CSF markers of neuroinflammation, synaptic dysfunction and [<sup>18</sup>F]DOPA-PET in Parkinson's disease.

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IntroductionNeuromelanin containing cell loss, neuroinflammation and synaptic dysfunction are believed to contribute to Parkinson's disease (PD) pathogenesis. [18F]DOPA PET reflects dopamine storage capacity in the putamen, while midbrain off-target retention of [18F]RO948 is hypothesized to reflect neuromelanin.ObjectivesTo investigate associations between disease duration, cerebrospinal fluid (CSF) markers of neurodegeneration, synaptic dysfunction, neuroinflammation, and dopamine synaptic loss as measured by [18F]DOPA PET in PD patients. We further aimed to explore whether reduced midbrain retention of [18F]RO948 relates to [18F]DOPA PET and CSF markers.MethodsParticipants were part of the BioFINDER studies. CSF biomarkers were analyzed for controls (n = 623), PD participants (n = 226) and Dementia with Lewy bodies (DLB; n = 33). [18F]RO948 PET was performed in controls (n = 514), PD (n = 77) and DLB (n = 47) and [18F]DOPA PET in PD (n = 58) and DLB (n = 22).ResultsPD patients showed higher CSF neurofilament light (NfL) levels (pg/ml [mean ± SD] 159 ± 139) vs. controls (137 ± 90, p 18F]DOPA uptake correlated with longer disease duration (ρ = -0.46, p 18F]DOPA PET. Substantia nigra [18F]RO948 signal was lower in PD ([mean ± SD] 1.67 ± 0.22) vs controls (1.76 ± 0.3, p 18F]DOPA-PET.ConclusionsIn PD patients, a decrease in [18F]DOPA PET retention correlated with disease duration as well as CSF neurodegenerative and synaptic biomarkers but not with inflammatory biomarkers or [18F]RO948 PET midbrain off-target retention.

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