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Parkinson Disease: HELP
Articles from Beijing
Based on 451 articles published since 2008
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These are the 451 published articles about Parkinson Disease that originated from Beijing during 2008-2019.
 
+ Citations + Abstracts
Pages: 1 · 2 · 3 · 4 · 5 · 6 · 7 · 8 · 9 · 10 · 11 · 12 · 13 · 14 · 15 · 16 · 17 · 18 · 19
1 Editorial Non-glaucomatous peripapillary retinal nerve fiber layer defect. 2013

Wei, Wen-bin / Pan, Cheng / Zhou, Jin-qiong. ·Beijing Tongren Eye Center, Beijing Tongren Hospital, Capital Medical University; Beijing Ophthalmology & Visual Sciences Key Laboratory, Beijing 100730, China (Email: trweiwenbin@yahoo.com.cn). ·Chin Med J (Engl) · Pubmed #23595367.

ABSTRACT: -- No abstract --

2 Review The mechanisms of NLRP3 inflammasome/pyroptosis activation and their role in Parkinson's disease. 2019

Wang, Shuo / Yuan, Yu-He / Chen, Nai-Hong / Wang, Hong-Bo. ·State Key Laboratory of Bioactive Substances and Functions of Natural Medicines, Institute of Materia Medica, Neuroscience Center, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100050, China. · State Key Laboratory of Bioactive Substances and Functions of Natural Medicines, Institute of Materia Medica, Neuroscience Center, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100050, China. Electronic address: yuanyuhe@imm.ac.cn. · State Key Laboratory of Bioactive Substances and Functions of Natural Medicines, Institute of Materia Medica, Neuroscience Center, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100050, China; College of Pharmacy, Hunan University of Chinese Medicine, Changsha, Hunan 410208, China. Electronic address: chennh@imm.ac.cn. · Key Laboratory of Molecular Pharmacology and Drug Evaluation (Yantai University), Ministry of Education, Yantai University, Yantai 264005, China. ·Int Immunopharmacol · Pubmed #30594776.

ABSTRACT: Parkinson's disease (PD) is a typical neurodegenerative disease and the pathological feature of which is the death of dopamine neurons in the substantia nigra region. At present, neuronal death caused by inflammatory cytokine-mediated neuroinflammation is being extensively studied. The nucleotide-binding oligomerization domain-, leucine-rich repeat and pyrin domain-containing 3 (NLRP3) inflammasome is an inflammatory complex existing in microglia. Its activation promotes the secretion of the inflammatory cytokine interleukin-1β/18 (IL-1β/18) and induces pyroptosis, a type of cell death that possesses the potential for inflammation, to rupture microglia to further release IL-1β. In this review we focus on the mechanisms of activation of the NLRP3 inflammasome and pyroptosis and their inflammatory effects on the development of PD. In addition, we focus on some inhibitors of NLRP3 inflammatory pathways to alleviate the progression of PD by inhibiting central inflammation and provide new therapeutic strategies for the treatment of PD.

3 Review SNCA REP1 and Parkinson's disease. 2018

Shu, Li / Zhang, Yuan / Sun, Qiying / Pan, Hongxu / Guo, Jifeng / Tang, Beisha. ·Department of Neurology, Xiangya Hospital, Central South University, Changsha, Hunan 410008, China. · Department of Geriatrics, Xiangya Hospital, Central South University, Changsha, Hunan 410008, China; National Clinical Research Center for Geriatric Disorders, Changsha, Hunan 410078, China; Key Laboratory of Hunan Province in Neurodegenerative Disorders, Central South University, Changsha, Hunan 410008, China. · Department of Neurology, Xiangya Hospital, Central South University, Changsha, Hunan 410008, China; National Clinical Research Center for Geriatric Disorders, Changsha, Hunan 410078, China; Key Laboratory of Hunan Province in Neurodegenerative Disorders, Central South University, Changsha, Hunan 410008, China; Parkinson's Disease Center of Beijing Institute for Brain Disorders, Beijing 100069, China; Collaborative Innovation Center for Brain Science, Shanghai 200032, China; Collaborative Innovation Center for Genetics and Development, Shanghai 200438, China. · Department of Neurology, Xiangya Hospital, Central South University, Changsha, Hunan 410008, China; Department of Geriatrics, Xiangya Hospital, Central South University, Changsha, Hunan 410008, China; National Clinical Research Center for Geriatric Disorders, Changsha, Hunan 410078, China; Key Laboratory of Hunan Province in Neurodegenerative Disorders, Central South University, Changsha, Hunan 410008, China; Center for Medical Genetics, School of Life Sciences, Central South University, Changsha, Hunan 410008, China; Parkinson's Disease Center of Beijing Institute for Brain Disorders, Beijing 100069, China; Collaborative Innovation Center for Brain Science, Shanghai 200032, China; Collaborative Innovation Center for Genetics and Development, Shanghai 200438, China. Electronic address: bstang7398@163.com. ·Neurosci Lett · Pubmed #29859327.

ABSTRACT: REP1 is a polymorphic dinucleotide repeat sequence located in the promoter region of the SNCA gene (OMIM 163890). Opinions regarding the interaction between the various REP1 alleles and Parkinson's disease (PD) or its phenotypes have been inconsistent and have thus far not been comprehensively analyzed. In this study, we searched Medline, Embase and Cochrane databases as well as the Chinese-language Wanfang and CNKI databases using strict inclusion and exclusion criteria and conducted our analysis using Revman 5.3 software. Our search produced 28 articles describing REP1 alleles and their associated PD risks and 8 articles which discussed the relationship between REP1 variation and PD phenotypes. We found that the 265-, 269-, and 271-bp alleles of REP1 (using the nomenclature established by Xia et al.) increased the risk of PD (OR: 1.81, 1.05, 1.17; p: 0.0002, 0.003, 0.002) while the 267-bp allele decreased PD risk (OR: 0.86, p: <0.00001) when taking all populations into account. By ethnicity, we observed an obvious population heterogeneity in the effects of various alleles, where the 269-, 271-, and 273-bp alleles increased PD risk (OR: 1.06, 1.22, 1.89; p: 0.001, 0.003, 0.001) and the 267-bp allele decreased PD risk (OR: 0.85; p: <0.00001) in Caucasian populations, and the 263- and 265-bp alleles increased the risk of PD (OR: 2.22, 2.03; p: 0.03, 0.0002) and the 267- and 273-bp alleles decreased PD risk (OR: 0.90, 0.78; p: 0.02, 0.03) in Asian populations. We also determined that the 267-, 269-, and 271-bp alleles occurred the most frequently, although the frequency distribution varied among different ethnicities. Phenotypic analysis demonstrated that PD patients carrying the 271-bp allele were prone to early onset PD (OR: 1.75, p: 0.02) while the 267-bp had the opposite effect (OR: 0.81; p: 0.01).

4 Review Relationships between Rapid Eye Movement Sleep Behavior Disorder and Neurodegenerative Diseases: Clinical Assessments, Biomarkers, and Treatment. 2018

Li, Min / Wang, Li / Liu, Jiang-Hong / Zhan, Shu-Qin. ·Department of Neurology, Xuanwu Hospital, Capital Medical University, Beijing 100053, China. ·Chin Med J (Engl) · Pubmed #29664058.

