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Parkinson Disease: HELP
Articles from Institute of Neurology
Based on 609 articles published since 2008

These are the 609 published articles about Parkinson Disease that originated from Institute of Neurology 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 What would James Parkinson think? A virtual dialogue on factors influencing the development of Parkinson's disease. 2017

Schapira, Anthony Hv. ·Department of Clinical Neurosciences, UCL Institute of Neurology, London, UK. ·Mov Disord · Pubmed #29124789.

ABSTRACT: -- No abstract --

2 Editorial What Would Dr. James Parkinson Think Today? I. The Role of Functional Neurosurgery for Parkinson's Disease. 2017

Hariz, Marwan / Obeso, Jose A. ·UCL-Institute of Neurology, London, United Kingdom. · Department of Clinical Neuroscience, Umeå University, Umeå, Sweden. · CINAC-HM Puerta del Sur, Mostoles and CEU-San Pablo University, Madrid, Spain. · CIBERNED, Insituto Carlos III, Madrid, Spain. ·Mov Disord · Pubmed #28124429.

ABSTRACT: -- No abstract --

3 Editorial A new scale for the assessment of pain in Parkinson's disease. 2015

Schrag, Anette. ·Department of Clinical Neurosciences, UCL Institute of Neurology, London, United Kingdom. ·Mov Disord · Pubmed #26230748.

ABSTRACT: -- No abstract --

4 Editorial The treatment of mild cognitive impairment associated with Parkinson's disease. 2015

Burn, David J. ·Institute of Neuroscience, and Professor of Movement Disorders Neurology, Henry Wellcome Building, Faculty of Medical Sciences, Newcastle University, Newcastle upon Tyne, NE2 4HH. ·Mov Disord · Pubmed #26011710.

ABSTRACT: -- No abstract --

5 Editorial Targeting mitochondria for neuroprotection in Parkinson disease. 2014

Schapira, Anthony H V / Patel, Sandip. ·Department of Clinical Neurosciences, Institute of Neurology, University College London, London, England. · Department of Cell and Developmental Biology, University College London, London, England. ·JAMA Neurol · Pubmed #24664140.

ABSTRACT: -- No abstract --

6 Editorial Genetics of Parkinson's disease: alpha-synuclein and other insights from Greece. 2014

Proukakis, C. ·UCL Institute of Neurology, Clinical Neuroscience Department, London, UK. c.proukakis@ucl.ac.uk. ·Eur J Neurol · Pubmed #24460978.

ABSTRACT: -- No abstract --

7 Editorial Cerebrospinal fluid α-synuclein levels in Parkinson's disease--changed or unchanged? 2014

Zetterberg, H / Petzold, M / Magdalinou, N. ·Clinical Neurochemistry Laboratory, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden; UCL Institute of Neurology, Queen Square, London, UK. henrik.zetterberg@clinchem.gu.se. ·Eur J Neurol · Pubmed #24330157.

ABSTRACT: -- No abstract --

8 Editorial Risky choices link the subthalamic nucleus with pathological gambling in Parkinson's disease. 2013

Jahanshahi, Marjan. ·UCL Institute of Neurology, The National Hospital for Neurology and Neurosurgery, London, United Kingdom. ·Mov Disord · Pubmed #23843183.

ABSTRACT: -- No abstract --

9 Editorial Timing the initiation of treatment in Parkinson's disease. 2008

Grosset, Donald G / Schapira, Anthony H. ·Institute of Neurological Sciences, Department of Neurology, Southern General Hospital, 1345 Govan Rd, Glasgow G51 4TF, UK. d.grosset@clinmed.gla.ac.uk ·J Neurol Neurosurg Psychiatry · Pubmed #18487552.

ABSTRACT: -- No abstract --

10 Review Chaperone-mediated autophagy as a therapeutic target for Parkinson disease. 2018

Campbell, Philip / Morris, Huw / Schapira, Anthony. ·a Department of Clinical and Movement Neurosciences, UCL Queen Square Institute of Neurology , University College London , London , UK. ·Expert Opin Ther Targets · Pubmed #30185079.

