• Stefanie Lerche, Isabel Wurster, Benjamin Röben, Gerrit Machetanz, Milan Zimmermann, Felix Bernhard, Elke Stransky, Christian Deuschle, Claudia Schulte, Oskar Hansson, Henrik Zetterberg, Thomas Gasser, Daniela Berg, Walter Maetzler, and Kathrin Brockmann.
• Center of Neurology, Department of Neurodegeneration and Hertie-Institute for Clinical Brain Research, University of Tuebingen, Tuebingen, Germany stefanie.lerche@uni-tuebingen.de.
• J. Neurol. Neurosurg. Psychiatr. 2019 Feb 1; 90 (2): 165-170.

ObjectiveTo evaluate the evolution of cognitive impairment in relation to cerebrospinal fluid (CSF) profiles of amyloid-β (Aβ), total-Tau and phosphorylated-Tau in Parkinson's disease (PD).MethodsProspective, longitudinal, observational study up to 10 years with follow-up every 2  years. We assessed CSF profiles in 415 patients with sporadic PD (median age 66; 63% men) and 142 healthy controls (median age 62; 43% men).ResultsPatients with PD with low CSF Aβ1-42 levels at baseline were more often cognitively impaired than patients with intermediate and high Aβ1-42 levels. Sixty-seven per cent of the patients with low Aβ1-42 levels at baseline and normal cognition developed cognitive impairment during follow-up, compared with 41% and 37% of patients having intermediate and high CSF Aβ1-42 levels. Kaplan-Meier survival curves and Cox regression revealed that patients with low CSF Aβ1-42 levels at baseline developed cognitive impairment more frequently and earlier during follow-up.ConclusionWe conclude that in patients with sporadic PD, low levels of Aβ1-42 are associated with a higher risk of developing cognitive impairment earlier in the disease process at least in a subgroup of patients.© Author(s) (or their employer(s)) 2019. No commercial re-use. See rights and permissions. Published by BMJ.

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