Activation of N-methyl-D-aspartate receptor glycine site temporally ameliorates neuropsychiatric symptoms of Parkinson%26apos;s disease with dementia

作者:Tsai Chon Haw*; Huang Hui Chun; Liu Bey Ling; Li Chia Ing; Lu Ming Kuei; Chen Xianxiu; Tsai Mu Chieh; Yang Yu Wan; Lane Hsien Yuan
来源:Psychiatry and Clinical Neurosciences, 2014, 68(9): 692-700.
DOI:10.1111/pcn.12175

摘要

Aim: We have previously found that sarcosine, a glycine transporter I inhibitor, can improve the psychiatric symptoms of schizophrenia. In this study, we aimed to investigate whether the agent can also ameliorate neuropsychiatric symptoms of Parkinson%26apos;s disease (PD) patients with dementia. %26lt;br%26gt;Methods: An 8-week, double-blind, placebo-controlled trial was conducted in patients who had PD with dementia (PD-D). Neuropsychiatric manifestations were measured before and at week 2 (V1), week 4 (V2) and week 8 (V3) after treatment. Linear regression with the generalized estimating equations was applied for data analysis. %26lt;br%26gt;Results: Fifteen patients were randomized into a sarcosine group; the other 15 into a placebo group. The generalized estimating equations model revealed significant differences in Hamilton Depression Rating Scale score (P = 0.049) at V1 and Neuropsychiatry Inventory (P = 0.039) at V2 between the treatment and placebo groups. By excluding the advanced patients from analysis, there were significant differences in Unified Parkinson%26apos;s Disease Rating Scale V2 (P = 0.004) and V3 (P = 0.040), Hamilton Depression Rating Scale V1 (P = 0.014) and V2 (P = 0.047), Neuropsychiatry Inventory V1 (P = 0.002) and V2 (P %26lt; 0.001) and Behavior Pathology in Alzheimer%26apos;s Disease Rating Scale V2 (P = 0.025) in favor of sarcosine. %26lt;br%26gt;Conclusion: Sarcosine temporally improved depression and neuropsychiatric symptoms in PD-D patients without exacerbating the motor or cognitive features; the beneficial effects were more prominent in patients with mild-moderate severity. Enhancement of N-methyl-D-aspartate receptor-glycine cascade may lead to a novel path for the management of PD-D.