ArticleJournal of neurology2026
Preliminary insights into whole-blood mitochondrial DNA copy number and telomere length in Parkinson's disease and multiple system atrophy.
Article in Journal of neurology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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8 authors.
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Abstract
backgroundParkinson's disease (PD) and multiple system atrophy (MSA) are α-synucleinopathies characterized by progressive neurodegeneration and overlapping clinical features but distinct pathological mechanisms with peripheral biomarkers remaining limited. Mitochondrial dysfunction and telomere attrition are hallmarks of cellular aging implicated in neurodegeneration, yet their combined role remains unclear.
methodsWhole-blood mitochondrial DNA copy number (mtDNA-CN) and telomere length (TL) were assessed in 58 PD patients, 35 MSA patients, and 62 healthy controls from Southern Italy. Mitochondrially encoded NADH dehydrogenase 1 (ND1) gene levels and TL were measured by quantitative PCR and normalized to the β-actin gene. Group differences were tested using multivariable linear regression adjusted for age and sex, with statistical significance defined as p < 0.05 after false discovery rate (FDR)-corrected Wald tests.
resultsND1-CN was significantly reduced in PD (p
conclusionsOur findings support the involvement of mitochondrial dysfunction and telomere attrition in PD and MSA. However, mtDNA-CN provided a clearer distinction between the two α-synucleinopathies than TL, suggesting that peripheral mtDNA-CN may represent a more informative non-invasive biomarker of disease-specific mitochondrial alterations. Further longitudinal studies in larger, independent cohorts are warranted to validate its diagnostic and prognostic utility.
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