CSF d18:1 sphingolipid species in Parkinson disease and dementia with Lewy bodies with and without GBA1 variants

CSF d18:1 sphingolipid species in Parkinson disease and dementia with Lewy bodies with and without GBA1 variants

Variants in GBA1 result in dysregulated sphingolipids. We investigated five CSF d18:1 sphingolipid species in a longitudinal multicenter cohort comprising people with Parkinson’s Disease and Dementia with Lewy bodies with and without GBA1 variants and healthy controls. We found no increase of sphing...

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Veröffentlicht in:NPJ Parkinson's Disease 2024-10, Vol.10 (1), p.198-6, Article 198
Hauptverfasser: Lerche, Stefanie, Wurster, Isabel, Valente, Enza Maria, Avenali, Micol, Samaniego, Daniela, Martínez-Vicente, Marta, Hernández-Vara, Jorge, Laguna, Ariadna, Sturchio, Andrea, Svenningsson, Per, France, Nicholas P., Barlow, Carrolee, Sankaranarayanan, Sethu, Brockmann, Kathrin
Format: Artikel
Sprache:eng
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692/617/375/1718
692/617/375/364
Biomedical and Life Sciences
Biomedicine
Brief Communication
Cognitive ability
Dementia
Disease
Genotype & phenotype
Neurodegeneration
Neurology
Neurosciences
Parkinson's disease
Plasma
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Zusammenfassung:Variants in GBA1 result in dysregulated sphingolipids. We investigated five CSF d18:1 sphingolipid species in a longitudinal multicenter cohort comprising people with Parkinson’s Disease and Dementia with Lewy bodies with and without GBA1 variants and healthy controls. We found no increase of sphingolipid species in heterozygous GBA1 variant participants and no effect on development of cognitive impairment. Thus, CSF d18:1 sphingolipids are not suitable as state markers in Parkinson’s Disease.
ISSN:2373-8057
2373-8057
DOI:10.1038/s41531-024-00820-0