ABSTRACT: Objective: Rapid eye movement sleep behavior disorder (RBD) is characterized by dream enactment and loss of muscle atonia during rapid eye movement sleep. RBD is closely related to α-synucleinopathies including Parkinson's disease, dementia with Lewy bodies, and multiple system atrophy. Many studies have investigated the markers of imaging and neurophysiological, genetic, cognitive, autonomic function of RBD and their predictive value for neurodegenerative diseases. This report reviewed the progress of these studies and discussed their limitations and future research directions. Data Sources: Using the combined keywords: "RBD", "neurodegenerative disease", "Parkinson disease", and "magnetic resonance imaging", the PubMed/MEDLINE literature search was conducted up to January 1, 2018. Study Selection: A total of 150 published articles were initially identified citations. Of the 150 articles, 92 articles were selected after further detailed review. This study referred to all the important English literature in full. Results: Single-nucleotide polymorphisms in SCARB2 (rs6812193) and MAPT (rs12185268) were significantly associated with RBD. The olfactory loss, autonomic dysfunction, marked electroencephalogram slowing during both wakefulness and rapid eye movement sleep, and cognitive impairments were potential predictive markers for RBD conversion to neurodegenerative diseases. Traditional structural imaging studies reported relatively inconsistent results, whereas reduced functional connectivity between the left putamen and substantia nigra and dopamine transporter uptake demonstrated by functional imaging techniques were relatively consistent findings. Conclusions: More longitudinal studies should be conducted to evaluate the predictive value of biomarkers of RBD. Moreover, because the glucose and dopamine metabolisms are not specific for assessing cognitive cognition, the molecular metabolism directly related to cognition should be investigated. There is a need for more treatment trials to determine the effectiveness of interventions of RBD on preventing the conversion to neurodegenerative diseases.

5 Review The Promise of Telemedicine for Movement Disorders: an Interdisciplinary Approach. 2018

Ben-Pazi, H / Browne, P / Chan, P / Cubo, E / Guttman, M / Hassan, A / Hatcher-Martin, J / Mari, Z / Moukheiber, E / Okubadejo, N U / Shalash, A / Anonymous1401121. ·Neuropediatric unit, Shaare Zedek Medical Center, Jerusalem, Israel. · Neurology Department, University Hospital Galway, Newcastle Road, Galway, Ireland. · School of Medicine, National University of Ireland Galway, Galway, Ireland. · Department of Neurobiology, Neurology and Geriatrics, Xuanwu Hospital of Capital Medical University Beijing, Beijing, China. · Neurology Department, University Hospital, Burgos, Spain. mcubo@saludcastillayleon.es. · University of Toronto, Toronto, ON, Canada. · Department of Neurology, Mayo Clinic, Rochester, MN, USA. · Movement Disorders Program, Department of Neurology, Emory University School of Medicine, Atlanta, GA, USA. · Parkinson's Disease and Movement Disorders Program, Cleveland Clinic Lou Ruvo Center for Brain Health, Las Vegas, USA. · Department of Neurology, Johns Hopkins Medicine, Baltimore, MD, USA. · Neurology Unit, Department of Medicine, College of Medicine, University of Lagos, Lagos State, Nigeria. · Department of Neurology, Faculty of Medicine, Ain Shams University, Cairo, Egypt. ·Curr Neurol Neurosci Rep · Pubmed #29654523.

ABSTRACT: PURPOSE OF REVIEW: Advances in technology have expanded telemedicine opportunities covering medical practice, research, and education. This is of particular importance in movement disorders (MDs), where the combination of disease progression, mobility limitations, and the sparse distribution of MD specialists increase the difficulty to access. In this review, we discuss the prospects, challenges, and strategies for telemedicine in MDs. RECENT FINDINGS: Telemedicine for MDs has been mainly evaluated in Parkinson's disease (PD) and compared to in-office care is cost-effective with similar clinical care, despite the barriers to engagement. However, particular groups including pediatric patients, rare MDs, and the use of telemedicine in underserved areas need further research. Interdisciplinary telemedicine and tele-education for MDs are feasible, provide similar care, and reduce travel costs and travel time compared to in-person visits. These benefits have been mainly demonstrated for PD but serve as a model for further validation in other movement disorders.

6 Review MiRNAs participate in the diagnosis, pathogenesis and therapy of Parkinson's disease. 2018

Lu, Xuexin / Cui, Zhijie / Liu, Shuang / Yin, Feng. ·Department of Neurosurgery, Navy General Hospital, PLA, Beijing, China. · Chinese Center for Disease Control and Prevention, National institute for virus disease control and prevention, Beijing, China. · Beijing Si Ji Qing Hospital, Beijing, China. ·Histol Histopathol · Pubmed #29135019.

ABSTRACT: MicroRNAs (miRNAs), one kind of post-transcriptional modification, mediate transcriptional silencing of various metabolic enzymes that are involved in various life processes, including Parkinson's disease. At present, the pathogenesis of Parkinson's disease is not clear, although many studies suggest that miRNAs play a very important role in the progress of Parkinsonism. This paper reviews the biological characteristics of miRNAs and summarizes the progress of miRNAs in reference to the diagnosis and pathogenesis of Parkinson's disease. It even considers miRNAs as a potential target for Parkinson's disease therapy.

7 Review The significance of uric acid in the diagnosis and treatment of Parkinson disease: An updated systemic review. 2017

Yu, Zhange / Zhang, Shuai / Wang, Dongdong / Fan, Meng / Gao, Fuqiang / Sun, Wei / Li, Zirong / Li, Shiliang. ·aDepartment of Acupuncture, China-Japan Friendship Hospital, Beijing bDepartment of Neurology, The Affiliated Hospital of Yangzhou University, Yangzhou University, Yangzhou, Jiangsu Province cDepartment of Orthopedics, Tumd Right Banner Hospital, Baotou City dDepartment of Orthopedics, China-Japan Friendship Hospital, Beijing, China. ·Medicine (Baltimore) · Pubmed #29137045.

ABSTRACT: BACKGROUND: Parkinson disease (PD) is a neurodegenerative disease characterized by chronic and progressive loss of dopaminergic neurons in substansia nigra pars compacta. Oxidative stress is proposed to play a critical role in the pathogenesis of PD. Uric acid (UA), as an important physiological antioxidant, is identified a molecular predictor associated with a decreased risk and a slower disease progression for PD and potential neuroprotectant of PD by increasing epidemiological and clinical evidences. Within this review, we will present a comprehensive overview of the data linking UA to PD in recent years. METHODS: We searched PubMed, EMBASE, Web of Science databases for relevant studies. Any observational or experimental studies that evaluated UA and PD were our goal of searching the electric databases. RESULTS: Twelve studies that evaluated UA and PD were identified in this review. We reviewed the roles of UA in the pathogenesis of PD, the association of UA with morbidity, severity/progression, nonmotor symptoms, motor complications of PD, with an attempt to provide new ideas for diagnosis and treatment in PD. CONCLUSION: Our findings supported that lots of clinical and epidemiological data observed lower UA levels in PD patients. Manipulation of UA or its precursors' concentration could be effective to treat or prevent PD. However, it is still suspectable that higher UA levels are better enough to PD patients. Furthermore, for the complex nature of PD and its heterogeneous genetic and environmental influences, it is inadequate for just manipulating UA in treating the disease.

