ReviewNature reviews. Neurology2025
Parkinson disease is a fatty acidopathy.
Review in Nature reviews. Neurology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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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
8 citing papers in PubMed.
- Cellular and systemic modifiers of alpha-synuclein proteostasis.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2026Review
- Mapping the causal chain from genetic risk variants to lipid dysmetabolism in Parkinson's disease.Brain : a journal of neurology · 2026Article
- Parkinson's Disease: Pathophysiology, Treatment Strategies, Wellness Approaches, and Obstacles/Paths Forward.NeuroSci · 2026Review
- Elevation of Stearoyl-Coenzyme A Desaturase and Monounsaturated Fatty Acids in Parkinson's Disease Serum.Movement disorders : official journal of the Movement Disorder Society · 2026Article
- The Emerging Parkinson's Disease Oxylipin-Ome.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Shared and distinct lipid profiles in amygdala from sporadic and GBA-associated Parkinson's diseases.NPJ Parkinson's disease · 2026Article
- Unlocking Parkinson's disease: harnessing the untapped potential of fatty acid metabolism in disease pathogenesis.Frontiers in immunology · 2026Review
- Interplay between lipid droplets and alpha-synuclein: implication in Parkinson's disease pathogenesis.Frontiers in molecular neuroscience · 2025Review
Corrections and comments
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Authors and funding
2 authors.
Funding
Abstract
On the basis of extensive mechanistic research over three decades, Parkinson disease (PD) and related synucleinopathies have been proposed to be combined proteinopathies and lipidopathies. Evidence strongly supports a physiological and pathogenic interplay between the disease-associated protein α-synuclein and lipids, with a demonstrable role for lipids in modulating PD phenotypes in the brain. Here, we refine this hypothesis by proposing PD to be a disease specifically involving metabolic dysregulation of fatty acids, a 'fatty acidopathy'. We review extensive findings from many laboratories supporting the perspective that PD centres on fatty acid dyshomeostasis - alterations in the fatty acid-ome - as the critical feature of lipid aberration in PD and other α-synucleinopathies. This construct places transient α-synuclein binding to fatty acid side chains of cytoplasmic vesicles as a principal contributor to the biology of PD-relevant α-synuclein-membrane interactions. We propose that α-synuclein-fatty acid interactions in the fatty acid-rich brain are interdependent determinants of the gradual progression from neuronal health to PD, with attendant therapeutic implications.
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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.