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Clinical Significance of REM Sleep Behavior Disorders and Other Non-motor Symptoms of Parkinsonism

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neuroscience Bulletin 2017年第5期33卷 576-584页

作者： Hong Jin Jin-Ru Zhang Yun Shen Chun-Feng Liu department of neurology and Sleep center The Second Affiliated Hospital of Soochow University Institute of neuroscience Soochow University

Rapid eye movement sleep behavior disorder （RBD） is one of the most common non-motor symptoms of parkinsonism, and it may serve as a prodromal marker of neurodegenerative disease. The mechanism underlying RBD is unclear. Several prospective studies have reported that specific non-motor symptoms predict a conversion risk of developing a neurodegenerative disease, including olfactory dysfunction, abnormal color vision, autonomic dysfunction, excessive daytime sleepiness, depression, and cognitive impairment. Parkinson＇s disease （PD） with RBD exhibits clinical heterogeneity with respect to motor and non-motor symptoms compared with PD without RBD. In this review, we describe the main clinical and pathogenic features of RBD, focusing on its association with other non-motor symptoms of parkinsonism.

关键词： Parkinson＇s disease · Rapid eye movement sleep behavior disorder · Risk factors ·Parkinsonism

Seasonal variations of nonmotor symptoms in patients with Parkinson's disease in Southeast China

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Chinese Medical Journal 2023年第4期136卷 415-422页

作者： Jingyi Wang Kangping Xiong Jingyuan Chao Sheng Zhuang Jie Li Chunfeng Liu department of neurology and Clinical Research center of Neurological Disease The Second Affiliated Hospital of Soochow UniversitySuzhouJiangsu 215004China Sleep center The Second Affiliated Hospital of Soochow UniversitySuzhouJiangsu 215004China Institute of neuroscience Soochow UniversitySuzhouJiangsu 215123China

Background:Studies suggest seasonal fluctuations of symptoms in Parkinson’s disease(PD)patients in Western countries.However,the association between seasonal change and variation in nonmotor symptoms(NMS)in Chinese PD patients is unclear.Here,we studied whether there is a change rule with annual cycle with severity of NMS for patients with PD in Southeast China.Methods:We studied 1005 PD patients between April 2008 and October 2020.Patients were classified into four seasons according to the 24 Chinese solar terms,based on assessment date.We compared comprehensive NMS scales and polysomnography parameters among groups and conducted further analysis of disease severity.Results:Among the 1005 patients studied,the mean age was 64.2±9.7 years and 569(56.6%)of them were men.Relative to the summer group,patients assessed during winter had higher Scales for Outcomes in Parkinson’s disease-Autonomic Dysfunction(SCOPA-AUT)scores(P=0.045).The sleep efficiency factor scores of Pittsburgh Sleep Quality Index in patients were higher during spring than summer(P=0.009).Among patients who completed polysomnography during the same period(n=135),compared with summer follow-ups,we observed a higher percentage of NREMS1 in winter and spring follow-ups(P=0.042,P=0.011),a higher NREMS1 time in spring follow-ups(P=0.0024),a lower NREMS2 time in winter follow-ups(P=0.007),and a higher percentage of phasic rapid eye movement(REM)-sleep without atonia in autumn and winter follow-ups(P=0.026 and P=0.020,respectively).In a subset of patients with PD and REM sleep behavior disorder(RBD;n=182),those visited during winter had higher scores for RBD questionnaire-Hong Kong and its factor 1(dream-related sub-score)than those visited during summer(P=0.034,P=0.020).We observed similar findings for SCOPA-AUT and sleep efficiency factor scores in early stage patients in subgroup analysis.Conclusions:PD patients assessed for follow-up during summer showed less severe symptoms of autonomic dysfunction and RBD symptoms than those assessed in winter,and l

关键词： Nonmotor symptoms Parkinson’s disease Seasonal variations

A New Perspective for Parkinson's Disease:Circadian Rhythm

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neuroscience Bulletin 2017年第1期33卷 62-72页

作者： Siyue Li Yali Wang Fen Wang Li-Fang Hu Chun-Feng Liu department of neurology and Suzhou Clinical Research center of Neurological Disease The Second Affiliated Hospital of Soochow University Institutes of neuroscience Soochow University

Circadian rhythm is manifested by the behavioral and physiological changes from day to night, which is controlled by the pacemaker and its regulator. The former is located at the suprachiasmatic nuclei （SCN） in the anterior hypothalamus, while the latter is composed of clock genes present in all tissues. Circadian desynchronization influences normal patterns of day-night rhythms such as sleep and alertness cycles, rest and activity cycles. Parkinson＇s disease （PD） exhibits diurnal fluctuations. Circadian dysfunction has been observed in PD patients and animal models, which may result in negative conse- quences to the homeostasis and even exacerbate the disease progression. Therefore, circadian therapies, including light stimulation, physical activity, dietary and social schedules, may be helpful for PD patients. However, the cellular and molecular mechanisms that underlie the circadian dysfunction in PD remain elusive. Further research on circadian patterns is needed. This article summarizes the existing research on the circadian rhythms in PD, focusing on the clinical symptom variations, molecular changes, as well as the available treatment options.

