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Parkinson Disease: HELP
Articles from Maryland
Based on 684 articles published since 2008
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These are the 684 published articles about Parkinson Disease that originated from Maryland 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 · 20
1 Editorial Are Alzheimer's disease and other neurodegenerative disorders caused by impaired signalling of insulin and other hormones? 2018

Hölscher, Christian / De Felice, Fernanda G / Greig, Nigel H / Ferreira, Sergio T. ·Biomedical and Life Sciences, Lancaster University, Lancaster, UK. Electronic address: c.holscher@lancaster.ac.uk. · Centre for Neuroscience Studies, Department of Biomedical and Molecular Sciences, Queen's University, Kingston, Ontario, Canada. · Drug Design & Development Section, Translational Gerontology Branch, National Institute on Aging, National Institutes of Health, Baltimore, USA. · Institute of Biophysics Carlos Chagas Filho, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil. ·Neuropharmacology · Pubmed #29782874.

ABSTRACT: -- No abstract --

2 Editorial Anxiety in Parkinson's: a complex syndrome of non-dopaminergic and dopaminergic etiology. 2017

Pontone, G M. ·Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, MD, USA. ·Eur J Neurol · Pubmed #28177179.

ABSTRACT: -- No abstract --

3 Editorial Identification of bona-fide LRRK2 kinase substrates. 2016

West, Andrew B / Cookson, Mark R. ·Center for Neurodegeneration and Experimental Therapeutics, Department of Neurology, The University of Alabama at Birmingham, Birmingham, Alabama, USA. · Cell Biology and Gene Expression Section, Laboratory of Neurogenetics, National Institute on Aging, Bethesda, Maryland, USA. ·Mov Disord · Pubmed #27126091.

ABSTRACT: -- No abstract --

4 Editorial Editorial overview: Neurobiology of disease. 2016

Selkoe, Dennis J / Weinberger, Daniel R. ·Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA. Electronic address: dselkoe@partners.org. · Lieber Institute for Brain Development and Johns Hopkins School of Medicine, Baltimore, MD, USA. Electronic address: drweinberger@libd.org. ·Curr Opin Neurobiol · Pubmed #26797413.

ABSTRACT: -- No abstract --

5 Editorial GBA mutations and Parkinson disease: when genotype meets phenotype. 2015

Scholz, Sonja W / Jeon, Beom S. ·From the Department of Neurology (S.W.S.), Johns Hopkins Hospital, Baltimore · Laboratory of Neurogenetics (S.W.S.), National Institute on Aging, National Institutes of Health, Bethesda, MD · and Department of Neurology (B.S.J.), Seoul National University Hospital, Republic of Korea. ·Neurology · Pubmed #25653294.

ABSTRACT: -- No abstract --

6 Editorial The pharmacodynamics of placebo: expectation effects of price as a proxy for efficacy. 2015

LeWitt, Peter A / Kim, Scott. ·From the Department of Neurology (P.A.L.), Parkinson's Disease and Movement Disorders Center, Henry Ford West Bloomfield Hospital · Department of Neurology (P.A.L.), Wayne State University School of Medicine, Detroit, MI · and Department of Bioethics (S.K.), National Institutes of Health, Bethesda, MD. ·Neurology · Pubmed #25632090.

ABSTRACT: -- No abstract --

7 Editorial Lardy brains make Parkinson's disease mice worse. 2014

Cookson, Mark R. ·Cell Biology and Gene Expression Section, Laboratory of Neurogenetics, National Institute on Aging, National Institutes of Health, Bethesda, Maryland, USA. ·J Neurochem · Pubmed #25142063.

ABSTRACT: -- No abstract --

8 Review Essential Tremor. 2019

Reich, Stephen G. ·Department of Neurology, University of Maryland School of Medicine, 110 South Paca Street, 3rd Floor, Baltimore, MD 21201, USA. Electronic address: sreich@som.umaryland.edu. ·Med Clin North Am · Pubmed #30704686.