ABSTRACT: INTRODUCTION: Parkinson disease (PD) is the most common neurodegenerative movement disorder. Currently only symptomatic treatments exist for PD, and so the search for potential neuroprotective drug targets is of great importance. Chaperone mediated autophagy (CMA) is one of the key cellular mechanisms in protein homeostasis. Many of the pathogenic pathways thought to be important in PD converge on CMA, thus rendering it an attractive therapeutic target. Areas covered: In this review we discuss current up-to-date knowledge of the molecular mechanisms involved in CMA function and regulation. We go on to discuss the links between CMA and PD including CMA's role in ɑ-synuclein processing, oxidative stress, and mitochondrial function. We finish by exploring the potential benefits of how upregulation of CMA may be beneficial in PD and strategies to achieve this. Expert opinion: Upregulation of CMA is an attractive therapeutic target in PD due to its links with several pathogenic pathways . Currently more knowledge of the mechanisms that regulate CMA is required to allow for the development of specific CMA modulators. However, recent studies demonstrating the role of retinoic acid derivatives and miRNAs in regulating CMA are promising, and indirect upregulation of CMA by modulating other lysosomal pathways may be helpful.

11 Review Neuroimaging advances in Parkinson's disease. 2018

Rispoli, Vittorio / Schreglmann, Sebastian R / Bhatia, Kailash P. ·Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, UCL, London, UK. · Department of Neuroscience, University Hospital Arcispedale S. Anna, Ferrara, Italy. ·Curr Opin Neurol · Pubmed #29878908.

ABSTRACT: PURPOSE OF REVIEW: Neuroimaging in Parkinson's disease is an evolving field, providing in-vivo insights into the structural and biochemical changes of the condition, although its diagnosis remains clinical. Here, we aim to summarize the most relevant recent advances in neuroimaging in Parkinson's disease to assess the underlying disease process, identify a biomarker of disease progression and guide or monitor therapeutic interventions. RECENT FINDINGS: The clinical applications of imaging technology increasingly allow to quantify pigments (iron, neuromelanin) on MRI, proteins (tau), cell markers (phosphodiesterases, microglia) and neurotransmitter receptors (dopamine, serotonin, noradrenalin, cholin) via PET protocols, activity maps by resting-state and task-dependent functional MRI, as well as microstructural changes (free water) through diffusion-based assessments. Their application provides increasing insight on the temporal and spatial dynamics of dopaminergic and other neurotransmitter systems as well as anatomical structures and circuits in Parkinson's disease. An expanding list of PET tracers increases the yield of functional studies. SUMMARY: This review summarizes the most recent, relevant advances in neuroimaging technology in Parkinson's disease. In particular, the combination of different imaging techniques seems promising to maximize the scope of future work, which should, among others, aim at identifying the best imaging marker of disease progression.

12 Review Exploring autophagy with Gene Ontology. 2018

Denny, Paul / Feuermann, Marc / Hill, David P / Lovering, Ruth C / Plun-Favreau, Helene / Roncaglia, Paola. ·a Functional Gene Annotation , Institute of Cardiovascular Science, University College London , London , UK. · b SIB Swiss Institute of Bioinformatics , Geneva , Switzerland. · c The Jackson Laboratory , Bar Harbor , ME , USA. · f The Gene Ontology Consortium. · d Department of Molecular Neuroscience , UCL Institute of Neurology , London , UK. · e European Bioinformatics Institute (EMBL-EBI) , European Molecular Biology Laboratory, Wellcome Genome Campus , Hinxton , Cambridge , UK. ·Autophagy · Pubmed #29455577.

ABSTRACT: Autophagy is a fundamental cellular process that is well conserved among eukaryotes. It is one of the strategies that cells use to catabolize substances in a controlled way. Autophagy is used for recycling cellular components, responding to cellular stresses and ridding cells of foreign material. Perturbations in autophagy have been implicated in a number of pathological conditions such as neurodegeneration, cardiac disease and cancer. The growing knowledge about autophagic mechanisms needs to be collected in a computable and shareable format to allow its use in data representation and interpretation. The Gene Ontology (GO) is a freely available resource that describes how and where gene products function in biological systems. It consists of 3 interrelated structured vocabularies that outline what gene products do at the biochemical level, where they act in a cell and the overall biological objectives to which their actions contribute. It also consists of 'annotations' that associate gene products with the terms. Here we describe how we represent autophagy in GO, how we create and define terms relevant to autophagy researchers and how we interrelate those terms to generate a coherent view of the process, therefore allowing an interoperable description of its biological aspects. We also describe how annotation of gene products with GO terms improves data analysis and interpretation, hence bringing a significant benefit to this field of study.

