ArticleMolecular neurobiology2025
Pathway Analysis and Genetic Markers in Parkinson's Disease: Insights into Subtype-Specific Mechanisms.
Article in Molecular neurobiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- Maternal Traumatic Brain Injury Increases Fetal Brain Cis p-tau Levels: Evidence for Potential Transplacental Effects in a Murine Model.Journal of molecular neuroscience : MN · 2026Article
- Effects of transmembrane protein 106B genetic variations on disease progression in Parkinson's disease.Frontiers in aging neuroscience · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Parkinson's disease (PD) is a complex disease influenced by both genetic and environmental factors. Despite advances in understanding PD genetics, subtype-specific mechanisms remain poorly characterized. This study aims to identify distinct genetic markers and pathways across PD subtypes, addressing this gap to enable targeted diagnostics and therapies. Genes associated with PD were collected from various databases and categorized into groups based on the PD type to assess the PD risk. Protein interaction analysis was conducted to identify functional clusters and key genes within each group. KEGG enrichment analysis revealed common genes and pathways among the different PD groups. This study conformed to the PRISMA 2020 guidelines for systematic data collection and analysis. Hub genes such as PRKN, SNCA, and LRRK2 have demonstrated considerable potential as biomarkers for genetic predisposition in PD, alongside the identification of additional complementary genes. Analysis of hub node variants highlighted specific genetic variations in these genes. We identified several microRNAs, including hsa-miR-335-5p, hsa-miR-19a-3p, and hsa-miR-106a-5p, as well as transcription factors that interact with crucial hub genes. This study refines subtype-specific mechanisms for established PD genes and identifies novel genetic markers and pathways associated with juvenile, young-onset, late-onset, familial, and sporadic Parkinson's disease, enhancing our understanding of their molecular mechanisms and potential for targeted diagnostics and therapies. Specifically, we highlight the roles of hub genes, such as PRKN, SNCA, and LRRK2, alongside significant microRNA interactions, which may serve as biomarkers for early detection and personalized treatment approaches.
Indexed as
Identifiers
40601219What 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.