ABSTRACT: Essential tremor is one of the most common movement disorders. It is characterized by a bilateral action tremor of the upper limbs. It may be accompanied by tremor of the head, voice, or lower limbs. Essential tremor is often present for years or decades before presentation and it progresses insidiously. It is often familial and transiently responsive to alcohol. For patients requiring treatment, the two first-line medications are propranolol and primidone, which are synergistic. Patients with disabling essential tremor that cannot be managed medically are candidates for either deep brain stimulation or focused ultrasound.

9 Review Parkinson's Disease. 2019

Reich, Stephen G / Savitt, Joseph M. ·Department of Neurology, University of Maryland School of Medicine, 110 South Paca Street, 3rd Floor, Baltimore, MD 21201, USA. Electronic address: sreich@som.umaryland.edu. · Department of Neurology, University of Maryland School of Medicine, 110 South Paca Street, 3rd Floor, Baltimore, MD 21201, USA. ·Med Clin North Am · Pubmed #30704685.

ABSTRACT: The diagnosis of Parkinson disease (PD) is based on the presence of bradykinesia and either resting tremor or rigidity and there should be no features from the history or examination to suggest an alternative cause of parkinsonism. In addition to the motor manifestations of PD, there is a long list of nonmotor symptoms, several of which occur before motor signs and are considered "prodromal" PD. These are classified as neuropsychiatric, autonomic, sleep, and sensory. There are many medical options for the treatment of PD but levodopa remains the mainstay. Deep brain stimulation and other advanced therapies are also available.

10 Review Molecular Imaging of the Noradrenergic System in Idiopathic Parkinson's Disease. 2018

Nahimi, Adjmal / Kinnerup, Martin B / Sommerauer, Michael / Gjedde, Albert / Borghammer, Per. ·Department of Nuclear Medicine and PET Centre, Aarhus University Hospital, Aarhus, Denmark; Department of Clinical Pharmacology, Aarhus University Hospital, Aarhus, Denmark; Department of Nuclear Medicine, Odense University Hospital, Odense, Denmark. Electronic address: anah@clin.au.dk. · Department of Nuclear Medicine and PET Centre, Aarhus University Hospital, Aarhus, Denmark. · Department of Nuclear Medicine, Odense University Hospital, Odense, Denmark; Department of Neuroscience and Pharmacology, University of Copenhagen, Copenhagen, Denmark; Department of Radiology and Radiological Science, Johns Hopkins University, Baltimore, MD, United States; Department of Neurology, McGill University, Montreal, QC, Canada. ·Int Rev Neurobiol · Pubmed #30314598.

ABSTRACT: Noradrenergic neurons in both the peripheral nervous system and in the central nervous system (CNS) undergo severe degeneration in patients with Parkinson's disease (PD). This loss of noradrenaline may play essential roles in the occurrence of a wide range of prevalent non-motor symptoms and can further complicate the lives of PD patients. In vivo molecular imaging of noradrenaline may provide insights into to the extent of degeneration of noradrenergic neurons and subsequent depletion of noradrenergic projections. Molecular imaging methods exist to quantify the noradrenergic deficiency in peripheral autonomic terminals, such as [

11 Review Parkinson's disease research: adopting a more human perspective to accelerate advances. 2018

Marshall, Lindsay J / Willett, Catherine. ·Humane Society International, The Humane Society of the United States, 700 Professional Drive, Gaithersburg, MD 20879, USA. · Humane Society International, The Humane Society of the United States, 700 Professional Drive, Gaithersburg, MD 20879, USA. Electronic address: kwillett@humanesociety.org. ·Drug Discov Today · Pubmed #30240875.

ABSTRACT: Parkinson's disease (PD) affects 1% of the population over 60 years old and, with global increases in the aging population, presents huge economic and societal burdens. The etiology of PD remains unknown; most cases are idiopathic, presumed to result from genetic and environmental risk factors. Despite 200 years since the first description of PD, the mechanisms behind initiation and progression of the characteristic neurodegenerative processes are not known. Here, we review progress and limitations of the multiple PD animal models available and identify advances that could be implemented to better understand pathological processes, improve disease outcome, and reduce dependence on animal models. Lessons learned from reducing animal use in PD research could serve as guideposts for wider biomedical research.