13 Review Glucocerebrosidase and Parkinson Disease: Molecular, Clinical, and Therapeutic Implications. 2018

Balestrino, Roberta / Schapira, Anthony H V. ·1 Department of Neuroscience, University of Turin, Turin, Italy. · 2 Department of Clinical Neurosciences, UCL Institute of Neurology, Royal Free Campus, London, UK. ·Neuroscientist · Pubmed #29400127.

ABSTRACT: Parkinson disease (PD) is a complex neurodegenerative disease characterised by multiple motor and non-motor symptoms. In the last 20 years, more than 20 genes have been identified as causes of parkinsonism. Following the observation of higher risk of PD in patients affected by Gaucher disease, a lysosomal disorder caused by mutations in the glucocerebrosidase (GBA) gene, it was discovered that mutations in this gene constitute the single largest risk factor for development of idiopathic PD. Patients with PD and GBA mutations are clinically indistinguishable from patients with idiopathic PD, although some characteristics emerge depending on the specific mutation, such as slightly earlier onset. The molecular mechanisms which lead to this increased PD risk in GBA mutation carriers are multiple and not yet fully elucidated, they include alpha-synuclein aggregation, lysosomal-autophagy dysfunction and endoplasmic reticulum stress. Moreover, dysfunction of glucocerebrosidase has also been demonstrated in non-GBA PD, suggesting its interaction with other pathogenic mechanisms. Therefore, GBA enzyme function represents an interesting pharmacological target for PD. Cell and animal models suggest that increasing GBA enzyme activity can reduce alpha-synuclein levels. Clinical trials of ambroxol, a glucocerebrosidase chaperone, are currently ongoing in PD and PD dementia, as is a trial of substrate reduction therapy. The aim of this review is to summarise the main features of GBA-PD and discuss the implications of glucocerebrosidase modulation on PD pathogenesis.

14 Review Review: Somatic mutations in neurodegeneration. 2018

Leija-Salazar, M / Piette, C / Proukakis, C. ·Department of Clinical Neuroscience, University College London Institute of Neurology, London, UK. ·Neuropathol Appl Neurobiol · Pubmed #29369391.

ABSTRACT: Somatic mutations are postzygotic mutations which may lead to mosaicism, the presence of cells with genetic differences in an organism. Their role in cancer is well established, but detailed investigation in health and other diseases has only been recently possible. This has been empowered by the improvements of sequencing techniques, including single-cell sequencing, which can still be error-prone but is rapidly improving. Mosaicism appears relatively common in the human body, including the normal brain, probably arising in early development, but also potentially during ageing. In this review, we first discuss theoretical considerations and current evidence relevant to somatic mutations in the brain. We present a framework to explain how they may be integrated with current views on neurodegeneration, focusing mainly on sporadic late-onset neurodegenerative diseases (Parkinson's disease, Alzheimer's disease and amyotrophic lateral sclerosis). We review the relevant studies so far, with the first evidence emerging in Alzheimer's in particular. We also discuss the role of mosaicism in inherited neurodegenerative disorders, particularly somatic instability of tandem repeats. We summarize existing views and data to present a model whereby the time of origin and spatial distribution of relevant somatic mutations, combined with any additional risk factors, may partly determine the development and onset age of sporadic neurodegenerative diseases.

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 Pedunculopontine nucleus deep brain stimulation in Parkinson's disease: A clinical review. 2018