8 Review Dysregulated microRNAs in neural system: Implication in pathogenesis and biomarker development in Parkinson's disease. 2017

Lu, Jiangkun / Xu, Yan / Quan, Zhenzhen / Chen, Zixuan / Sun, Zhenzhen / Qing, Hong. ·School of Life Science, Beijing Institute of Technology, No 5 South Zhongguancun Street, Haidian District, Beijing 100081, PR China. · School of Basic Medical Sciences, Zhengzhou University, Zhengzhou 450001, PR China. · School of Life Science, Beijing Institute of Technology, No 5 South Zhongguancun Street, Haidian District, Beijing 100081, PR China. Electronic address: hqing@bit.edu.cn. ·Neuroscience · Pubmed #28964753.

ABSTRACT: Parkinson's disease is a debilitating neurodegenerative movement disorder, characterized by the progressive and selective loss of dopaminergic neurons located in the substantia nigra, leading to clinical motor symptoms. The factors involved in PD are rather multifaceted. There are many cellular pathways contributing to its neuro-pathogenesis, which include abnormal protein aggregation, impaired ubiquitin proteasome system, autophagy, and neuroinflammation. However, despite years of investigation, still little is known about early events in the molecular pathogenesis. MicroRNAs are small non-coding RNAs that can regulate post-transcriptional expression of mRNAs. Since they somewhat modulate many mRNA targets simultaneously, many cellular pathways may be affected by one individual miRNA. Moreover, miRNAs can stably circulate in cerebrospinal fluid and blood, and their expression pattern can reflect the molecular pathophysiology, thus making them promising biomarkers in PD diagnosis and prognosis. In this review, we will review the recent progress on miRNA's mechanism in PD pathogenesis and discuss the possibilities of miRNAs as PD molecular biomarkers.

9 Review Past, present, and future of Parkinson's disease: A special essay on the 200th Anniversary of the Shaking Palsy. 2017

Obeso, J A / Stamelou, M / Goetz, C G / Poewe, W / Lang, A E / Weintraub, D / Burn, D / Halliday, G M / Bezard, E / Przedborski, S / Lehericy, S / Brooks, D J / Rothwell, J C / Hallett, M / DeLong, M R / Marras, C / Tanner, C M / Ross, G W / Langston, J W / Klein, C / Bonifati, V / Jankovic, J / Lozano, A M / Deuschl, G / Bergman, H / Tolosa, E / Rodriguez-Violante, M / Fahn, S / Postuma, R B / Berg, D / Marek, K / Standaert, D G / Surmeier, D J / Olanow, C W / Kordower, J H / Calabresi, P / Schapira, A H V / Stoessl, A J. ·HM CINAC, Hospital Universitario HM Puerta del Sur, Mostoles, Madrid, Spain. · Universidad CEU San Pablo, Madrid, Spain. · CIBERNED, Madrid, Spain. · Department of Neurology, Philipps University, Marburg, Germany. · Parkinson's Disease and Movement Disorders Department, HYGEIA Hospital and Attikon Hospital, University of Athens, Athens, Greece. · Department of Neurological Sciences, Rush University Medical Center, Chicago, Illinois, USA. · Department of Neurology, Medical University Innsbruck, Innsbruck, Austria. · Morton and Gloria Shulman Movement Disorders Clinic and the Edmond J Safra Program in Parkinson's Disease, Toronto Western Hospital, Toronto, Canada. · Department of Medicine, University of Toronto, Toronto, Canada. · Department of Psychiatry, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania, USA. · Parkinson's Disease and Mental Illness Research, Education and Clinical Centers (PADRECC and MIRECC), Corporal Michael J. Crescenz Veteran's Affairs Medical Center, Philadelphia, Pennsylvania, USA. · Medical Sciences, Newcastle University, Newcastle, UK. · Brain and Mind Centre, Sydney Medical School, The University of Sydney, Sydney, Australia. · School of Medical Sciences, University of New South Wales and Neuroscience Research Australia, Sydney, Australia. · Université de Bordeaux, Institut des Maladies Neurodégénératives, Centre National de la Recherche Scientifique Unité Mixte de Recherche 5293, Institut des Maladies Neurodégénératives, Bordeaux, France. · China Academy of Medical Sciences, Institute of Lab Animal Sciences, Beijing, China. · Departments of Neurology, Pathology, and Cell Biology, the Center for Motor Neuron Biology and Disease, Columbia University, New York, New York, USA. · Columbia Translational Neuroscience Initiative, Columbia University, New York, New York, USA. · Institut du Cerveau et de la Moelle épinière - ICM, Centre de NeuroImagerie de Recherche - CENIR, Sorbonne Universités, UPMC Univ Paris 06, Inserm U1127, CNRS UMR 7225, Paris, France. · Groupe Hospitalier Pitié-Salpêtrière, Paris, France. · Clinical Sciences Department, Newcastle University, Newcastle, UK. · Department of Nuclear Medicine, Aarhus University, Aarhus, Denmark. · Human Neurophysiology, Sobell Department, UCL Institute of Neurology, London, UK. · Human Motor Control Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland, USA. · Department of Neurology, Emory University School of Medicine, Atlanta, Georgia, USA. · Morton and Gloria Shulman Movement Disorders Centre and the Edmond J Safra Program in Parkinson's disease, Toronto Western Hospital, University of Toronto, Toronto, Canada. · Movement Disorders and Neuromodulation Center, Department of Neurology, University of California-San Francisco, San Francisco, California, USA. · Parkinson's Disease Research, Education and Clinical Center, San Francisco Veterans Affairs Medical Center, San Francisco, California, USA. · Veterans Affairs Pacific Islands Health Care System, Honolulu, Hawaii, USA. · Parkinson's Institute, Sunnyvale, California, USA. · Institute of Neurogenetics, University of Luebeck, Luebeck, Germany. · Department of Clinical Genetics, Erasmus University Medical Center, Rotterdam, The Netherlands. · Parkinson's Disease Center and Movement Disorders Clinic, Department of Neurology, Baylor College of Medicine, Houston, Texas, USA. · Department of Neurosurgery, Toronto Western Hospital, University of Toronto, Toronto, Canada. · Department of Neurology, Universitätsklinikum Schleswig-Holstein, Christian Albrechts University Kiel, Kiel, Germany. · Department of Medical Neurobiology, Institute of Medical Research Israel-Canada, Jerusalem, Israel. · Edmond and Lily Safra Center for Brain Sciences, The Hebrew University, Jerusalem, Israel. · Department of Neurosurgery, Hadassah University Hospital, Jerusalem, Israel. · Parkinson's Disease and Movement Disorders Unit, Neurology Service, Institut Clínic de Neurociències, Hospital Clínic de Barcelona, Barcelona, Spain. · Department of Medicine, Universitat de Barcelona, IDIBAPS, Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED) Barcelona, Spain. · Movement Disorders Clinic, Clinical Neurodegenerative Research Unit, Mexico City, Mexico. · Instituto Nacional de Neurología y Neurocirugía, Mexico City, Mexico. · Department of Neurology, Columbia University Medical Center, New York, New York, USA. · Department of Neurology, McGill University, Montreal General Hospital, Montreal, Quebec, Canada. · Klinik für Neurologie, UKSH, Campus Kiel, Christian-Albrechts-Universität, Kiel, Germany. · Institute for Neurodegenerative Disorders, New Haven, Connecticut, USA. · Department of Neurology, University of Alabama at Birmingham, Birmingham, Alabama, USA. · Department of Physiology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, USA. · Departments of Neurology and Neuroscience, Mount Sinai School of Medicine, New York, New York, USA. · Research Center for Brain Repair, Rush University Medical Center, Chicago, Illinois, USA. · Neuroscience Graduate Program, Rush University Medical Center, Chicago, Illinois, USA. · Neurological Clinic, Department of Medicine, Hospital Santa Maria della Misericordia, University of Perugia, Perugia, Italy. · Laboratory of Neurophysiology, Santa Lucia Foundation, IRCCS, Rome, Italy. · University Department of Clinical Neurosciences, UCL Institute of Neurology, University College London, London, UK. · Pacific Parkinson's Research Centre, Division of Neurology & Djavadf Mowafaghian Centre for Brain Health, University of British Columbia, British Columbia, Canada. · Vancouver Coastal Health, Vancouver, British Columbia, Canada. ·Mov Disord · Pubmed #28887905.

