ReviewNeurology and therapy2025
Neuroprotection in Parkinson Disease.
Review in Neurology and therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed.
- Lifestyle medicine for neuroprotection: evidence and implementation in Asian contexts.Journal of neural transmission (Vienna, Austria : 1996) · 2026Review
- Neuroprotection Across Cerebellar and Nigrostriatal Degeneration: Translational Insights from Parkinson's Disease to Spinocerebellar Ataxia Type 2.Cerebellum (London, England) · 2026Review
- Neuroprotective Potential of Synaptamide in MPTP-Induced Parkinson's Disease.Pathophysiology : the official journal of the International Society for Pathophysiology · 2026Article
- Stem Cell-Derived Exosomes Regulate Mitochondrial Function: A Novel Strategy for Parkinson's Disease Therapy.Molecular neurobiology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Parkinson disease (PD) is a progressive neurodegenerative condition characterised by tremor, bradykinesia and rigidity, as well as other motor and non-motor symptoms, for which no effective disease-modifying treatments have been discovered. Neuroprotection in PD is limited by its clinical and biological heterogeneity, suboptimal preclinical models, lack of established disease progression biomarkers, complex pathophysiology, the existence of effective symptomatic therapies which hamper the detection of actual disease modification, and trial design. This review discusses the above issues and other important concepts in neuroprotection in PD. The main pathophysiological mechanisms in PD are classified into mitochondrial dysfunction, lysosomal dysfunction, inflammation, protein aggregation/propagation, and "other", and discussed briefly. The most relevant disease-modifying candidates in PD are classified into the aforementioned categories and reviewed. Finally, conclusions and recommendations for future improvements in the field of disease modification in PD are provided.
Indexed as
Identifiers
What Socratic 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 Socratic graph.