关键词： Parkinson＇s disease Circadian rhythm Sleep Dopamine

Selegiline improves excessive daytime sleepiness in Parkinson’s disease:an open-label observational study

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Chinese Medical Journal 2022年第14期135卷 1762-1764页

作者： Jinru Zhang Juping Chen Jia Li Jian Li Hong Miao Xiangyang Zhu Meng Meng Yang Han Jing Chen Xiaoyu Cheng Kangping Xiong Hong Jin Weifeng Luo Chengjie Mao Chunfeng Liu department of neurology and Clinical Research center of Neurological Disease The Second Affiliated Hospital of Soochow UniversitySuzhouJiangsu 215004China department of neurology Changshu Hospital Affiliated to Nanjing University of Chinese MedicineChangshuJiangsu 215516China department of neurology The Second Affiliated Hospital of Nantong UniversityNantongJiangsu 226001China department of neurology JiangYuan Hospital Affiliated to Jiangsu Institute of Nuclear MedicineWuxiJiangsu 214063China Jiangsu Key Laboratory of Neuropsychiatric Diseases and Institute of neuroscience Soochow UniversitySuzhouJiangsu 215123China

To the Editor:Parkinson’s disease(PD)is the second most common neurodegenerative disorder,and sleep disturbance is a major disabling non-motor symptom.[1]Excessive daytime sleepiness(EDS)is defined as inappropriate and undesirable sleepiness during waking hours,which may occur during activities such as talking or driving.In PD patients,EDS increased the risk of accidents and resulted in a poor quality of life.[2]

关键词： sleep driving patients

Expression and Function of Zinc-α2-Glycoprotein

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neuroscience Bulletin 2019年第3期35卷 540-550页

作者： Xin Wei Xi Liu Changhong Tan Lijuan Mo Hui Wang Xi Peng Fen Deng Lifen Chen department of neurology The Second Affiliated Hospital of Chongqing Medical University

Zinc-α2-glycoprotein(ZAG), encoded by the AZGP1 gene, is a major histocompatibility complex I molecule and a lipid-mobilizing factor. ZAG has been demonstrated to promote lipid metabolism and glucose utilization, and to regulate insulin sensitivity. Apart from adipose tissue, skeletal muscle, liver, and kidney, ZAG also occurs in brain tissue, but its distribution in brain is debatable. Only a few studies have investigated ZAG in the brain. It has been found in the brains of patients with Krabbe disease and epilepsy, and in the cerebrospinal fluid of patients with Alzheimer disease, frontotemporal lobe dementia, and amyotrophic lateral sclerosis. Both ZAG protein and AZGP1 m RNA are decreased in epilepsy patients and animal models, while overexpression of ZAG suppresses seizure and epileptic discharges in animal models of epilepsy, but knowledge of the specific mechanism of ZAG in epilepsy is limited. In this review, we summarize the known roles and molecular mechanisms of ZAG in lipid metabolism and glucose metabolism, and in the regulation of insulin sensitivity, and discuss the possible mechanisms by which it suppresses epilepsy.

关键词： Zinc-α2-glycoprotein Metabolism Glucose Lipid Insulin sensitivity Neuron

Cortical spreading depression-induced preconditioning in the brain

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Neural Regeneration Research 2016年第11期11卷 1857-1864页

作者： Ping-ping Shen Shuai Hou Di Ma Ming-ming Zhao Ming-qin Zhu Jing-dian Zhang Liang-shu Feng Li Cui Jia-chun Feng Institute of neuroscience center and neurology department the First Affiliated Hospital of Jilin University

Cortical spreading depression is a technique used to depolarize neurons. During focal or global ischemia, cortical spreading depression-induced preconditioning can enhance tolerance of further injury. However, the underlying mechanism for this phenomenon remains relatively unclear. To date, numerous issues exist regarding the experimental model used to precondition the brain with cortical spreading depression, such as the administration route, concentration of potassium chloride, induction time, duration of the protection provided by the treatment, the regional distribution of the protective effect, and the types of neurons responsible for the greater tolerance. In this review, we focus on the mechanisms underlying cor- tical spreading depression-induced tolerance in the brain, considering excitatory neurotransmission and metabolism, nitric oxide, genomic reprogramming, inflammation, neurotropic factors, and cellular stress response. Specifically, we clarify the procedures and detailed information regarding cortical spreading depression-induced preconditioning and build a foundation for more comprehensive investigations in the field of neural regeneration and clinical application in the future.