ABSTRACT: This article reviews and summarizes 200 years of Parkinson's disease. It comprises a relevant history of Dr. James Parkinson's himself and what he described accurately and what he missed from today's perspective. Parkinson's disease today is understood as a multietiological condition with uncertain etiopathogenesis. Many advances have occurred regarding pathophysiology and symptomatic treatments, but critically important issues are still pending resolution. Among the latter, the need to modify disease progression is undoubtedly a priority. In sum, this multiple-author article, prepared to commemorate the bicentenary of the shaking palsy, provides a historical state-of-the-art account of what has been achieved, the current situation, and how to progress toward resolving Parkinson's disease. © 2017 International Parkinson and Movement Disorder Society.

10 Review Can music-based movement therapy improve motor dysfunction in patients with Parkinson's disease? Systematic review and meta-analysis. 2017

Zhang, Shuai / Liu, Dong / Ye, Dan / Li, Haiyu / Chen, Feng. ·Department of Emergency, Beijing Aerospace General Hospital, Beijing, China. · Department of Neurosurgery, Sanbo Brain Hospital of Eleven Clinical College of Capital Medical University, Beijing, China. · Department of Emergency, Beijing Aerospace General Hospital, Beijing, China. zhangshu0890@163.com. ·Neurol Sci · Pubmed #28634878.

ABSTRACT: This study aimed to quantify whether there is association between music-based movement therapy and motor dysfunction in patients with Parkinson's disease, and, if so, whether music-based movement therapy can be used as first-line non-pharmacological treatment. To conduct a systematic review and meta-analysis of clinical trials that examined the effect of music-based movement therapy on patient-relevant and disease-specific outcomes. Comprehensive literature was searched of PubMed, EMbase, and the Cochrane Library from inception to November 2016. Randomized controlled trial of patients with Parkinson's disease was searched to identify trials comparing music-based movement therapy with no music care. A total of 8 studies (11 analyses, 241 subjects) were included; all of them had acceptable quality by PEDro scale score. Studies based on any type of Parkinson's disease patients were combined and subgroup analyzed. Compared with the control group, the SMD of Berg Balance Scale score was 0.85(0.46 to 1.25), -0.60 (-0.98 to -0.22) in Parkinson Disease Questionnaire-39 summary index, -0.90s (-1.56 to -0.23) in Time Up and Go text, and -0.43 (-1.11 to 0.25) in Unified Parkinson's Disease Rating Scale Motor Subscale 3 as instrument methods for motor function. Secondary outcomes included cognitive function and quality of life. There was positive evidence to support the use of music-based movement therapy on treatment of motor function; there was neutral evidence to support the use of music for the treatment of cognitive function quality of life.

11 Review Efficacy of antidepressive medication for depression in Parkinson disease: a network meta-analysis. 2017

Zhuo, Chuanjun / Xue, Rong / Luo, Lanlan / Ji, Feng / Tian, Hongjun / Qu, Hongru / Lin, Xiaodong / Jiang, Ronghuan / Tao, Ran. ·aDepartment of Psychological Medicine, Wenzhou Seventh People's Hospital, Wenzhou, Zhejiang bInstitute of Mental Health, Jining Medical University, Jining, Shandong cDepartment of Psychological Medicine, Tianjin Mental Health Center dDepartment of Psychological Medicine, Tianjin Anning Hospital eDepartment of Neurology, Tianjin Medical University General Hospital, Tianjin fDepartment of Psychological Medicine, Chinese PLA (People's Liberation Army) General Hospital gDepartment of Psychological Medicine, General Hospital of Beijing Military Region, Chinese PLA, Beijing, China. ·Medicine (Baltimore) · Pubmed #28562526.

ABSTRACT: BACKGROUND: Parkinson disease (PD) was considered as the 2nd most prevalent neurodegenerative disorder after Alzheimer disease, while depression is a prevailing nonmotor symptom of PD. Typically used antidepression medication includes tricyclic antidepressants (TCA), selective serotonin reuptake inhibitors (SSRI), serotonin and norepinephrine reuptake inhibitors (SNRI), monoamine-oxidase inhibitors (MAOI), and dopamine agonists (DA). Our study aimed at evaluating the efficacy of antidepressive medications for depression of PD. METHODS: Web of Science, PubMed, Embase, and the Cochrane library were searched for related articles. Traditional meta-analysis and network meta-analysis (NMA) were performed with outcomes including depression score, UPDRS-II, UPDRS-III, and adverse effects. Surface under the cumulative ranking curve (SUCRA) was also performed to illustrate the rank probabilities of different medications on various outcomes. The consistency of direct and indirect evidence was also assessed by node-splitting method. RESULTS: Results of traditional pairwise meta-analysis were performed. Concerning depression score, significant improvement was observed in AD, MAOI, SSRI, and SNRI compared with placebo. NMA was performed and more information could be obtained. DA was illustrated to be effective over placebo concerning UPDRS-III, MAOI, and SNRI. DA demonstrated a better prognosis in UPDRS-II scores compared with placebo and MAOI. However, DA and SSRI demonstrated a significant increase in adverse effects compared with placebo. The SUCRA value was calculated to evaluate the ranking probabilities of all medications on investigated outcomes, and the consistency between direct and indirect evidences was assessed by node-splitting method. CONCLUSION: SSRI had a satisfying efficacy for the depression of PD patients and could improve activities of daily living and motor function of patient but the adverse effects are unneglectable. SNRI are the safest medication with high efficacy for depression as well while other outcomes are relatively poor.

