Multiple comorbid sleep disorders adversely affect quality of life in Parkinson's disease patients.

Sleep disorders are common non-motor symptoms in patients with Parkinson's disease (PD). The characteristics and impact of multiple comorbid sleep disorders remain to be elucidated. Our goal was to investigate the characteristics of various sleep disorder comorbidities, and their association with motor complications and the impact on the quality of life in PD patients. In this multicenter, observational, cross-sectional study, data concerning the clinical characteristics of complicated sleep disorders were collected from PD patients treated at 40 different hospitals in Shanghai. Sleep disorders were evaluated using the PD Sleep Scale-2, Epworth Sleepiness Scale, Rapid Eye Movement Sleep Behavior Disorder Questionnaire-Hong Kong, and the International Restless Legs Scale. Among the 1006 subjects evaluated, 77.53% exhibited signs of sleep disorders, and most had multiple sleep disorders (n = 502, 49.9%). A smaller percentage of patients with sleep disorders had a single disorder (n = 278, 27.6%). Furthermore, an increased number of sleep disorders, including nighttime problems, excessive daytime sleepiness, rapid eye movement sleep behavior disorder, and restless legs syndrome was a significant contributor to a poor quality of life (ß = 4.33, CI: 3.33-5.33, P for trend <0.001), even when controlling for multiple factors. Moreover, motor complications partially mediated this relationship (indirect effect: ß = 0.355, 95% boot CI: 0.134, 0.652).Our study showed that a large proportion of PD patients suffer from multiple comorbid sleep disorders, which greatly decreases the quality of life in PD patients and is partially mediated by motor complications.

Benfotiamine prevents increased ß-amyloid production in HEK cells induced by high glucose.

OBJECTIVE: To determine whether high glucose enhances ß-amyloid (Aß) production in HEK293 Swedish mutant (APPsw) cells with Aß precursor protein (APP) overexpression, and whether under this condition benfotiamine reduces the increased Aß production. METHODS: HEK293 APPsw cells were cultured with different concentrations of glucose for different times. The Aß content in the supernatant was determined by ELISA. To investigate the mechanism by which benfotiamine reduced Aß production, glycogen synthase kinase-3 (GSK-3) activity and expression were measured after the cells were cultured with 5.5 g/L glucose for 12 h. RESULTS: With 1.0, 3.0, 4.5, 5.5, 6.5, 7.5, 8.5, or 10.5 g/L glucose, Aß production by HEK293 APPsw cells was highest in the presence of 5.5 g/L glucose for 6 and 12 h. The difference in Aß content between 5.5 and 1.0 g/L was most marked after incubation for 12 h. Benfotiamine at 20 and 40 µg/mL significantly reduced Aß production in cells incubated with 5.5 g/L glucose for 12 h. Moreover, 40 µg/mL benfotiamine significantly enhanced the ratio of phosphorylated GSK-3 to total GSK-3, together with consistent down-regulation of GSK-3 activity. CONCLUSION: High glucose increases Aß production by HEK293 APPsw cells while benfotiamine prevents this increase. This is correlated with the modulation of GSK-3 activity.