关键词： nerve regeneration cortical spreading depression neuronal depolarization ischemic tolerance peri-infarct depolarization excitatory neurotransmission nitric oxide genomic reprogramming inflammation neurotropic factors cellular stress response neural regeneration

Volumetric Changes in Hippocampal Subregions and Memory Performance in Mesial Temporal Lobe Epilepsy with Hippocampal Sclerosis

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neuroscience Bulletin 2018年第2期34卷 389-396页

作者： Caihong Ji Lujia Zhu Cong Chen Shuang Wang Leilei Zheng Hong Li department of neurology Epilepsy Center Second Affiliated Hospital School of Medicine Zhejiang University department of Psychology Second Affiliated HospitalSchool of Medicine Zhejiang University department of Radiology Second Affiliated Hospital School of Medicine Zhejiang University

In the present study we explored the different patterns of volumetric atrophy in hippocampal subregions of patients with left and right mesial temporal lobe epilepsy with hippocampal sclerosis(TLE-HS). Meanwhile, the memory impairment patterns in Chinese-speaking TLE-HS patients and potential influencing factors were also determined. TLE-HS patients(21 left and 17 right) and 21 healthy controls were recruited to complete T2-weighted imaging and verbal/nonverbal memory assessment. The results showed that both left and right TLE-HS patients had overall reduced hippocampal subregion volumes on the sclerotic side, and cornu ammonis sectors(CA1) exhibited maximum atrophy. The verbal memory of left TLE-HS patients was significantly impaired(P \ 0.001) and was not associated with the volumes of the left hippocampal subregions. Verbal or nonverbal memory impairment was not found in the patients with right TLE-HS. These results suggested that the atrophy of hippocampal subregion volumes cannot account for the verbal memory impairment, which might be related to the functional network.

关键词： HIGH-RESOLUTION MRI IMPAIRMENT DISEASE ATROPHY SUBFIELDS RECALL SHAPE RISK

The Pathology of Primary Familial Brain Calcification:Implications for Treatment

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neuroscience Bulletin 2023年第4期39卷 659-674页

作者： Xuan Xu Hao Sun Junyu Luo Xuewen Cheng Wenqi Lv Wei Luo Wan-Jin Chen Zhi-Qi Xiong Jing-Yu Liu Institute of neuroscience State Key Laboratory of NeuroscienceCenter for Excellence in Brain Science and Intelligence TechnologyChinese Academy of SciencesShanghai200031China College of Life Science and Technology Huazhong University of Science and TechnologyWuhan430074China department of neurology and Institute of neurology of First affiliated hospital Institute of Neuroscienceand Fujian Key Laboratory of Molecular NeurologyFujian Medical UniversityFuzhou350005China department of neurology The Second Affiliated HospitalZhejiang University School of MedicineHangzhou310009China

Primary familial brain calcification(PFBC)is an inherited neurodegenerative disorder mainly characterized by progressive calcium deposition bilaterally in the brain,accompanied by various symptoms,such as dystonia,ataxia,parkinsonism,dementia,depression,headaches,and epilepsy.Currently,the etiology of PFBC is largely unknown,and no specific prevention or treatment is available.During the past 10 years,six causative genes(SLC20A2,PDGFRB,PDGFB,XPR1,MYORG,and JAM2)have been identified in PFBC.In this review,considering mechanistic studies of these genes at the cellular level and in animals,we summarize the pathogenesis and potential preventive and therapeutic strategies for PFBC patients.Our systematic analysis suggests a classification for PFBC genetic etiology based on several characteristics,provides a summary of the known composition of brain calcification,and identifies some potential therapeutic targets for PFBC.

关键词： Primary familial brain calcification Causative gene Pathogenesis Preventive and therapeutic strategy

Norepinephrine from the Locus Coeruleus Regulates Microglia Dynamics During Wakefulness

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neuroscience Bulletin 2020年第5期36卷 554-556页

作者： Yaling Hu Peng Shi Zhihua Gao neuroscience Research center and department of neurology The Second Affiliated HospitalKey Laboratory of Medical Neurobiology of Zhejiang ProvinceZhejiang University School of MedicineHangzhou 310058China department of Cardiology The Second Affiliated HospitalZhejiang University School of MedicineHangzhou 310058China

Microglia,the brain’s"busy bees",continuously survey the microenvironment by extending and retracting their ramified processes to maintain brain homeostasis[1,2].Upon disease or injury,microglia quickly transform their morphology and extend their processes towards the disease/injury sites to clear damage[2].The mechanisms underlying the high motility of microglial processes and the rapid morphological transformation of microglia have been extensively investigated.

关键词： homeostasis motility maintain