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dc.contributor.authorSelnes, Per
dc.contributor.authorStav, Ane Løvli
dc.contributor.authorJohansen, Krisztina Kunszt
dc.contributor.authorBjørnerud, Atle
dc.contributor.authorCoello, Sebastien Christopher
dc.contributor.authorAuning, Eirik
dc.contributor.authorKalheim, Lisa Flem
dc.contributor.authorAlmdahl, Ina Selseth
dc.contributor.authorHessen, Erik
dc.contributor.authorZetterberg, Henrik
dc.contributor.authorBlennow, Kaj
dc.contributor.authorÅrsland, Dag
dc.contributor.authorFladby, Tormod
dc.identifier.citationSelnes, P., Stav, A. L., Johansen, K. K., Bjørnerud, A., Coello, C., Auning, E., ... & Blennow, K. (2017). Impaired synaptic function is linked to cognition in Parkinson's disease. Annals of clinical and translational neurology, 4(10), 700-713.en
dc.description.abstractObjective Cognitive impairment is frequent in Parkinson's disease, but the underlying mechanisms are insufficiently understood. Because cortical metabolism is reduced in Parkinson's disease and closely associated with cognitive impairment, and CSF amyloid‐β species are reduced and correlate with neuropsychological performance in Parkinson's disease, and amyloid‐β release to interstitial fluid may be related to synaptic activity; we hypothesize that synapse dysfunction links cortical hypometabolism, reduced CSF amyloid‐β, and presynaptic deposits of α‐synuclein. We expect a correlation between hypometabolism, CSF amyloid‐β, and the synapse related‐markers CSF neurogranin and α‐synuclein. Methods Thirty patients with mild‐to‐moderate Parkinson's disease and 26 healthy controls underwent a clinical assessment, lumbar puncture, MRI, 18F‐fludeoxyglucose‐PET, and a neuropsychological test battery (repeated for the patients after 2 years). Results All subjects had CSF amyloid‐β 1‐42 within normal range. In Parkinson's disease, we found strong significant correlations between cortical glucose metabolism, CSF Aβ, α‐synuclein, and neurogranin. All PET CSF biomarker‐based cortical clusters correlated strongly with cognitive parameters. CSF neurogranin levels were significantly lower in mild‐to‐moderate Parkinson's disease compared to controls, correlated with amyloid‐β and α‐synuclein, and with motor stage. There was little change in cognition after 2 years, but the cognitive tests that were significantly different, were also significantly associated with cortical metabolism. No such correlations were found in the control group. Interpretation CSF Aβ, α‐synuclein, and neurogranin concentrations are related to cortical metabolism and cognitive decline. Synaptic dysfunction due to Aβ and α‐synuclein dysmetabolism may be central in the evolution of cognitive impairment in Parkinson's disease.en
dc.relation.ispartofseriesAnnals of Clinical and Translational Neurology;4(10)
dc.rightsAttribution-NonCommercial 3.0 United States This is an open acces article, originally published at
dc.titleImpaired synaptic function is linked to cognition in Parkinson's diseaseen
dc.typeJournal articleen
dc.typePeer revieweden

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Attribution-NonCommercial 3.0 United States
This is an open acces article, originally published at
Med mindre annet er angitt, så er denne innførselen lisensiert som Attribution-NonCommercial 3.0 United States This is an open acces article, originally published at