Thevathasan, Wesley / Debu, Bettina / Aziz, Tipu / Bloem, Bastiaan R / Blahak, Christian / Butson, Christopher / Czernecki, Virginie / Foltynie, Thomas / Fraix, Valerie / Grabli, David / Joint, Carole / Lozano, Andres M / Okun, Michael S / Ostrem, Jill / Pavese, Nicola / Schrader, Christoph / Tai, Chun-Hwei / Krauss, Joachim K / Moro, Elena / Anonymous621156. ·Department of Medicine, Royal Melbourne Hospital, University of Melbourne, Australia and the Bionics Institute of Australia, Melbourne, Australia. · Movement Disorders Center, Division of Neurology, Centre Hospitalier Universitaire (CHU) Grenoble, Grenoble Alpes University, Grenoble, France. · Department of Neurosurgery, John Radcliffe Hospital, University of Oxford, Oxford, UK. · Department of Neurology, Donders Institute for Brain, Cognition and Behaviour, Radboud University, Nijmegen, the Netherlands. · Department of Neurology, Universitätsmedizin Mannheim, University of Heidelberg, Heidelberg, Germany. · Department of Bioengineering, Scientific Computing and Imaging Institute, University of Utah, Salt Lake City, USA. · Department of Neurology, Institut de Cerveau et de la Moelle épinière, Sorbonne Universités, University Pierre-and-Marie-Curie (UPMC) Université, Paris, France. · Sobell Department of Motor Neuroscience, University College London (UCL) Institute of Neurology, United Kingdom. · Department of Neurology, Assistance Publique-Hôpitaux de Paris, Pitié-Salpêtière University Hospital, Paris, France. · Department of Neurosurgery, Toronto Western Hospital, University of Toronto, Toronto, Canada. · Departments of Neurology and Neurosurgery, University of Florida Center for Movement Disorders, Gainesville, Florida, USA. · Department of Neurology, UCSF Movement Disorder and Neuromodulation Center, University of California, San Francisco, USA. · Institute of Neuroscience, Newcastle University, Newcastle upon Tyne, UK. · Department of Clinical Medicine, Centre for Functionally Integrative Neuroscience, University of Aarhus, Aarhus, Denmark. · Department of Neurology, Hannover Medical School, Hannover, Germany. · Department of Neurology, National Taiwan University Hospital, College of Medicine, National Taiwan University, Taipei, Taiwan. · Department of Neurosurgery, Hannover Medical School, Hannover, Germany. ·Mov Disord · Pubmed #28960543.

ABSTRACT: Pedunculopontine nucleus region deep brain stimulation (DBS) is a promising but experimental therapy for axial motor deficits in Parkinson's disease (PD), particularly gait freezing and falls. Here, we summarise the clinical application and outcomes reported during the past 10 years. The published dataset is limited, comprising fewer than 100 cases. Furthermore, there is great variability in clinical methodology between and within surgical centers. The most common indication has been severe medication refractory gait freezing (often associated with postural instability). Some patients received lone pedunculopontine nucleus DBS (unilateral or bilateral) and some received costimulation of the subthalamic nucleus or internal pallidum. Both rostral and caudal pedunculopontine nucleus subregions have been targeted. However, the spread of stimulation and variance in targeting means that neighboring brain stem regions may be implicated in any response. Low stimulation frequencies are typically employed (20-80 Hertz). The fluctuating nature of gait freezing can confound programming and outcome assessments. Although firm conclusions cannot be drawn on therapeutic efficacy, the literature suggests that medication refractory gait freezing and falls can improve. The impact on postural instability is unclear. Most groups report a lack of benefit on gait or limb akinesia or dopaminergic medication requirements. The key question is whether pedunculopontine nucleus DBS can improve quality of life in PD. So far, the evidence supporting such an effect is minimal. Development of pedunculopontine nucleus DBS to become a reliable, established therapy would likely require a collaborative effort between experienced centres to clarify biomarkers predictive of response and the optimal clinical methodology. © 2017 International Parkinson and Movement Disorder Society.

17 Review Protective effects of the GLP-1 mimetic exendin-4 in Parkinson's disease. 2018

Athauda, Dilan / Foltynie, Thomas. ·Sobell Department of Motor Neuroscience, UCL Institute of Neurology, The National Hospital for Neurology and Neurosurgery, Queen Square, London, WC1N 3BG, United Kingdom. · Sobell Department of Motor Neuroscience, UCL Institute of Neurology, The National Hospital for Neurology and Neurosurgery, Queen Square, London, WC1N 3BG, United Kingdom. Electronic address: T.Foltynie@ucl.ac.uk. ·Neuropharmacology · Pubmed #28927992.

ABSTRACT: There is increasing interest in the potential role of glucagon-like peptide-1 (GLP-1) receptor agonists as neuroprotective treatments in neurodegenerative diseases including Parkinson's disease following the publication of the results of the Exenatide-PD trial. Of the current GLP-1 receptor agonists already licensed to treat Type 2 diabetes several including exenatide, liraglutide and lixisenatide are the subject of ongoing clinical trials in PD. The underlying rationale for using drugs licensed and effective for T2DM in PD patients therefore needs to be scrutinized, and the results obtained to date critically reviewed. We review the relationship between insulin resistance and Parkinson's disease, the implications on pathogenesis and the efforts to reposition GLP-1 agonists as potential treatments for Parkinson's disease and give an overview of the pre-clinical and clinical data supporting the use of exenatide in Parkinson's disease with a discussion regarding possible mechanisms of action. This article is part of the Special Issue entitled 'Metabolic Impairment as Risk Factors for Neurodegenerative Disorders.'

