ArticleAnnals of neurology2025
Plasma Glucosylceramide Levels Are Regulated by ATP10D and Are Not Involved in Parkinson's Disease Pathogenesis.
Article in Annals of neurology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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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.
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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.
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Who cites it
6 citing papers in PubMed.
- Clinical Trials in GBA1-Associated Parkinson's Disease: A Need for Molecular Classification.Movement disorders : official journal of the Movement Disorder Society · 2026Article
- Genome-wide association studies identify genetic determinants of synucleinopathy biomarkers.Research square · 2026Article
- Plasma Glucosylsphingosine in GBA1 E365K, N409S, and L483P Heterozygous Mutation Carriers.Movement disorders : official journal of the Movement Disorder Society · 2026Article
- Modest improvement of metabolic and behavioral deficits with long-term ambroxol treatment in a Pink1Acta pharmacologica Sinica · 2026Article
- Age at onset of Parkinson's disease modulates the sphingolipid-dopaminergic interplay in autonomic progression.NPJ Parkinson's disease · 2026Article
- Genome-wide association studies identify genetic determinants of synucleinopathy biomarkers.medRxiv : the preprint server for health sciences · 2025Article
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Authors and funding
14 authors.
Funding
Abstract
GBA1 variants and decreased glucocerebrosidase activity are implicated in Parkinson's disease (PD). We investigated the hypothesis that increased levels of glucosylceramide (GlcCer), a main substrate of glucocerebrosidase, are involved in PD pathogenesis. Using multiple genetic methods, we show that ATPase phospholipid transporting 10D (ATP10D), not GBA1, is the main regulator of plasma GlcCer levels, yet it is not involved in PD pathogenesis. Plasma GlcCer levels were associated with PD, but not in a causative manner, and are not predictive of disease status. These results argue against targeting GlcCer in GBA1-PD, and underscore the need to explore alternative mechanisms and biomarkers for PD. ANN NEUROL 2025;97:873-878.
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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.