Xiao-Tong Wang1, Feng-Tao Liu2, Huan Yu2, Can Zhang3, Ya-Hui Ma1, Jian Wang2, Qiang Dong2, Lan Tan4, Han Wang5, Jin-Tai Yu6. 1. Department of Neurology, Qingdao Municipal Hospital, School of Medicine, Qingdao University, No.5 Donghai Middle Road, Qingdao, China. 2. Department of Neurology and Institute of Neurology, Huashan Hospital, Shanghai Medical College, Fudan University, 12th Wulumuqi Zhong Road, Shanghai, 200040, China. 3. Department of Neurology, Genetics and Aging Research Unit, McCance Center for Brain Health, MassGeneral Institute for Neurodegenerative Diseases (MIND), Massachusetts General Hospital, Harvard Medical School, Charlestown, MA, 02129-2060, USA. 4. Department of Neurology, Qingdao Municipal Hospital, School of Medicine, Qingdao University, No.5 Donghai Middle Road, Qingdao, China. dr.tanlan@163.com. 5. Department of Neurology, Peking Union Medical College Hospital, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing, 100730, China. wanghan4179@pumch.cn. 6. Department of Neurology and Institute of Neurology, Huashan Hospital, Shanghai Medical College, Fudan University, 12th Wulumuqi Zhong Road, Shanghai, 200040, China. jintai_yu@fudan.edu.cn.
Abstract
OBJECTIVES: Our aim is to investigate the associations of sleep disorders with cerebrospinal fluid (CSF) α-synuclein (α-syn) in healthy controls (HCs), and patients with prodromal and early Parkinson's disease (PD). METHODS: We included a total of 575 individuals, consisting of 360 PD individuals, 46 prodromal PD individuals, and 169 HCs. Multiple linear regression models and linear mixed-effects models were used to investigate the associations of sleep disorders with baseline and longitudinal CSF α-syn. Associations between the change rates of sleep disorders and CSF α-syn were further investigated via multiple linear regression models. RESULTS: In PD, probable Rapid-eye-movement sleep Behavior Disorder (pRBD) (β = - 0.1199; P = 0.0444) and RBD sub-items, such as aggressive dreams (β = - 0.1652; P = 0.0072) and hurting bed partner (β = - 0.2468; P = 0.0010), contributed to lower CSF α-syn. The association between aggressive dreams and lower CSF α-syn further survived Bonferroni correction (P < 0.0036). In prodromal PD, dream-enacting (a specific RBD behavior) was significantly associated with decreased CSF α-syn during the follow-up (β = - 0.0124; P = 0.0237). HCs with daytime sleepiness when inactive-sitting in public places (β = - 0.0033; P = 0.0135) showed decreased CSF α-syn. Furthermore, increased possibilities of daytime sleepiness when sitting and reading contributed to a greater decrease of CSF α-syn in HCs (β = - 196.8779; P = 0.0433). CONCLUSIONS: Sleep disorders were associated with decreased CSF α-syn. Sleep management may be important for disease monitoring and preventing the progression of α-syn pathology.
OBJECTIVES: Our aim is to investigate the associations of sleep disorders with cerebrospinal fluid (CSF) α-synuclein (α-syn) in healthy controls (HCs), and patients with prodromal and early Parkinson's disease (PD). METHODS: We included a total of 575 individuals, consisting of 360 PD individuals, 46 prodromal PD individuals, and 169 HCs. Multiple linear regression models and linear mixed-effects models were used to investigate the associations of sleep disorders with baseline and longitudinal CSF α-syn. Associations between the change rates of sleep disorders and CSF α-syn were further investigated via multiple linear regression models. RESULTS: In PD, probable Rapid-eye-movement sleep Behavior Disorder (pRBD) (β = - 0.1199; P = 0.0444) and RBD sub-items, such as aggressive dreams (β = - 0.1652; P = 0.0072) and hurting bed partner (β = - 0.2468; P = 0.0010), contributed to lower CSF α-syn. The association between aggressive dreams and lower CSF α-syn further survived Bonferroni correction (P < 0.0036). In prodromal PD, dream-enacting (a specific RBD behavior) was significantly associated with decreased CSF α-syn during the follow-up (β = - 0.0124; P = 0.0237). HCs with daytime sleepiness when inactive-sitting in public places (β = - 0.0033; P = 0.0135) showed decreased CSF α-syn. Furthermore, increased possibilities of daytime sleepiness when sitting and reading contributed to a greater decrease of CSF α-syn in HCs (β = - 196.8779; P = 0.0433). CONCLUSIONS: Sleep disorders were associated with decreased CSF α-syn. Sleep management may be important for disease monitoring and preventing the progression of α-syn pathology.