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Phenotype of postural instability/gait difficulty in Parkinson disease: relevance to cognitive impairment and mechanism relating pathological proteins and neurotransmitters

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机构： [1]Department of Neurology, Beijing Tiantan Hospital, Capital Medical University, Beijing, 100050, China. [2]Department of Geriatrics, Beijing Tiantan Hospital, Capital Medical University, Beijing, 100050, China. [3]Core Laboratory for Clinical Medical Research, Beijing Tiantan Hospital, Capital Medical University, Beijing, 100050, China. [4]Department of Neurobiology and Physiology, Capital Medical University, Beijing, 100069, China. [5]Key Laboratory for Neurodegenerative Disorders of the Ministry of Education, Capital Medical University, Beijing, 100069, China. [6]Beijing Institute for Brain Disorders, Capital Medical University, Beijing, 100069, China. [7]Beijing Key Laboratory on Parkinson disease, Beijing, 100053, China. [8]Department of Neurobiology, Beijing Institute of Geriatrics, Xuanwu Hospital of Capital Medical University, Beijing, 100053, China. [9]Department of Neurology, Ruijin Hospital Affiliated to Shanghai Jiaotong University School of Medicine, Shanghai, 200025, China. [10]China National Clinical Research Center for Neurological Diseases, Beijing, 100050, China.

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Parkinson disease (PD) is identified as tremor-dominant (TD) and postural instability and gait difficulty (PIGD) phenotypes. The relationships between motor phenotypes and cognitive impairment and the underlying mechanisms relating pathological proteins and neurotransmitters in cerebrospinal fluid (CSF) are unknown. We evaluated the motor symptoms and cognitive function by scales, and detected the levels of pathological proteins and neurotransmitters in CSF. TD group and PIGD group had significantly higher levels of total tau, tau phosphorylated at the position of threonine 181(P-tau181t), threonine 231, serine 396, serine 199 and lower beta amyloid (A beta)(1-42) level in CSF than those in control group; PIGD group had significantly higher P-tau181t level and lower A beta(1-42) level than those in TD group. In PD group, PIGD severity was negatively correlated with MoCA score and A beta(1-42) level in CSF, and positively correlated with Hoehn-Yahr stage and P-tau181t level in CSF. In PIGD group, PIGD severity was negatively correlated with homovanillic acid (HVA) level in CSF, and HVA level was positively correlated with A beta(1-42) level in CSF. PIGD was significantly correlated with cognitive impairment, which underlying mechanism might be involved in A beta(1-42) aggregation in brain and relevant neurochemical disturbance featured by the depletion of HVA in CSF.

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出版当年[2016]版：

大类 | 2 区综合性期刊

小类 | 2 区综合性期刊

最新[2023]版：

大类 | 2 区综合性期刊

小类 | 2 区综合性期刊

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出版当年[2015]版：

Q1 MULTIDISCIPLINARY SCIENCES

最新[2023]版：

Q1 MULTIDISCIPLINARY SCIENCES

影响因子： 3.8 最新[2023版] 4.3 最新五年平均 5.228 出版当年[2015版] 5.525 出版当年五年平均 5.578 出版前一年[2014版] 4.259 出版后一年[2016版]

第一作者：

第一作者机构： [1]Department of Neurology, Beijing Tiantan Hospital, Capital Medical University, Beijing, 100050, China.

通讯作者：

通讯机构： [1]Department of Neurology, Beijing Tiantan Hospital, Capital Medical University, Beijing, 100050, China. [2]Department of Geriatrics, Beijing Tiantan Hospital, Capital Medical University, Beijing, 100050, China. [5]Key Laboratory for Neurodegenerative Disorders of the Ministry of Education, Capital Medical University, Beijing, 100069, China. [6]Beijing Institute for Brain Disorders, Capital Medical University, Beijing, 100069, China. [7]Beijing Key Laboratory on Parkinson disease, Beijing, 100053, China. [10]China National Clinical Research Center for Neurological Diseases, Beijing, 100050, China.

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