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Parkinson Disease: HELP
Articles from Illinois
Based on 507 articles published since 2008
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These are the 507 published articles about Parkinson Disease that originated from Illinois 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 Closing the celebration of 200 years of Parkinson's Essay on the Shaking Palsy: Where do we go in the next 200 years? 2017

Goetz, Christopher G. ·Rush University Medical Center, Chicago, Illinois, USA. ·Mov Disord · Pubmed #29119602.

ABSTRACT: -- No abstract --

2 Editorial Virtually reducing fall risk in Parkinson disease. 2017

Moreau, Caroline / Barton, Brandon R / Devos, David. ·From the Service de Neurologie (C.M., D.D.) and Services de Pharmacologie and Médicale (D.D.), LICEND COEN Center, Université de Lille, CHU de Lille, INSERM UMRS_1171, France · Department of Neurological Sciences (B.R.B.), Rush University Medical Center · and Neurology Service (B.R.B.), Jesse Brown VA Medical Center, Chicago, IL. ·Neurology · Pubmed #28954881.

ABSTRACT: -- No abstract --

3 Editorial What would Dr. James Parkinson think today? parcelling out the circuitry of levodopa-induced dyskinesias. 2017

Kordower, Jeffrey H. ·Department of Neurological Sciences, Rush University Medical Center, Chicago, Illinois, 60612. · The Van Andel Research Institute, Grand Rapids Michigan, 49503. ·Mov Disord · Pubmed #28425143.

ABSTRACT: -- No abstract --

4 Editorial Fetal grafts for Parkinson's disease: Decades in the making. 2016

Kordower, Jeffrey H / Olanow, C Warren. ·Department of Neurological Sciences, Rush University Medical Center, Chicago, IL 60612; Van Andel Institute, Grand Rapids, MI 49503; jkordowe@rush.edu. · Department of Neurology, Mt. Sinai School of Medicine, New York, NY 10029; Department of Neuroscience, Mt. Sinai School of Medicine, New York, NY 10029. ·Proc Natl Acad Sci U S A · Pubmed #27247420.

ABSTRACT: -- No abstract --

5 Editorial Preface. 2015

Poewe, Werner / Goetz, Christopher G. ·Innsbruck Medical University, Austria. · Rush University Medical Center, Chicago, Illinois. ·Mov Disord · Pubmed #26301896.

ABSTRACT: -- No abstract --

6 Review Synaptic, Mitochondrial, and Lysosomal Dysfunction in Parkinson's Disease. 2019

Nguyen, Maria / Wong, Yvette C / Ysselstein, Daniel / Severino, Alex / Krainc, Dimitri. ·Ken and Ruth Davee Department of Neurology, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA. · Ken and Ruth Davee Department of Neurology, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA. Electronic address: dkrainc@nm.org. ·Trends Neurosci · Pubmed #30509690.

ABSTRACT: The discovery of genetic forms of Parkinson's disease (PD) has highlighted the importance of the autophagy/lysosomal and mitochondrial/oxidative stress pathways in disease pathogenesis. However, recently identified PD-linked genes, including DNAJC6 (auxilin), SYNJ1 (synaptojanin 1), and the PD risk gene SH3GL2 (endophilin A1), have also highlighted disruptions in synaptic vesicle endocytosis (SVE) as a significant contributor to disease pathogenesis. Additionally, the roles of other PD genes such as LRRK2, PRKN, and VPS35 in the regulation of SVE are beginning to emerge. Here we discuss the recent work on the contribution of dysfunctional SVE to midbrain dopaminergic neurons' selective vulnerability and highlight pathways that demonstrate the interplay of synaptic, mitochondrial, and lysosomal dysfunction in the pathogenesis of PD.

7 Review Molecular mechanisms of α-synuclein and GBA1 in Parkinson's disease. 2018

Stojkovska, Iva / Krainc, Dimitri / Mazzulli, Joseph R. ·The Ken and Ruth Davee Department of Neurology, Northwestern University Feinberg School of Medicine, 303 E. Chicago Ave, Ward 12-369, Chicago, IL, 60611, USA. · The Ken and Ruth Davee Department of Neurology, Northwestern University Feinberg School of Medicine, 303 E. Chicago Ave, Ward 12-369, Chicago, IL, 60611, USA. jmazzulli@northwestern.edu. ·Cell Tissue Res · Pubmed #29064079.

ABSTRACT: Parkinson's disease (PD) is a neurodegenerative movement disorder characterized pathologically by the presence of Lewy bodies comprised of insoluble alpha (α)-synuclein. Pathological, clinical and genetic studies demonstrate that mutations in the GBA1 gene, which encodes the lysosomal enzyme glucocerebrosidase (GCase) that is deficient in Gaucher's disease, are important risk factors for the development of PD. The molecular mechanism for the association between these two diseases is not completely understood. We discuss several possible mechanisms that may lead to GBA1-related neuronal death and α-synuclein accumulation including disruptions in lipid metabolism, protein trafficking and impaired protein quality control mechanisms. Elucidating the mechanism between GCase and α-synuclein may provide insight into potential therapeutic pathways for PD and related synucleinopathies.