12 Review Variable frequency stimulation of subthalamic nucleus in Parkinson's disease: Rationale and hypothesis. 2017

Jia, Fumin / Hu, Wei / Zhang, Jianguo / Wagle Shukla, Aparna / Almeida, Leonardo / Meng, Fan-Gang / Okun, Michael S / Li, Luming. ·National Engineering Laboratory for Neuromodulation, Tsinghua University, Beijing, China. · University of Florida Center for Movement Disorders and Neurorestoration, Gainesville, FL, USA. · Beijing Tian Tan Hospital, Capital Medical University, Beijing, China. · Beijing Neurosurgical Institute, Capital Medical University, Beijing, China. · University of Florida Center for Movement Disorders and Neurorestoration, Gainesville, FL, USA. Electronic address: Okun@neurology.ufl.edu. · National Engineering Laboratory for Neuromodulation, Tsinghua University, Beijing, China; Precision Medicine & Healthcare Research Center, Tsinghua-Berkeley Shenzhen Institute, Shenzhen, China; Man-machine-environment Engineering Institute, School of Aerospace Engineering, Tsinghua University, Beijing, China; Center of Epilepsy, Beijing Institute for Brain Disorders, Beijing, China. Electronic address: lilm@tsinghua.edu.cn. ·Parkinsonism Relat Disord · Pubmed #28392298.

ABSTRACT: -- No abstract --

13 Review Expression, Purification, and Enzymatic Characterization of Intramembrane Proteases. 2017

Zhou, R / Shi, Y / Yang, G. ·Ministry of Education Key Laboratory of Protein Science, Tsinghua-Peking Joint Center for Life Sciences, Beijing Advanced Innovation Center for Structural Biology, School of Life Sciences, Tsinghua University, Beijing, China. Electronic address: zhour13@mails.tsinghua.edu.cn. · Ministry of Education Key Laboratory of Protein Science, Tsinghua-Peking Joint Center for Life Sciences, Beijing Advanced Innovation Center for Structural Biology, School of Life Sciences, Tsinghua University, Beijing, China. Electronic address: shil-lab@tsinghua.edu.cn. · Ministry of Education Key Laboratory of Protein Science, Tsinghua-Peking Joint Center for Life Sciences, Beijing Advanced Innovation Center for Structural Biology, School of Life Sciences, Tsinghua University, Beijing, China. Electronic address: ygh12@mails.tsinghua.edu.cn. ·Methods Enzymol · Pubmed #28065261.

ABSTRACT: Intramembrane proteases catalyze peptide bond hydrolysis in the lipid bilayer and play a key role in numerous cellular processes. These integral membrane enzymes consist of four classes: site-2 protease (S2P), rhomboid serine protease, Rce1-type glutamyl protease, and aspartyl protease exemplified by presenilin and signal peptide peptidase (SPP). Structural elucidation of these enzymes is important for mechanistic understanding of their functions, particularly their roles in cell signaling and debilitating diseases such as Parkinson's disease and Alzheimer's disease. In the past decade, rigorous effort has led to determination of the crystal structures of S2P from archaebacterium, rhomboid serine protease from E. coli (GlpG), and presenilin/SPP from archaebacterium (PSH). A novel method has been developed to express well-behaved human γ-secretase, which facilitated its structure determination by cryoelectron microscopy (cryo-EM). In this chapter, we will discuss the expression and purification of intramembrane proteases including human γ-secretase and describe the enzymatic activity assays for these intramembrane proteases.

14 Review Pathological α-synuclein exacerbates the progression of Parkinson's disease through microglial activation. 2017

Zhang, Qiu-Shuang / Heng, Yang / Yuan, Yu-He / Chen, Nai-Hong. ·State Key Laboratory of Bioactive Substances and Functions of Natural Medicines, Institute of Materia Medica & Neuroscience Center, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100050, China. · State Key Laboratory of Bioactive Substances and Functions of Natural Medicines, Institute of Materia Medica & Neuroscience Center, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100050, China. Electronic address: yuanyuhe@imm.ac.cn. · State Key Laboratory of Bioactive Substances and Functions of Natural Medicines, Institute of Materia Medica & Neuroscience Center, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100050, China; Hunan University of Chinese Medicine, Changsha, 410208, China. Electronic address: chennh@imm.ac.cn. ·Toxicol Lett · Pubmed #27865851.

ABSTRACT: Parkinson's disease (PD) is characterized by α-synuclein accumulation, dopaminergic neuron loss and inflammation. α-Synuclein can be secreted by neurons and activate microglia to different degrees. Excessive microglial activation can increase the production of tumor necrosis factor alpha (TNF-α), interleukin-1-β (IL-1β), interleukin-6 (IL-6), interferon-γ (INF-γ), inducible nitric oxide synthase (iNOS), reactive oxygen species (ROS) and nitric oxide (NO), and can also enhance microglial phagocytosis and migration as well as lymphocyte infiltration. Pathological α-synuclein and microglial activation can potentiate each other, leading to the loss of dopaminergic neurons and accelerated PD degeneration. This review will mainly describe the profiles of α-synuclein-activated microglia, with particular emphasis on the signaling cascades involved in this process.

15 Review Synucleinopathies: common features and hippocampal manifestations. 2017

Yang, Weiwei / Yu, Shun. ·Department of Neurobiology, Xuanwu Hospital of Capital Medical University, 45 Changchun Street, Beijing, 100053, China. · Department of Neurobiology, Xuanwu Hospital of Capital Medical University, 45 Changchun Street, Beijing, 100053, China. yushun103@163.com. · Center of Parkinson's Disease, Beijing Institute for Brain Disorders, Beijing, China. yushun103@163.com. · Beijing Key Laboratory for Parkinson's Disease, Beijing, China. yushun103@163.com. ·Cell Mol Life Sci · Pubmed #27826641.

ABSTRACT: Parkinson's disease (PD), dementia with Lewy Bodies (DLB), and multiple system atrophy (MSA) are three major synucleinopathies characterized by α-synuclein-containing inclusions in the brains of patients. Because the cell types and brain structures that are affected vary markedly between the disorders, the patients have different clinical manifestations in addition to some overlapping symptoms, which are the basis for differential diagnosis. Cognitive impairment and depression associated with hippocampal dysfunction are frequently observed in these disorders. While various α-synuclein-containing inclusions are found in the hippocampal formation, increasing evidence supports that small α-synuclein aggregates or oligomers may be the real culprit, causing deficits in neurotransmission and neurogenesis in the hippocampus and related brain regions, which constitute the major mechanism for the hippocampal dysfunctions and associated neuropsychiatric manifestations in synucleinopathies.

16 Review mTOR Signaling in Parkinson's Disease. 2017

Lan, Ai-Ping / Chen, Jun / Zhao, Yuliang / Chai, Zhifang / Hu, Yi. ·CAS Key Laboratory for Biomedical Effects of Nanomaterials and Nanosafety, Multi-disciplinary Research Division, Institute of High Energy Physics, Chinese Academy of Sciences (CAS), Beijing, 100049, China. · CAS Key Laboratory for Biomedical Effects of Nanomaterials and Nanosafety, Multi-disciplinary Research Division, Institute of High Energy Physics, Chinese Academy of Sciences (CAS), Beijing, 100049, China. huyi@ihep.ac.cn. ·Neuromolecular Med · Pubmed #27263112.

