Evidence map›Paper›PMID 42809157›Full record

ArticleJournal of neurology2026

Preliminary insights into whole-blood mitochondrial DNA copy number and telomere length in Parkinson's disease and multiple system atrophy.

Monica Gagliardi, Alessia Felicetti, Radha Procopio, Antonio Augimeri, Maurizio Morelli, Andrea Quattrone, Grazia Annesi, Aldo Quattrone

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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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1 · What the graph read from it

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2 · The registry

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3 · Its place in the literature

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No citing paper in PubMed yet.

4 · The record

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5 · Who and what money

Authors and funding

8 authors.

Monica GagliardiNeuroscience Research Center, Magna Graecia University, Viale Europa, 88100, Catanzaro, Italy. monica.gagliardi@unicz.it.ORCID http://orcid.org/0000-0002-3386-9808
Alessia FelicettiDepartment of Medical and Surgical Sciences, Institute of Neurology, Magna Graecia University, 88100, Catanzaro, Italy.
Radha ProcopioNeuroscience Research Center, Magna Graecia University, Viale Europa, 88100, Catanzaro, Italy.
Antonio AugimeriBiotecnomed S.C.aR.L., 88100, Catanzaro, Italy.
Maurizio MorelliDepartment of Medical and Surgical Sciences, Institute of Neurology, Magna Graecia University, 88100, Catanzaro, Italy.
Andrea QuattroneNeuroscience Research Center, Magna Graecia University, Viale Europa, 88100, Catanzaro, Italy.
Grazia AnnesiInstitute for Biomedical Research and Innovation, National Research Council, 87050, Cosenza, Italy.
Aldo QuattroneNeuroscience Research Center, Magna Graecia University, Viale Europa, 88100, Catanzaro, Italy.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

DNA Copy Number VariationsDNA, MitochondrialMultiple System AtrophyParkinson DiseaseTelomereAgedFemaleHumansMaleMiddle AgedNADH DehydrogenaseDNA, MitochondrialNADH DehydrogenaseNADH dehydrogenase subunit 1, humanMitochondrial DNA copy numberMultiple system atrophyParkinson’s diseaseTelomere length

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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.