8 Review Striatal synapses, circuits, and Parkinson's disease. 2018

Zhai, Shenyu / Tanimura, Asami / Graves, Steven M / Shen, Weixing / Surmeier, D James. ·Department of Physiology, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA. · Department of Physiology, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA. Electronic address: j-surmeier@northwestern.edu. ·Curr Opin Neurobiol · Pubmed #28843800.

ABSTRACT: The striatum is a hub in the basal ganglia circuitry controlling goal directed actions and habits. The loss of its dopaminergic (DAergic) innervation in Parkinson's disease (PD) disrupts the ability of the two principal striatal projection systems to respond appropriately to cortical and thalamic signals, resulting in the hypokinetic features of the disease. New tools to study brain circuitry have led to significant advances in our understanding of striatal circuits and how they adapt in PD models. This short review summarizes some of these recent studies and the gaps that remain to be filled.

9 Review Falls in Parkinson's disease: A complex and evolving picture. 2017

Fasano, Alfonso / Canning, Colleen G / Hausdorff, Jeffrey M / Lord, Sue / Rochester, Lynn. ·Morton and Gloria Shulman Movement Disorders Centre and the Edmond J. Safra Program in Parkinson's Disease, Toronto Western Hospital, UHN, Division of Neurology, University of Toronto, Toronto, Ontario, Canada. · Krembil Research Institute, Toronto, Ontario, Canada. · Discipline of Physiotherapy, Faculty of Health Sciences, University of Sydney, Sydney, Australia. · Center for Study of Movement, Cognition and Mobility, Department of Neurology, Tel Aviv Sourasky Medical Center, Tel Aviv, Israel. · Sagol School of Neuroscience and Department of Physical Therapy, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel. · Rush Alzheimer's Disease Center and Department of Orthopaedic Surgery, Rush University Medical Center, Chicago, Illinois, US. · Institute of Neuroscience, Newcastle University, Newcastle upon Tyne, UK. · Auckland University of Technology, Auckland, New Zealand. · Newcastle upon Tyne Hospitals National Health Service (NHS) Foundation Trust, Newcastle upon Tyne, UK. ·Mov Disord · Pubmed #29067726.

ABSTRACT: Falls are a major determinant of poor quality of life, immobilization, and reduced life expectancy in people affected by Parkinson's disease (PD) and in older adults more generally. Although many questions remain, recent research has advanced the understanding of this complex problem. The goal of this review is to condense new knowledge of falls in PD from prodromal to advanced disease, taking into account risk factors, assessment, and classification as well as treatment. The fundamental steps of clinical and research-based approaches to falls are described, namely, the identification of fall risk factors, clinical and instrumental methods to evaluate and classify fall risk, and the latest evidence to reduce or delay falls in PD. We summarize recent developments, the direction in which the field should be heading, and what can be recommended at this stage. We also provide a practical algorithm for clinicians.© 2017 International Parkinson and Movement Disorder Society.

10 Review Parkinson's Disease Is Not Simply a Prion Disorder. 2017

Surmeier, D James / Obeso, José A / Halliday, Glenda M. ·Department of Physiology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois 60611, j-surmeier@northwestern.edu. · CINAC, HM Puerta del Sur, Hospitales de Madrid, Mostoles and CEU-San Pablo University, 28938 Madrid, Spain. · Network Center for Biomedical Research on Neurodegenerative Diseases, Instituto Carlos III, 28029 Madrid, Spain. · Brain and Mind Centre, Sydney Medical School, University of Sydney, Sydney, 2006 New South Wales, Australia, and. · School of Medical Sciences, University of New South Wales and Neuroscience Research Australia, Sydney, 2052 New South Wales, Australia. ·J Neurosci · Pubmed #29021297.

ABSTRACT: The notion that prion-like spreading of misfolded α-synuclein (α-SYN) causes Parkinson's disease (PD) has received a great deal of attention. Although attractive in its simplicity, the hypothesis is difficult to reconcile with postmortem analysis of human brains and connectome-mapping studies. An alternative hypothesis is that PD pathology is governed by regional or cell-autonomous factors. Although these factors provide an explanation for the pattern of neuronal loss in PD, they do not readily explain the apparently staged distribution of Lewy pathology in many PD brains, the feature of the disease that initially motivated the spreading hypothesis by Braak and colleagues. While each hypothesis alone has its shortcomings, a synthesis of the two can explain much of what we know about the etiopathology of PD.

11 Review Therapeutic approaches to target alpha-synuclein pathology. 2017

Brundin, Patrik / Dave, Kuldip D / Kordower, Jeffrey H. ·Center for Neurodegenerative Science, Van Andel Research Institute, Grand Rapids, MI 49503, USA. Electronic address: Patrik.Brundin@vai.org. · The Michael J Fox Foundation, New York, NY 10017, USA. · Center for Neurodegenerative Science, Van Andel Research Institute, Grand Rapids, MI 49503, USA; Department of Neurological Sciences, Rush University Medical Center, Chicago, IL 60612, USA. ·Exp Neurol · Pubmed #28987463.

