Laboratory of Biological Psychiatry, Institute of Mental Health, Tianjin Anding Hospital, Mental Health Center of Tianjin Medical University, 13 Liulin Road, Hexi District, 300222, Tianjin, China.
Department of Genetics, College of Basic Medical Sciences, Tianjin Medical University, Tianjin, 300070, China.
J Neural Transm (Vienna). 2022 Jun;129(5-6):563-573. doi: 10.1007/s00702-021-02437-6. Epub 2021 Nov 27.
Depressive symptoms and abnormal glycolipid metabolisms are common in patients with Parkinson's disease (PD), but their relationship has not been fully reported. It is not clear whether glycolipid impairments lead to poor cognitive and motor function, and aggravate depressive symptoms. Therefore, we aimed to explore the relationships between glycolipid variables, cognition, motor and depressive symptoms in PD patients cross-sectionally. Two hundred ten PD patients were recruited. Glycolipid parameters and Uric acid (UA) were measured. Depressive symptoms, cognitive function and motor symptoms were assessed using the Hamilton Depression Rating Scale-17 (HAMD-17), the Montreal Cognitive Assessment (MOCA) and the Movement Disorder Society Unified Parkinson's Disease Rating Scale Part-III (UPDRS-III). Depressive PD patients had significantly worse motor symptoms and higher levels of fasting plasma glucose (FPG) than those in non-depressive patients (F = 24.145, P < 0.001). Further, logistic regression analysis indicated that UPDRS-III (OR = 1.039, 95% CI 1.019-1.057, P = 0.044), FPG (OR = 1.447, 95% CI 1.050-1.994, P = 0.024) were independently associated with depression. In PD patients without depression, UA (β = - 0.068, t = - 2.913, P = 0.005) and cholesterol (CHOL) (β = - 3.941, t = - 2.518, P = 0.014) were independent predictors of the UPDRS-III score; in addition, UPDRS-III score was negatively associated with MOCA score (β = - 0.092, t = - 2.791, P = 0.007). FPG levels and motor symptoms were related to depressive symptoms in PD patients. Further, in non-depressive PD patients, UA and CHOL showed putative biomarkers of motor symptoms.
抑郁症状和异常糖脂代谢在帕金森病（PD）患者中很常见，但它们之间的关系尚未完全阐明。目前尚不清楚糖脂代谢紊乱是否会导致认知和运动功能下降，并加重抑郁症状。因此，我们旨在探讨 PD 患者横断面糖脂变量与认知、运动和抑郁症状之间的关系。共纳入 210 例 PD 患者，检测糖脂参数和尿酸（UA）。采用 Hamilton 抑郁评定量表-17（HAMD-17）、蒙特利尔认知评估（MOCA）和运动障碍协会统一帕金森病评定量表第 3 部分（UPDRS-III）评估抑郁症状、认知功能和运动症状。与非抑郁患者相比，抑郁 PD 患者的运动症状更差，空腹血糖（FPG）水平更高（F=24.145，P<0.001）。进一步的 logistic 回归分析表明，UPDRS-III（OR=1.039，95%CI 1.019-1.057，P=0.044）和 FPG（OR=1.447，95%CI 1.050-1.994，P=0.024）与抑郁独立相关。在无抑郁的 PD 患者中，UA（β=-0.068，t=-2.913，P=0.005）和胆固醇（CHOL）（β=-3.941，t=-2.518，P=0.014）是 UPDRS-III 评分的独立预测因子；此外，UPDRS-III 评分与 MOCA 评分呈负相关（β=-0.092，t=-2.791，P=0.007）。PD 患者的 FPG 水平和运动症状与抑郁症状相关。此外，在非抑郁的 PD 患者中，UA 和 CHOL 显示出运动症状的潜在生物标志物。