ABSTRACT: As a key regulator of cell metabolism and survival, mechanistic target of rapamycin (mTOR) emerges as a novel therapeutic target for Parkinson's disease (PD). A growing body of research indicates that restoring perturbed mTOR signaling in PD models can prevent neuronal cell death. Nevertheless, molecular mechanisms underlying mTOR-mediated effects in PD have not been fully understood yet. Here, we review recent progress in characterizing the association of mTOR signaling with PD risk factors and further discuss the potential roles of mTOR in PD.

17 Review Oxidative Modification and Its Implications for the Neurodegeneration of Parkinson's Disease. 2017

Zhao, Junjun / Yu, Shuqing / Zheng, Yan / Yang, Hui / Zhang, Jianliang. ·Department of Neurobiology, Beijing Institute of Brain Disorders, Capital Medical University, Key Laboratory for Neurodegenerative Disease of the Ministry of Education, Beijing Center of Neural Regeneration and Repair, Beijing Key Laboratory of Brain Major Disorders-State Key Lab Incubation Base, Beijing Neuroscience Disciplines, Beijing, 100069, China. · Department of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University, China National Clinical Research Center for Neurological Diseases, State Key Disciplinary of Neurosurgery Department, Beijing, 100050, China. · Department of Neurobiology, Beijing Institute of Brain Disorders, Capital Medical University, Key Laboratory for Neurodegenerative Disease of the Ministry of Education, Beijing Center of Neural Regeneration and Repair, Beijing Key Laboratory of Brain Major Disorders-State Key Lab Incubation Base, Beijing Neuroscience Disciplines, Beijing, 100069, China. jlzhang@ccmu.edu.cn. ·Mol Neurobiol · Pubmed #26843115.

ABSTRACT: Parkinson's disease (PD) is the second most common neurodegenerative disease. The major characteristics of PD include the loss of dopaminergic neurons in the substantia nigra and Lewy body depositions. Genetic defects, environment toxicants, and aging have been recognized as risk factors for the development of PD. Currently, although the pathogenesis of PD is still obscure, overwhelming evidence demonstrates that oxidative stress plays a central role in the progress of PD. Reactive oxygen species (ROS) function mainly through chemical reactions with atomic targets that lead to covalent oxidative modifications. Through the oxidative modification of ions, amino acids, amines, and nucleic acids, ROS exert augmented effects on the structures and functions of multiple macromolecules. These oxidative modifications can affect nucleic acid stability by oxidizing RNA, increasing mitochondrial DNA (mtDNA) mutation, and launching translesion synthesis (TLS); disturb protein homeostasis by accelerating α-synuclein aggregation, parkin aggregation, and proteasome dissociation; modulate dopamine release by activating ATP-sensitive potassium channels (K

18 Review Aberrations in Peripheral Inflammatory Cytokine Levels in Parkinson Disease: A Systematic Review and Meta-analysis. 2016

Qin, Xiao-Yan / Zhang, Shu-Ping / Cao, Chang / Loh, Y Peng / Cheng, Yong. ·Center on Translational Neuroscience, College of Life and Environmental Sciences, MinZu University of China, Beijing, China. · Section on Cellular Neurobiology, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland. ·JAMA Neurol · Pubmed #27668667.

ABSTRACT: Importance: The association of nonmotor features and Parkinson disease (PD) is increasingly recognized. Evidence suggests that inflammation may play a role in PD pathologic features and symptoms. Objective: To quantitatively summarize the peripheral inflammatory cytokine data available for patients with PD. Data Source: A systematic search of peer-reviewed English-language articles from PubMed, PsycINFO, and the Cochrane Library without year limitation was performed from December 7, 2015, to March 23, 2016. The search terms included inflammation or cytokine or chemokine or tumor necrosis factor or interleukin or interferon or C-reactive protein AND Parkinson disease. Study Selection: Studies were included if they provided data on peripheral blood cytokine concentrations in patients with PD and a healthy control group. Studies were excluded if they contained in vitro analysis of stimulated or unstimulated levels of cytokines, samples that overlapped with other studies, patients not diagnosed with PD at blood sampling, or if the cytokine analyzed was assessed in fewer than 3 studies. Data Extraction and Synthesis: Data were extracted from the 25 included studies encompassing 1547 unique patients with PD and 1107 unique controls by 2 independent investigators. Data were pooled using a random-effects model with the Comprehensive Meta-analysis software. Effect sizes were generated as standardized mean differences of cytokine concentrations between patients with PD and healthy controls and converted to the Hedges g statistic. Main Outcomes and Measures: Blood cytokine concentrations in patients with PD compared with controls. Aberrations in peripheral cytokine levels were hypothesized to be related to PD. Results: Among the 2654 study participants, concentrations of interleukin 6 (IL-6) (Hedges g, 0.325; 95% CI, 0.007-0.643; P = .045) in 13 studies, tumor necrosis factor (Hedges g, 0.354; 95% CI, 0.144-0.563; P = .001) in 9 studies, IL-1β (Hedges g, 0.382; 95% CI, 0.142-0.621; P = .002) in 6 studies, C-reactive protein (Hedges g, 0.323; 95% CI, 0.052-0.593; P = .02) in 6 studies, IL-10 (Hedges g, 0.329; 95% CI, 0.051-0.607; P = .02) in 5 studies, RANTES (regulated on activation, normal T-expressed, and presumably secreted) (Hedges g, 0.605; 95% CI, 0.111-1.099; P = .02) in 5 studies, and IL-2 (Hedges g, 0.789; 95% CI, 0.105-1.472; P = .02) in 3 studies were significantly higher in patients with PD compared with healthy controls. No differences were found between patients with PD and healthy controls for concentrations of interferon-γ (Hedges g, 0.745; 95% CI, -0.192 to 1.682; P = .12) in 5 studies, IL-4 (Hedges g, 0.031; 95% CI, -0.191 to 0.253; P = .79) in 3 studies, and IL-8 (Hedges g, 0.072; 95% CI, -0.136 to 0.279; P = .50) in 3 studies. Conclusions and Relevance: The findings of the meta-analysis demonstrated higher peripheral concentrations of IL-6, tumor necrosis factor, IL-1β, IL-2, IL-10, C-reactive protein, and RANTES in patients with PD, strengthening the clinical evidence that PD is accompanied by an inflammatory response.

19 Review The neurotoxicity of iron, copper and cobalt in Parkinson's disease through ROS-mediated mechanisms. 2016

Lan, A P / Chen, J / Chai, Z F / Hu, Y. ·CAS Key Laboratory for Biomedical Effects of Nanomaterials and Nanosafety, Multi-disciplinary Research Division, Institute of High Energy Physics, Chinese Academy of Sciences (CAS), Beijing, 100049, China. · School of Radiological and Interdisciplinary Sciences, Soochow University, Suzhou, 215123, China. · CAS Key Laboratory for Biomedical Effects of Nanomaterials and Nanosafety, Multi-disciplinary Research Division, Institute of High Energy Physics, Chinese Academy of Sciences (CAS), Beijing, 100049, China. huyi@ihep.ac.cn. ·Biometals · Pubmed #27349232.