12 Review MR-Guided Functional Neurosurgery: Laser Ablation and Deep Brain Stimulation. 2018

Boone, Christine E / Wojtasiewicz, Teresa / Moukheiber, Emile / Butala, Ankur / Jordao, Ligia / Mills, Kelly A / Sair, Haris / Anderson, William S. ·Department of Neurosurgery. · Department of Neurology. · Department of Pediatric Cardiology. · Department of Radiology, Neuroradiology, The Johns Hopkins University, Baltimore, MD. ·Top Magn Reson Imaging · Pubmed #29870469.

ABSTRACT: Intraoperative magnetic resonance imaging (iMRI) is increasingly implemented for image-guided procedures in functional neurosurgery. iMRI facilitates accurate electrode implantation for deep brain stimulation (DBS) and is currently an alternative method for DBS electrode targeting. The application of iMRI also allows for greater accuracy and precision in laser-induced thermal therapy (LITT). The expanding use of functional neurosurgical procedures makes safety and feasibility of iMRI important considerations, particularly in patients with comorbidities or complex medical histories. We review here the applications of iMRI and discuss its safety, feasibility, and limitations in functional neurosurgery.To motivate discussion of this topic, we also present a 52-year-old patient with an implanted cardioverter-defibrillator (ICD) who successfully underwent iMRI-guided DBS electrode implantation for advanced Parkinson disease (PD). Neither iMRI nor the passage of electrical current through the implanted DBS electrodes demonstrated detectable interference in ICD function. This case demonstrates that, even in complex clinical contexts, iMRI is a promising tool that merits further exploration for procedures requiring highly accurate and precise identification of target structures.

13 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.

14 Review Genetic risk factors in Parkinson's disease. 2018

Billingsley, K J / Bandres-Ciga, S / Saez-Atienzar, S / Singleton, A B. ·Laboratory of Neurogenetics, National Institute on Aging, National Institutes of Health, 35 Convent Drive, Bethesda, MD, 20892, USA. · Department of Molecular and Clinical Pharmacology, Institute of Translational Medicine, University of Liverpool, L69 3BX, Liverpool, UK. · Laboratory of Neurogenetics, National Institute on Aging, National Institutes of Health, 35 Convent Drive, Bethesda, MD, 20892, USA. singleta@mail.nih.gov. ·Cell Tissue Res · Pubmed #29536161.

ABSTRACT: Over the last two decades, we have witnessed a revolution in the field of Parkinson's disease (PD) genetics. Great advances have been made in identifying many loci that confer a risk for PD, which has subsequently led to an improved understanding of the molecular pathways involved in disease pathogenesis. Despite this success, it is predicted that only a relatively small proportion of the phenotypic variability has been explained by genetics. Therefore, it is clear that common heritable components of disease are still to be identified. Dissecting the genetic architecture of PD constitutes a critical effort in identifying therapeutic targets and although such substantial progress has helped us to better understand disease mechanism, the route to PD disease-modifying drugs is a lengthy one. In this review, we give an overview of the known genetic risk factors in PD, focusing not on individual variants but the larger networks that have been implicated following comprehensive pathway analysis. We outline the challenges faced in the translation of risk loci to pathobiological relevance and illustrate the need for integrating big-data by noting success in recent work which adopts a broad-scale screening approach. Lastly, with PD genetics now progressing from identifying risk to predicting disease, we review how these models will likely have a significant impact in the future.

