Abstract Variants in GBA1 result in dysregulated sphingolipids. We investigated five CSF sphingolipid species in a 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 carriers. Sphingolipid levels had no effect on development of cognitive impairment. Thereby, CSF Sphingolipids seem not useful as state marker in Parkinson’s Disease.
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Brockmann et al. (2024) studied this question.
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