Journal
AMERICAN JOURNAL OF PATHOLOGY
Volume 184, Issue 4, Pages 966-975Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.ajpath.2013.12.007
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Funding
- Michael J. Fox Foundation
- Parkinson Study Group
- NTH grants [NIEHS T32ES015459, AG033398, ES004696-5897, ES007033-6364, ES016873, ES019277, NS057567, NS060252, NS062684-6221, NS082137]
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Most patients with Parkinson disease (PD) develop both cognitive and motor impairment, and biomarkers for progression are urgently needed. Although alpha-synuclein is altered in cerebrospinal fluid of patients with PD, it is not known whether it predicts motor or cognitive deterioration. We examined clinical data and alpha-synuclein in >300 unmedicated patients with PD who participated in the deprenyl and tocopherol antioxidative therapy of parkinsonism (DATATOP) study, with up to 8 years of follow-up. Longitudinal measures of motor and cognitive function were studied before (phase 1) and during (phase 2) levodopa therapy; cerebrospinal fluid was collected at the beginning of each phase. Correlations and linear mixed models were used to assess alpha-synuclein association with disease severity and prediction of progression in the subsequent follow-up period. Despite decreasing cc-synuclein (phase 1 to phase 2 change of -0.05 +/- 0.21 log-transformed values, P < 0.001), no correlations were observed between alpha-synuclein and motor symptoms. Longitudinally, lower alpha-synuclein predicted better preservation of cognitive function by several measures [Selective Reminding Test total recall alpha-synuclein x time interaction effect coefficient, -0.12 (P = 0.037); delayed recall, -0.05 (P = 0.002); New Dot Test, -0.03 (P = 0.002)]. Thus, alpha-synuclein, although not clinically useful for motor progression, might predict cognitive decline, and future longitudinal studies should include this outcome for further validation.
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