Prospective longitudinal course of cognition in older subjects with mild parkinsonian signs. Issue 1 (December 2016)

• Record Type: Journal Article
• Authors: Lerche, Stefanie; Brockmann, Kathrin; Pilotto, Andrea; Wurster, Isabel; Sünkel, Ulrike; Hobert, Markus; von Thaler, Anna-Katharina; Schulte, Claudia; Stoops, Erik; Vanderstichele, Hugo; Herbst, Victor; Brix, Britta; Eschweiler, Gerhard; Metzger, Florian; Maetzler, Walter; Berg, Daniela
• Is Part Of: Alzheimer's research & therapy. Volume 8:Issue 1(2016)
• Page Start: 1
• Page End: 8
• Publication Date: 2016-12
• Subjects: Amyloid-beta -- Dementia -- Prospective -- Longitudinal -- Cohort study; Alzheimer's disease -- Periodicals; 616.831005
• DOI: 10.1186/s13195-016-0209-7
• Languages: English
• ISSNs: 1758-9193

Abstract

Abstract Background Mild parkinsonian signs (MPS) are common in older people and are associated with an increased risk of different neurodegenerative diseases. This study prospectively evaluates the longitudinal course of cognitive performance in older individuals with MPS. Methods From the TREND study, 480 individuals neurologically healthy at baseline, aged between 50 and 80 years, with complete follow-up data for three assessments within a mean of 43.8 months, were included in this analysis. Participants underwent a detailed cognitive test battery, evaluation of prodromal markers for neurodegenerative diseases and history of vascular diseases at each study visit. In addition, plasma levels of amyloid-beta (Aβ)1–40 and Aβ1–42 were evaluated longitudinally. Results In 52 (11 %) of the 480 participants, MPS could be detected at baseline. These individuals had cognitive deficits significantly more often compared with controls at each time point and their cognitive performance showed a steeper decline during follow-up. In addition, their levels of plasma Aβ1–42 were significantly lower than those of controls, and declined more rapidly over time. Conclusions This longitudinal study shows that MPS are associated with cognitive decline and decrease in plasma Aβ1–42, possibly indicating an ongoing neurodegenerative process.