Research Paper Volume 12, Issue 20 pp 20880—20887
SNCA Rep1 microsatellite length influences non-motor symptoms in early Parkinson’s disease
- 1 Department of Neurology, National Neuroscience Institute, Tan Tock Seng Hospital, Singapore, Singapore
- 2 Department of Clinical Translational Research, Singapore General Hospital, Singapore, Singapore
- 3 Department of Neurology, National Neuroscience Institute, Singapore General Hospital, Singapore, Singapore
- 4 Neuroscience and Behavioural Disorders Program, Duke-NUS Medical School, Singapore, Singapore
Received: May 7, 2020 Accepted: September 9, 2020 Published: October 20, 2020
https://doi.org/10.18632/aging.104111How to Cite
Copyright: © 2020 Yong et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Abstract
Long alpha-synuclein gene (SNCA) promoter (Rep1) allele-carriers are linked to higher risk for Parkinson’s disease (PD) and faster motor progression. Non-motor symptoms including autonomic, neuropsychiatric, and sleep disorders are common in PD. However, the relationship between SNCA Rep1 microsatellite lengths and non-motor symptoms in early PD remains to be elucidated. 171 consecutive early PD patients were recruited from tertiary clinics and genotyped for Rep1. Multivariable regression analyses were performed to examine associations between Rep1 alleles and non-motor outcome scores. Longer Rep1 alleles significantly associated with higher total Non-Motor Symptom Scale (NMSS) scores (p=.006) and Hospital Anxiety and Depression Scale (HADS) depression subscale scores (p=.002), after adjusting for covariates and Bonferroni correction. We demonstrated that SNCA Rep1 allele length influences overall non-motor symptom burden and depression in early PD patients. Further functional studies to evaluate the role of Rep1 in non-dopaminergic systems may unravel new therapeutic targets for non-motor symptoms in PD.