ArticleJournal of molecular neuroscience : MN2026
Association of Statin use with Parkinson's Disease Progression in a Prospective Cohort Study and Multi-omics Analyses.
Article in Journal of molecular neuroscience : MN, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundWhile more than 30% of patients with Parkinson’s disease (PD) are prescribed statins, the impact of statin use on the progression of PD remains incompletely elucidated. We aimed to comprehensively investigate the impact of statin use on PD progression. We analyzed longitudinal data from the Parkinson’s Progression Markers Initiative (PPMI) to examine associations between statin use and clinical manifestations and cerebrospinal fluid (CSF) biomarkers. Mendelian randomization and Bayesian colocalization analyses were employed to assess genetic relationships between HMGCR inhibition (a proxy for statins) and PD phenotypes. Multi-omics analyses utilized postmortem substantia nigra RNA-seq data and CSF proteomics from living patients to explore potential mechanisms. In the PPMI cohort, statin use was associated with a faster cognitive decline among PD patients during longitudinal follow-up, which was partially mediated by reduced CSF Aβ42. Genetic analyses indicated detrimental effects of HMGCR inhibition on cognitive function, dyskinesia, and restless legs syndrome in PD. In addition, RNA-seq analysis of substantia nigra suggested that HMGCR expression gradually decreases with PD progression, showing significant reductions in moderate and advanced stages. Finally, CSF proteomics revealed that statin use was associated with 238 upregulated and 203 downregulated proteins in PD, among which 28 proteins were linked to cognitive decline and significantly enriched in pathways related to substantia nigra development and PD. Our study suggests that statins may accelerate cognitive decline in PD patients through mechanisms potentially involving reduced CSF Aβ42 levels, inhibition of HMGCR in the substantia nigra, and disruption of PD-related protein pathways.
Indexed as
Identifiers
41721963What 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.