18 Review Mitochondrial calcium imbalance in Parkinson's disease. 2018

Ludtmann, Marthe H R / Abramov, Andrey Y. ·Department of Molecular Neuroscience, UCL Institute of Neurology, Queen Square, London WC1N 3BG, UK. Electronic address: m.ludtmann@ucl.ac.uk. · Department of Molecular Neuroscience, UCL Institute of Neurology, Queen Square, London WC1N 3BG, UK. Electronic address: a.abramov@ucl.ac.uk. ·Neurosci Lett · Pubmed #28838811.

ABSTRACT: Multiple factors are involved in the mechanism(s) of neuronal loss in neurodegenerative disorders whilst mitochondria are thought to play a central role in neurodegeneration of Parkinson's disease. Mitochondria are vital to cellular functions by supplying energy in form of ATP and affect cell physiology via calcium, ROS and signalling proteins. Changes in mitochondrial calcium homeostasis and ROS overproduction can induce cell death by triggering mitochondrial permeability transition pore opening. One of the major triggers for PTP is mitochondrial calcium overload. Mitochondrial Ca

19 Review Insights into the structural biology of Gaucher disease. 2017

Smith, Laura / Mullin, Stephen / Schapira, Anthony H V. ·Department of Clinical Neurosciences, Institute of Neurology, University College London, London, NW3 2PF, UK. · Department of Clinical Neurosciences, Institute of Neurology, University College London, London, NW3 2PF, UK. Electronic address: a.schapira@ucl.ac.uk. ·Exp Neurol · Pubmed #28923368.

ABSTRACT: Gaucher disease, the most common lysosomal storage disorder, is caused by mutations in the gene encoding the acid-β-glucosidase lysosomal hydrolase enzyme that cleaves glucocerebroside into glucose and ceramide. Reduced enzyme activity and impaired structural stability arise due to >300 known disease-causing mutations. Several of these mutations have also been associated with an increased risk of Parkinson disease (PD). Since the discovery of the acid-β-glucosidase X-ray structure, there have been major advances in our understanding of the structural properties of the protein. Analysis of specific residues has provided insight into their functional and structural importance and provided insight into the pathogenesis of Gaucher disease and the contribution to PD. Disease-causing mutations are positioned throughout the acid-β-glucosidase structure, with many located far from the active site and thus retaining some enzymatic activity however, thus far no clear relationship between mutation location and disease severity has been established. Here, we review the crystal structure of acid-β-glucosidase, while highlighting important structural aspects of the protein in detail. This review discusses the structural stability of acid-β-glucosidase, which can be altered by pH and glycosylation, and explores the relationship between known Gaucher disease and PD mutations, structural stability and disease severity.

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 Nonmotor Features in Atypical Parkinsonism. 2017

Bhatia, Kailash P / Stamelou, Maria. ·Institute of Neurology, London, United Kingdom. · HYGEIA Hospital, Athens, Greece; Neurology Clinic, Philipps University Marburg, Marburg, Germany; University of Athens, Athens, Greece. Electronic address: mariastamelou@gmail.com. ·Int Rev Neurobiol · Pubmed #28805573.

ABSTRACT: Atypical parkinsonism (AP) comprises mainly multiple system atrophy (MSA), progressive supranuclear palsy (PSP), and corticobasal degeneration (CBD), which are distinct pathological entities, presenting with a wide phenotypic spectrum. The classic syndromes are now called MSA-parkinsonism (MSA-P), MSA-cerebellar type (MSA-C), Richardson's syndrome, and corticobasal syndrome. Nonmotor features in AP have been recognized almost since the initial description of these disorders; however, research has been limited. Autonomic dysfunction is the most prominent nonmotor feature of MSA, but also gastrointestinal symptoms, sleep dysfunction, and pain, can be a feature. In PSP and CBD, the most prominent nonmotor symptoms comprise those deriving from the cognitive/neuropsychiatric domain. Apart from assisting the clinician in the differential diagnosis with Parkinson's disease, nonmotor features in AP have a big impact on quality of life and prognosis of AP and their treatment poses a major challenge for clinicians.