15 Review The LRRK2 signalling system. 2018

Price, Alice / Manzoni, Claudia / Cookson, Mark R / Lewis, Patrick A. ·School of Pharmacy, University of Reading, Whiteknights, Reading, RG6 6AP, UK. · Department of Molecular Neuroscience, UCL Institute of Neurology, Queen Square, London, WC1N 3BG, UK. · Laboratory of Neurogenetics, National Institute on Aging, National Institutes of Health, Building. 35, 35 Convent Drive, Bethesda, MD, 20892, USA. · School of Pharmacy, University of Reading, Whiteknights, Reading, RG6 6AP, UK. p.a.lewis@reading.ac.uk. · Department of Molecular Neuroscience, UCL Institute of Neurology, Queen Square, London, WC1N 3BG, UK. p.a.lewis@reading.ac.uk. ·Cell Tissue Res · Pubmed #29308544.

ABSTRACT: The LRRK2 gene is a major contributor to genetic risk for Parkinson's disease and understanding the biology of the leucine-rich repeat kinase 2 (LRRK2, the protein product of this gene) is an important goal in Parkinson's research. LRRK2 is a multi-domain, multi-activity enzyme and has been implicated in a wide range of signalling events within the cell. Because of the complexities of the signal transduction pathways in which LRRK2 is involved, it has been challenging to generate a clear idea as to how mutations and disease associated variants in this gene are altered in disease. Understanding the events in which LRRK2 is involved at a systems level is therefore critical to fully understand the biology and pathobiology of this protein and is the subject of this review.

16 Review Functional dissection of astrocyte-secreted proteins: Implications in brain health and diseases. 2018

Jha, Mithilesh Kumar / Kim, Jong-Heon / Song, Gyun Jee / Lee, Won-Ha / Lee, In-Kyu / Lee, Ho-Won / An, Seong Soo A / Kim, SangYun / Suk, Kyoungho. ·Department of Pharmacology, Brain Science and Engineering Institute, BK21 Plus KNU Biomedical Convergence Program, Kyungpook National University School of Medicine, Daegu, Republic of Korea; Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA. · Department of Pharmacology, Brain Science and Engineering Institute, BK21 Plus KNU Biomedical Convergence Program, Kyungpook National University School of Medicine, Daegu, Republic of Korea. · School of Life Sciences, BK21 Plus KNU Creative BioResearch Group, Kyungpook National University, Daegu, Republic of Korea. · Department of Internal Medicine, Division of Endocrinology and Metabolism, Kyungpook National University School of Medicine, Daegu, Republic of Korea. · Department of Neurology, Brain Science and Engineering Institute, Kyungpook National University School of Medicine, Daegu, Republic of Korea. · Department of BioNano Technology, Gachon University, Gyeonggi-do, Republic of Korea. · Department of Neurology, Seoul National University Bundang Hospital, Seoul National University College of Medicine, Gyeonggi-do, Republic of Korea. · Department of Pharmacology, Brain Science and Engineering Institute, BK21 Plus KNU Biomedical Convergence Program, Kyungpook National University School of Medicine, Daegu, Republic of Korea. Electronic address: ksuk@knu.ac.kr. ·Prog Neurobiol · Pubmed #29247683.

ABSTRACT: Astrocytes, which are homeostatic cells of the central nervous system (CNS), display remarkable heterogeneity in their morphology and function. Besides their physical and metabolic support to neurons, astrocytes modulate the blood-brain barrier, regulate CNS synaptogenesis, guide axon pathfinding, maintain brain homeostasis, affect neuronal development and plasticity, and contribute to diverse neuropathologies via secreted proteins. The identification of astrocytic proteome and secretome profiles has provided new insights into the maintenance of neuronal health and survival, the pathogenesis of brain injury, and neurodegeneration. Recent advances in proteomics research have provided an excellent catalog of astrocyte-secreted proteins. This review categorizes astrocyte-secreted proteins and discusses evidence that astrocytes play a crucial role in neuronal activity and brain function. An in-depth understanding of astrocyte-secreted proteins and their pathways is pivotal for the development of novel strategies for restoring brain homeostasis, limiting brain injury/inflammation, counteracting neurodegeneration, and obtaining functional recovery.

