ReviewBiomolecules2025
The Role of
Review in Biomolecules, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed.
- Epigenetic Dysregulation of the Wnt/β-Catenin Pathway via FTO-m6A in the mPFC Contributes to Autism-Like Behaviors.Molecular neurobiology · 2026Article
- Mitochondrial Quality Control and Pathogenic Signaling Networks in Parkinson's Disease.Current issues in molecular biology · 2026Review
- FTO-modulated mJournal of translational medicine · 2026Article
- Decoding the RNA Shield: HNRNPC and YTHDF2 Act as Guardians of Neurons in Parkinson's Disease.Neurotoxicity research · 2026Review
- Multi-omics and network pharmacology identify IGFBP1 as an m6A-Epigenetic target of pueraria in NSCLC therapy.PLoS computational biology · 2026Article
- Research advances in key genes and regulatory mechanisms of posttranslational modifications in Parkinson's disease.PloS one · 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
4 authors.
Funding
Abstract
Parkinson's disease (PD) is a neurodegenerative disease with a high prevalence among the middle-aged and elderly population. The pathogenesis of PD is closely linked to the misfolding and aggregation of α-synuclein, which contributes to the formation of Lewy bodies. These processes are associated with the degeneration of dopaminergic neurons, a key neuropathological change that underlies the motor symptoms of PD. In addition, genetic susceptibility, mitochondrial dysfunction, oxidative stress and neuroinflammation are involved in the progress of the disease. Previous studies indicated that the dysregulation of epigenetic modifications, including DNA methylation and histone acetylation, may be the key pathophysiological factors in PD.
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.