22 Review Nonmotor Symptoms in Experimental Models of Parkinson's Disease. 2017

Titova, Nataliya / Schapira, Anthony H V / Chaudhuri, K Ray / Qamar, Mubasher A / Katunina, Elena / Jenner, Peter. ·Federal State Budgetary Educational Institution of Higher Education "N.I. Pirogov Russian National Research Medical University" of the Ministry of Healthcare of the Russian Federation, Moscow, Russia. Electronic address: nattitova@yandex.ru. · UCL Institute of Neurology, London, United Kingdom. · National Parkinson Foundation International Centre of Excellence, King's College London and King's College Hospital, London, United Kingdom; The Maurice Wohl Clinical Neuroscience Institute, King's College London, National Institute for Health Research (NIHR) South London and Maudsley NHS Foundation Trust and King's College London, London, United Kingdom. · Neurodegenerative Diseases Research Group, Institute of Pharmaceutical Science, Faculty of Life Sciences and Medicine, King's College London, London, United Kingdom. ·Int Rev Neurobiol · Pubmed #28802936.

ABSTRACT: Nonmotor symptoms of Parkinson's disease (PD) range from neuropsychiatric, cognitive to sleep and sensory disorders and can arise from the disease process as well as from drug treatment. The clinical heterogeneity of nonmotor symptoms of PD is underpinned by a wide range of neuropathological and molecular pathology, affecting almost the entire range of neurotransmitters present in brain and the periphery. Understanding the neurobiology and pathology of nonmotor symptoms is crucial to the effective treatment of PD and currently a key unmet need. This bench-to-bedside translational concept can only be successful if robust animal models of PD charting the genesis and natural history of nonmotor symptoms can be devised. Toxin-based and transgenic rodent and primate models of PD have given us important clues to the underlying basis of motor symptomatology and in addition, can provide a snapshot of some nonmotor aspects of PD, although the data are far from complete. In this chapter, we discuss some of the nonmotor aspects of the available experimental models of PD and how the development of robust animal models to understand and treat nonmotor symptoms needs to become a research priority.

23 Review Depression and Anxiety in Parkinson's Disease. 2017

Schrag, Anette / Taddei, Raquel N. ·UCL Institute of Neurology, London, United Kingdom. Electronic address: a.schrag@ucl.ac.uk. · King's College Hospital, London, United Kingdom. ·Int Rev Neurobiol · Pubmed #28802935.

ABSTRACT: Depression and anxiety are some of the most common comorbidities arising in patients with Parkinson's disease. However, their timely recognition and diagnosis are often hindered by overlap with other somatic features and a low rate of self-report. There is a need for greater awareness and for better assessment and treatment options are highly required. Currently available scales can serve as tools to monitor change over time and the effect of interventional strategies. Development of new therapeutic strategies, including nonpharmacological approaches such as transcranial magnetic stimulation and deep brain stimulation, may provide alternatives to currently available treatment approaches. In this chapter we will give an overview of the most recent advances in the diagnosis and treatment of these important nonmotor symptoms.

24 Review Quality of Life and Nonmotor Symptoms in Parkinson's Disease. 2017

Barone, Paolo / Erro, Roberto / Picillo, Marina. ·Center for Neurodegenerative Diseases (CEMAND), Neuroscience Section, University of Salerno, Salerno, Italy. Electronic address: pbarone@unisa.it. · Center for Neurodegenerative Diseases (CEMAND), Neuroscience Section, University of Salerno, Salerno, Italy; University College London, Institute of Neurology, London, United Kingdom. · Center for Neurodegenerative Diseases (CEMAND), Neuroscience Section, University of Salerno, Salerno, Italy. ·Int Rev Neurobiol · Pubmed #28802930.

ABSTRACT: Health-related quality of life (HRQoL) is defined as "the perception and evaluation by patients themselves of the impact caused on their lives by the disease and its consequences." HRQoL is conceptualized as a combination of physical, psychological, and social well-being in the context of a particular disease. Following earlier studies revolving on the impact of the classic motor symptoms of Parkinson's disease on HRQoL, mounting evidence have been produced that nonmotor symptoms (NMS) significantly and independently contribute to worse HRQoL. This holds particularly true for such NMS such as neuropsychiatric disturbances, cognitive impairment, and fatigue, the burden of which might well exceed the effects of the motor symptoms. Nonetheless, there is very sparse evidence on how to manage these NMS and whether targeting NMS would in fact lead to an improvement of HRQoL, which calls for the need of future trials with NMS as primary outcomes.

25 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.