17 Review Advances and challenges in the search for D 2018

Moritz, Amy E / Free, R Benjamin / Sibley, David R. ·Molecular Neuropharmacology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, 35 Convent Drive, MSC-3723, Bethesda, MD 20892-3723, United States. · Molecular Neuropharmacology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, 35 Convent Drive, MSC-3723, Bethesda, MD 20892-3723, United States. Electronic address: sibleyd@ninds.nih.gov. ·Cell Signal · Pubmed #28716664.

ABSTRACT: Compounds that target D2-like dopamine receptors (DRs) are currently used as therapeutics for several neuropsychiatric disorders including schizophrenia (antagonists) and Parkinson's disease (agonists). However, as the D

18 Review A New Treatment Strategy for Parkinson's Disease through the Gut-Brain Axis: The Glucagon-Like Peptide-1 Receptor Pathway. 2017

Kim, Dong Seok / Choi, Ho-Il / Wang, Yun / Luo, Yu / Hoffer, Barry J / Greig, Nigel H. ·1 Peptron Inc., Yuseong-gu, Daejeon, Republic of Korea. · 2 Drug Design and Development Section, Translational Gerontology Branch, Intramural Research Program, National Institute on Aging, National Institutes of Health, Baltimore, MD, USA. · 3 Center for Neuropsychiatric Research, National Health Research Institutes, Zhunan, Miaoli County, Taiwan. · 4 Department of Neurosurgery, Case Western Reserve University School of Medicine, Cleveland, OH, USA. ·Cell Transplant · Pubmed #29113464.

ABSTRACT: Molecular communications in the gut-brain axis, between the central nervous system and the gastrointestinal tract, are critical for maintaining healthy brain function, particularly in aging. Epidemiological analyses indicate type 2 diabetes mellitus (T2DM) is a risk factor for neurodegenerative disorders including Alzheimer's disease (AD) and Parkinson's diseases (PD) for which aging shows a major correlative association. Common pathophysiological features exist between T2DM, AD, and PD, including oxidative stress, inflammation, insulin resistance, abnormal protein processing, and cognitive decline, and suggest that effective drugs for T2DM that positively impact the gut-brain axis could provide an effective treatment option for neurodegenerative diseases. Glucagon-like peptide-1 (GLP-1)-based antidiabetic drugs have drawn particular attention as an effectual new strategy to not only regulate blood glucose but also decrease body weight by reducing appetite, which implies that GLP-1 could affect the gut-brain axis in normal and pathological conditions. The neurotrophic and neuroprotective effects of GLP-1 receptor (R) stimulation have been characterized in numerous in vitro and in vivo preclinical studies using GLP-1R agonists and dipeptidyl peptidase-4 inhibitors. Recently, the first open label clinical study of exenatide, a long-acting GLP-1 agonist, in the treatment of PD showed long-lasting improvements in motor and cognitive function. Several double-blind clinical trials of GLP-1R agonists including exenatide in PD and other neurodegenerative diseases are already underway or are about to be initiated. Herein, we review the physiological role of the GLP-1R pathway in the gut-brain axis and the therapeutic strategy of GLP-1R stimulation for the treatment of neurodegenerative diseases focused on PD, for which age is the major risk factor.

19 Review NAD 2017

Fang, Evandro F / Lautrup, Sofie / Hou, Yujun / Demarest, Tyler G / Croteau, Deborah L / Mattson, Mark P / Bohr, Vilhelm A. ·Laboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, Baltimore, MD 21224, USA; Department of Clinical Molecular Biology, University of Oslo and Akershus University Hospital, 1478 Lørenskog, Norway; Co-first authors. · Laboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, Baltimore, MD 21224, USA; Danish Aging Research Center, Department of Molecular Biology and Genetics, University of Aarhus, 8000 Aarhus C, Denmark; Co-first authors. · Laboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, Baltimore, MD 21224, USA. · Laboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, Baltimore, MD 21224, USA; Laboratory of Neurosciences, National Institute on Aging, National Institutes of Health, Baltimore, MD 21224, USA. · Laboratory of Neurosciences, National Institute on Aging, National Institutes of Health, Baltimore, MD 21224, USA; Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA. · Laboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, Baltimore, MD 21224, USA; Danish Center for Healthy Aging, University of Copenhagen, Blegdamsvej 3B, 2200 Copenhagen, Denmark. Electronic address: vbohr@nih.gov. ·Trends Mol Med · Pubmed #28899755.