ABSTRACT: Parkinson's disease (PD) is the second most common neurodegenerative disease with gradual loss of dopaminergic neurons. Despite extensive research in the past decades, the etiology of PD remains elusive. Nevertheless, multiple lines of evidence suggest that oxidative stress is one of the common causes in the pathogenesis of PD. It has also been suggested that heavy metal-associated oxidative stress may be implicated in the etiology and pathogenesis of PD. Here we review the roles of redox metals, including iron, copper and cobalt, in PD. Iron is a highly reactive element and deregulation of iron homeostasis is accompanied by concomitant oxidation processes in PD. Copper is a key metal in cell division process, and it has been shown to have an important role in neurodegenerative diseases such as PD. Cobalt induces the generation of reactive oxygen species (ROS) and DNA damage in brain tissues.

20 Review MDS research criteria for prodromal Parkinson's disease. 2015

Berg, Daniela / Postuma, Ronald B / Adler, Charles H / Bloem, Bastiaan R / Chan, Piu / Dubois, Bruno / Gasser, Thomas / Goetz, Christopher G / Halliday, Glenda / Joseph, Lawrence / Lang, Anthony E / Liepelt-Scarfone, Inga / Litvan, Irene / Marek, Kenneth / Obeso, José / Oertel, Wolfgang / Olanow, C Warren / Poewe, Werner / Stern, Matthew / Deuschl, Günther. ·Department of Neurodegeneration, Hertie-Institute for Clinical Brain Research and German Center for Neurodegenerative Diseases, Tuebingen, Germany. · Department of Neurology, Montreal General Hospital, Montreal, Quebec, Canada. · The Parkinson's Disease and Movement Disorders Center, Department of Neurology, Mayo Clinic, Scottsdale, Arizona, USA. · Department of Neurology, Radboud University Medical Center, Donders Institute for Brain, Cognition and Behavior, Nijmegen, The Netherlands. · Xuanwu Hospital of Capitol of Medical University, Beijing, China. · Hopital De La Salpetriere, Paris, France. · Rush University Medical Center, Chicago, Illinois, USA. · Neuroscience Research Australia & University of NSW, Randwick, Australia. · Department of Epidemiology and Biostatistics, McGill University, Montreal, Quebec, Canada. · Division of Neurology, Toronto Western Hospital, Toronto, Ontario, Canada. · Department of Neurosciences, University of California San Diego, La Jolla, California, USA. · Institute for Neurodegenerative Disorders, New Haven, Connecticut, USA. · University of Navarra-FIMA, Pamplona, Spain. · Department of Neurology, Philipps University of Marburg, Marburg, Germany. · Department of Neurology, The Mount Sinai Hospital, New York, New York, USA. · Department of Neurology, Innsbruck Medical University, Innsbruck, Austria. · Penn Neurological Institute, Philadelphia, Pennsylvania, USA. · Department of Neurology, Christian-Albrechts University, Kiel, Germany. ·Mov Disord · Pubmed #26474317.

ABSTRACT: This article describes research criteria and probability methodology for the diagnosis of prodromal PD. Prodromal disease refers to the stage wherein early symptoms or signs of PD neurodegeneration are present, but classic clinical diagnosis based on fully evolved motor parkinsonism is not yet possible. Given the lack of clear neuroprotective/disease-modifying therapy for prodromal PD, these criteria were developed for research purposes only. The criteria are based upon the likelihood of prodromal disease being present with probable prodromal PD defined as ≥80% certainty. Certainty estimates rely upon calculation of an individual's risk of having prodromal PD, using a Bayesian naïve classifier. In this methodology, a previous probability of prodromal disease is delineated based upon age. Then, the probability of prodromal PD is calculated by adding diagnostic information, expressed as likelihood ratios. This diagnostic information combines estimates of background risk (from environmental risk factors and genetic findings) and results of diagnostic marker testing. In order to be included, diagnostic markers had to have prospective evidence documenting ability to predict clinical PD. They include motor and nonmotor clinical symptoms, clinical signs, and ancillary diagnostic tests. These criteria represent a first step in the formal delineation of early stages of PD and will require constant updating as more information becomes available.

21 Review MDS clinical diagnostic criteria for Parkinson's disease. 2015

Postuma, Ronald B / Berg, Daniela / Stern, Matthew / Poewe, Werner / Olanow, C Warren / Oertel, Wolfgang / Obeso, José / Marek, Kenneth / Litvan, Irene / Lang, Anthony E / Halliday, Glenda / Goetz, Christopher G / Gasser, Thomas / Dubois, Bruno / Chan, Piu / Bloem, Bastiaan R / Adler, Charles H / Deuschl, Günther. ·Department of Neurology, Montreal General Hospital, Montreal, Quebec, Canada. · Department of Neurodegeneration, Hertie-Institute for Clinical Brain Research and German Center for Neurodegenerative Diseases, Tuebingen, Germany. · Penn Neurological Institute, Philadelphia, Pennsylvania, USA. · Department of Neurology, Innsbruck Medical University, Innsbruck, Austria. · Department of Neurology, The Mount Sinai Hospital, New York, New York, USA. · Department of Neurology, Philipps University of Marburg, Marburg, Germany. · University of Navarra-FIMA, Pamplona, Spain. · Institute for Neurodegenerative Disorders, New Haven, Connecticut, USA. · Department of Neurosciences, UC San Diego, La Jolla, California, USA. · Division of Neurology, Toronto Western Hospital, Toronto, Ontario, Canada. · Neuroscience Research Australia & University of NSW, Randwick, Australia. · Rush University Medical Center, Chicago, Illinois, USA. · Hopital De La Salpetriere, Paris, France. · Xuanwu Hospital of Capitol of Medical University, Beijing, Peoples Republic of China. · Department of Neurology, Radboud University Medical Center, Donders Institute for Brain, Cognition and Behaviour, Nijmegen, Netherlands. · The Parkinson's Disease and Movement Disorders Center, Department of Neurology, Mayo Clinic, Scottsdale, Arizona, USA. · Department of Neurology, Christian-Albrechts University, Kiel, Germany. ·Mov Disord · Pubmed #26474316.

ABSTRACT: This document presents the Movement Disorder Society Clinical Diagnostic Criteria for Parkinson's disease (PD). The Movement Disorder Society PD Criteria are intended for use in clinical research but also may be used to guide clinical diagnosis. The benchmark for these criteria is expert clinical diagnosis; the criteria aim to systematize the diagnostic process, to make it reproducible across centers and applicable by clinicians with less expertise in PD diagnosis. Although motor abnormalities remain central, increasing recognition has been given to nonmotor manifestations; these are incorporated into both the current criteria and particularly into separate criteria for prodromal PD. Similar to previous criteria, the Movement Disorder Society PD Criteria retain motor parkinsonism as the core feature of the disease, defined as bradykinesia plus rest tremor or rigidity. Explicit instructions for defining these cardinal features are included. After documentation of parkinsonism, determination of PD as the cause of parkinsonism relies on three categories of diagnostic features: absolute exclusion criteria (which rule out PD), red flags (which must be counterbalanced by additional supportive criteria to allow diagnosis of PD), and supportive criteria (positive features that increase confidence of the PD diagnosis). Two levels of certainty are delineated: clinically established PD (maximizing specificity at the expense of reduced sensitivity) and probable PD (which balances sensitivity and specificity). The Movement Disorder Society criteria retain elements proven valuable in previous criteria and omit aspects that are no longer justified, thereby encapsulating diagnosis according to current knowledge. As understanding of PD expands, the Movement Disorder Society criteria will need continuous revision to accommodate these advances.

