investigated whether population-specific mtDNA variation is associated with risk of MSA, and our nominally significant findings suggest mitochondrial haplogroup background may influence MSA risk. Validation of these findings and additional meta-analytic studies will be important.
Indexed as
Identifiers
What OpenQuestion holds
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.