ABSTRACT: The coenzyme NAD

20 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.

21 Review Activation mechanisms of the E3 ubiquitin ligase parkin. 2017

Panicker, Nikhil / Dawson, Valina L / Dawson, Ted M. ·Neuroregeneration and Stem Cell Programs, Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, MD 21205, U.S.A. · Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, U.S.A. · Adrienne Helis Malvin Medical Research Foundation, New Orleans, LA 70130-2685, U.S.A. · Department of Physiology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, U.S.A. · Solomon H. Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205, U.S.A. · Diana Helis Henry Medical Research Foundation, New Orleans, LA 70130-2685, U.S.A. · Neuroregeneration and Stem Cell Programs, Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, MD 21205, U.S.A. tdawson@jhmi.edu. ·Biochem J · Pubmed #28860335.

ABSTRACT: Monogenetic, familial forms of Parkinson's disease (PD) only account for 5-10% of the total number of PD cases, but analysis of the genes involved therein is invaluable to understanding PD-associated neurodegenerative signaling. One such gene,

22 Review A user's guide for α-synuclein biomarker studies in biological fluids: Perianalytical considerations. 2017

Mollenhauer, Brit / Batrla, Richard / El-Agnaf, Omar / Galasko, Douglas R / Lashuel, Hilal A / Merchant, Kalpana M / Shaw, Lesley M / Selkoe, Dennis J / Umek, Robert / Vanderstichele, Hugo / Zetterberg, Henrik / Zhang, Jing / Caspell-Garcia, Chelsea / Coffey, Chris / Hutten, Samantha J / Frasier, Mark / Taylor, Peggy / Anonymous5870913. ·Paracelsus-Elena-Klinik, Kassel, Germany. · Department of Neurology, University Medical Center, Göttingen, Germany. · Roche Diagnostics International Ltd, Rotkreuz, Switzerland. · Neurological Disorders Research Center, Qatar Biomedical Research Institute (QBRI), and College of Science and Engineering, HBKU, Education City, Qatar Foundation, Doha, Qatar. · University of San Diego, San Diego, California, USA. · Laboratory of Molecular and Chemical Biology of Neurodegeneration, Brain Mind Institute, Faculty of Life Science, Ecole Polytechnique Federale de Lausanne (EPFL), Lausanne, Switzerland. · Northwestern University School of Medicine, Chicago, Illinois, USA. · Department of Pathology & Laboratory Medicine and Center for Neurodegenerative Disease Research, Institute on Aging, University of Pennsylvania, Philadelphia, Pennsylvania, USA. · Center for Neurodegenerative Disorders, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA. · MesoScale Discovery, Gaithersburg, Maryland, USA. · ADx NeuroSciences, Gent, Belgium. · Department of Psychiatry and Neurochemistry, Sahlgrenska Academy at the University of Gothenburg, Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden; and Department of Molecular Neuroscience, UCL Institute of Neurology, London, UK; UK Dementia Research Institute, London, UK. · University of Washington, Seattle, Washington, USA. · Department of Biostatistics, College of Public Health, University of Iowa, Iowa City, Iowa, USA. · Michael J. Fox Foundation for Parkinson's Research, New York, New York, USA. · BioLegend, Dedham, Massachusetts, USA. ·Mov Disord · Pubmed #28734051.