22 Review The phosphorylation of α-synuclein: development and implication for the mechanism and therapy of the Parkinson's disease. 2015

Xu, Yan / Deng, Yulin / Qing, Hong. ·School of Life Science, Beijing Institute of Technology, Beijing, China. ·J Neurochem · Pubmed #26134497.

ABSTRACT: Parkinson's disease (PD) is cited to be the second most common neuronal degenerative disorders; however, the exact mechanism of PD is still unclear. α-synuclein is one of the key proteins in PD pathogenesis as it's the main component of the PD hallmark Lewy bodies (LBs). Nowadays, the study of α-synuclein phosphorylation mechanism related to the PD pathology has become a research hotspot, given that 90% of α-synuclein deposition in LBs is phosphorylated at Ser129, whereas in normal brains, only 4% or less of α-synuclein is phosphorylated at the residue. Here, we review the related study of PD pathological mechanism involving the phosphorylation of α-synuclein mainly at Ser129, Ser87, and Tyr125 residues in recent years, as well as some explorations relating to potential clinical application, in an attempt to describe the development and implication for the mechanism and therapy of PD. Given that some of the studies have yielded paradoxical results, there is need for more comprehensive research in the field. The phosphorylation of α-synuclein might provide a breakthrough for PD mechanism study and even supply a new therapeutic strategy. The milestone study on the phosphorylation of α-synuclein mainly at Ser129, Ser87, and Tyr125 relating to PD in recent years as well as some clinical application exploration are overviewed. The potential pathways of the phosphorylated α-synuclein related to PD are also summarized. The review may supply more ideas and thinking on this issue for the scientists in related research field.

23 Review Motor automaticity in Parkinson's disease. 2015

Wu, Tao / Hallett, Mark / Chan, Piu. ·Department of Neurobiology, Key Laboratory on Neurodegenerative Disorders of Ministry of Education, Beijing Institute of Geriatrics, Xuanwu Hospital, Capital Medical University, Beijing, China; Beijing Key Laboratory on Parkinson's Disease, Parkinson Disease Center of Beijing Institute for Brain Disorders, Beijing, China. Electronic address: wutao69@gmail.com. · Human Motor Control Section, Medical Neurology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, USA. · Department of Neurobiology, Key Laboratory on Neurodegenerative Disorders of Ministry of Education, Beijing Institute of Geriatrics, Xuanwu Hospital, Capital Medical University, Beijing, China; Beijing Key Laboratory on Parkinson's Disease, Parkinson Disease Center of Beijing Institute for Brain Disorders, Beijing, China. ·Neurobiol Dis · Pubmed #26102020.

ABSTRACT: Bradykinesia is the most important feature contributing to motor difficulties in Parkinson's disease (PD). However, the pathophysiology underlying bradykinesia is not fully understood. One important aspect is that PD patients have difficulty in performing learned motor skills automatically, but this problem has been generally overlooked. Here we review motor automaticity associated motor deficits in PD, such as reduced arm swing, decreased stride length, freezing of gait, micrographia and reduced facial expression. Recent neuroimaging studies have revealed some neural mechanisms underlying impaired motor automaticity in PD, including less efficient neural coding of movement, failure to shift automated motor skills to the sensorimotor striatum, instability of the automatic mode within the striatum, and use of attentional control and/or compensatory efforts to execute movements usually performed automatically in healthy people. PD patients lose previously acquired automatic skills due to their impaired sensorimotor striatum, and have difficulty in acquiring new automatic skills or restoring lost motor skills. More investigations on the pathophysiology of motor automaticity, the effect of L-dopa or surgical treatments on automaticity, and the potential role of using measures of automaticity in early diagnosis of PD would be valuable.

24 Review Interaction between Neuromelanin and Alpha-Synuclein in Parkinson's Disease. 2015

Xu, Shengli / Chan, Piu. ·Beijing Institute of Geriatrics, Xuanwu Hospital of Capital University of Medical Sciences, No.45 changchun St., Xicheng District, Beijing 100053, China. xushngli_xw@163.com. · Parkinson's disease Center of Beijing Institute for Brain Disorders, Beijing 100053, China. xushngli_xw@163.com. · Beijing Institute of Geriatrics, Xuanwu Hospital of Capital University of Medical Sciences, No.45 changchun St., Xicheng District, Beijing 100053, China. pbchan90@gmail.com. · Parkinson's disease Center of Beijing Institute for Brain Disorders, Beijing 100053, China. pbchan90@gmail.com. ·Biomolecules · Pubmed #26057626.

ABSTRACT: Parkinson's disease (PD) is a very common neurodegenerative disorder characterized by the accumulation of α-synuclein (α-syn) into Lewy body (LB) inclusions and the loss of neuronmelanin (NM) containing dopamine (DA) neurons in the substantia nigra (SN). Pathological α-syn and NM are two prominent hallmarks in this selective and progressive neurodegenerative disease. Pathological α-syn can induce dopaminergic neuron death by various mechanisms, such as inducing oxidative stress and inhibiting protein degradation systems. Therefore, to explore the factors that trigger α-syn to convert from a non-toxic protein to toxic one is a pivotal question to clarify the mechanisms of PD pathogenesis. Many triggers for pathological α-syn aggregation have been identified, including missense mutations in the α-syn gene, higher concentration, and posttranslational modifications of α-Syn. Recently, the role of NM in inducing α-syn expression and aggregation has been suggested as a mechanism for this pigment to modulate neuronal vulnerability in PD. NM may be responsible for PD and age-associated increase and aggregation in α-syn. Here, we reviewed our previous study and other recent findings in the area of interaction between NM and α-syn.

25 Review Defective autophagy in Parkinson's disease: lessons from genetics. 2015

Zhang, H / Duan, C / Yang, H. ·Center of Parkinson's Disease Beijing Institute for Brain Disorders, Key Laboratory for Neurodegenerative Disease of the Ministry of Education, Department of Neurobiology Capital Medical University, Beijing, 100069, China. ·Mol Neurobiol · Pubmed #24990317.

ABSTRACT: Parkinson's disease (PD) is the most prevalent neurodegenerative movement disorder. Genetic studies over the past two decades have greatly advanced our understanding of the etiological basis of PD and elucidated pathways leading to neuronal degeneration. Recent studies have suggested that abnormal autophagy, a well conserved homeostatic process for protein and organelle turnover, may contribute to neurodegeneration in PD. Moreover, many of the proteins related to both autosomal dominant and autosomal recessive PD, such as α-synuclein, PINK1, Parkin, LRRK2, DJ-1, GBA, and ATPA13A2, are also involved in the regulation of autophagy. We propose that reduced autophagy enhances the accumulation of α-synuclein, other pathogenic proteins, and dysfunctional mitochondria in PD, leading to oxidative stress and neuronal death.

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