ArticleNeuropathology and applied neurobiology2025
Protein Coaggregation in Caribbean Atypical Parkinsonism: The Contribution of Annonacin.
Article in Neuropathology and applied neurobiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed.
- Squamocin as the Principal Toxic Constituent ofInternational journal of molecular sciences · 2026Article
- Emerging directions in tauopathy research.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Review
- Peripheral Immunological Signatures of Parkinsonism: Insights from the Caribbean vs. North America.Molecular neurobiology · 2026Article
- Protein Coaggregation in Caribbean Atypical Parkinsonism: The Contribution of Annonacin.Neuropathology and applied neurobiology · 2025Article
- Uric Acid, the End-Product of Purine Metabolism, Mitigates Tau-Related Abnormalities: Comparison with DOT, a Non-Antibiotic Oxytetracycline Derivative.Biomolecules · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors.
Funding
Abstract
aimsThere is an unexpectedly high proportion of atypical forms of degenerative parkinsonism in the French Caribbean islands. Residents of these islands are thought to be susceptible to Caribbean atypical parkinsonism (CAP) owing to their consumption of Annonaceae plant products containing the mitochondrial toxin annonacin. Here, we aimed to better correlate the clinical diagnosis of CAP with the misfolded protein pathology observed in affected individuals and to further investigate how annonacin could contribute to CAP pathogenesis.
methodsWe conducted postmortem histopathological analysis of brain samples from eight patients; more specifically, we assessed the distribution and burden of α-synuclein (αS) and tau pathologies. Additionally, we studied how annonacin influences αS and tau aggregation using biophysical assays, with the corresponding recombinant human proteins serving as substrates.
resultsCAP was associated with heterogeneous clinical and histopathological features. Tau/αS copathology with a predominance of either αS or tau aggregates was observed in the majority (5/8) of patients. Tau and αS aggregates were sometimes colocalised in the same brain regions or cells. In biophysical assays, we showed that annonacin leads to an increase in αS aggregation and the formation of αS fibrils that could cross-seed tau aggregation.
conclusionsAnnonacin may contribute to degenerative CAP by modulating the production of tau and αS pathogenic protein assemblies.
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.