ABSTRACT: Parkinson's disease biomarkers are needed to increase diagnostic accuracy, to objectively monitor disease progression and to assess therapeutic efficacy as well as target engagement when evaluating novel drug and therapeutic strategies. This article summarizes perianalytical considerations for biomarker studies (based on immunoassays) in Parkinson's disease, with emphasis on quantifying total α-synuclein protein in biological fluids. Current knowledge and pitfalls are discussed, and selected perianalytical variables are presented systematically, including different temperature of sample collection and types of collection tubes, gradient sampling, the addition of detergent, aliquot volume, the freezing time, and the different thawing methods. We also discuss analytical confounders. We identify gaps in the knowledge and delineate specific areas that require further investigation, such as the need to identify posttranslational modifications of α-synuclein and antibody-independent reference methods for quantification, as well as the analysis of potential confounders, such as comorbidities, medication, and phenotypes of Parkinson's disease in larger cohorts. This review could be used as a guideline for future Parkinson's disease biomarker studies and will require regular updating as more information arises in this growing field, including new technical developments as they become available. In addition to reviewing best practices, we also identify the current technical limitations and gaps in the knowledge that should be addressed to enable accurate and quantitative assessment of α-synuclein levels in the clinical setting. © 2017 International Parkinson and Movement Disorder Society.

23 Review Dichlorodiphenyltrichloroethane (DDT) induced extracellular vesicle formation: a potential role in organochlorine increased risk of Parkinson's disease. 2017

Rossi, Mario / Scarselli, Marco / Fasciani, Irene / Maggio, Roberto / Giorgi, Franco. ·Molecular Signaling Section, Laboratory of Bioorganic Chemistry, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, MD, United States. · Department of Translational Research and New Technologies in Medicine and Surgery, University of Pisa, Pisa, Italy. · Department of Biotechnological and Applied Clinical Sciences, University of L'Aquila, L'Aquila, Italy. · Department of Biotechnological and Applied Clinical Sciences, University of L'Aquila, L'Aquila, Italy; roberto.maggio@univaq.it. ·Acta Neurobiol Exp (Wars) · Pubmed #28691715.

ABSTRACT: A number of studies have demonstrated that rural living and exposure to pesticides such as dichlorodiphenyltrichloroethane (DDT) highly increase the chances of developing Parkinson's disease. In a previous work, we have found that DDT leads to the formation of vesicular buds that are released from the cells upon fusion of an intermediate endocytic compartment with the plasma membrane. Since extracellular vesicles like exosomes have been implicated in the development of neurodegenerative diseases through the propagation of neurotoxic misfolded proteins from neuron to neuron, in this minireview we propose that organochlorine pesticides could enhance the risk of neurodegenerative diseases by increasing the formation of exosomes.

24 Review Gene Linkage and Systems Biology. 2017

Cookson, Mark R. ·Laboratory of Neurogenetics, NIA, NIH. 35, Convent Drive, Bethesda, MD, 20892-3707, USA. cookson@mail.nih.gov. ·Adv Neurobiol · Pubmed #28674994.

ABSTRACT: In the past two decades it has become increasingly clear that the risk for many neurodegenerative disorders is at least partially genetic. Assignment of causality for a given gene depends on showing that a particular variant shows either segregation within a family or association with disease across a population. In terms of lifetime risk of disease, the former generally show strong effects compared to the latter. In rare, but interesting, circumstances there are genetic loci that contain different variants that encode either highly penetrant Mendelian disease but also that contribute to risk of sporadic disease. Here, we will discuss the current efforts to complete our understanding of the genetic architecture of neurodegenerative diseases of aging with a particular focus on Parkinson's disease. We will also briefly outline attempts to use systematic approaches to infer relationships between genes associated with the same diseases, which likely demonstrate that in each case there are a relatively small number of underlying biological pathways or processes that may explain pathogenesis.

25 Review Make dopamine neurons great again: An exciting new therapeutic option in parkinson's disease. 2017

Bonet-Ponce, Luis / Singleton, Andrew B. ·Cell Biology and Gene Expression Section, Laboratory of Neurogenetics, National Institute of Aging, National Institutes of Health, Bethesda, Maryland, USA. · Molecular Genetics Section, Laboratory of Neurogenetics, National Institute of Aging, National Institutes of Health, Bethesda, Maryland, USA. ·Mov Disord · Pubmed #28631854.

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