ABSTRACT: Starting two decades ago with the discoveries of genetic links between alpha-synuclein and Parkinson's disease risk and the identification of aggregated alpha-synuclein as the main protein constituent of Lewy pathology, alpha-synuclein has emerged as the major therapeutic target in Parkinson's disease and related synucleinopathies. Following the suggestion that alpha-synuclein pathology gradually spreads through the nervous system following a stereotypic pattern and the discovery that aggregated forms of alpha-synuclein can propagate pathology from one cell to another, and thereby probably aggravate existing deficits as well as generate additional symptoms, the idea that alpha-synuclein is a viable therapeutic target gained further support. In this review we describe current challenges and possibilities with alpha-synuclein as a therapeutic target. We briefly highlight gaps in the knowledge of the role of alpha-synuclein in disease, and propose that a deeper understanding of the pathobiology of alpha-synuclein can lead to improved therapeutic strategies. We describe several treatment approaches that are currently being tested in advanced animal experiments or already are in clinical trials. We have divided them into approaches that reduce alpha-synuclein production; inhibit alpha-synuclein aggregation inside cells; promote its degradation either inside or outside cells; and reduce its uptake by neighbouring cells following release from already affected neurons. Finally, we briefly discuss challenges related to the clinical testing of alpha-synuclein therapies, for example difficulties in monitoring target engagement and the need for relatively large trials of long duration. We conclude that alpha-synuclein remains one of the most compelling therapeutic targets for Parkinson's disease, and related synucleinopathies, and that the multitude of approaches being tested provides hope for the future.

12 Review Regulation of Striatal Neuron Activity by Cyclic Nucleotide Signaling and Phosphodiesterase Inhibition: Implications for the Treatment of Parkinson's Disease. 2017

Padovan-Neto, Fernando E / West, Anthony R. ·Department of Neuroscience, Rosalind Franklin University of Medicine and Science, 3333 Green Bay Road, North Chicago, IL, 60064, USA. fernando.padovanneto@rosalindfranklin.edu. · Department of Neuroscience, Rosalind Franklin University of Medicine and Science, 3333 Green Bay Road, North Chicago, IL, 60064, USA. anthony.west@rosalindfranklin.edu. ·Adv Neurobiol · Pubmed #28956336.

ABSTRACT: Cyclic nucleotide phosphodiesterase (PDE) enzymes catalyze the hydrolysis and inactivation of cyclic nucleotides (cAMP/cGMP) in the brain. Several classes of PDE enzymes with distinct tissue distributions, cyclic nucleotide selectivity, and regulatory factors are highly expressed in brain regions subserving cognitive and motor processes known to be disrupted in neurodegenerative diseases such as Parkinson's disease (PD). Furthermore, small-molecule inhibitors of several different PDE family members alter cyclic nucleotide levels and favorably enhance motor performance and cognition in animal disease models. This chapter will explore the roles and therapeutic potential of non-selective and selective PDE inhibitors on neural processing in fronto-striatal circuits in normal animals and models of DOPA-induced dyskinesias (LIDs) associated with PD. The impact of selective PDE inhibitors and augmentation of cAMP and cGMP signaling on the membrane excitability of striatal medium-sized spiny projection neurons (MSNs) will be discussed. The effects of cyclic nucleotide signaling and PDE inhibitors on synaptic plasticity of striatonigral and striatopallidal MSNs will be also be reviewed. New data on the efficacy of PDE10A inhibitors for reversing behavioral and electrophysiological correlates of L-DOPA-induced dyskinesias in a rat model of PD will also be presented. Together, these data will highlight the potential of novel PDE inhibitors for treatment of movement disorders such as PD which are associated with abnormal corticostriatal transmission.

13 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.

14 Review Pimavanserin, a novel antipsychotic for management of Parkinson's disease psychosis. 2017

Kianirad, Yasaman / Simuni, Tanya. ·a Department of Neurology , Northwestern University, Feinberg School of Medicine , Chicago , IL , USA. ·Expert Rev Clin Pharmacol · Pubmed #28817967.

ABSTRACT: INTRODUCTION: Parkinson's disease psychosis (PDP) may develop in up to 60% of Parkinson's patients and is associated with increased morbidity and mortality. It also correlates with depression and dementia, and can contribute to caregiver stress and burnout. Pimavanserin is the first FDA approved drug for the treatment of hallucinations and delusions associated with PDP. Areas covered: For this review, a MEDLINE literature search (via PubMed) and information provided by ACADIA Pharmaceuticals were used. This review will discuss the pathophysiology and current management of PDP. In addition, this review will focus on the rationales behind the development of pimavanserin, mechanism of action, pharmacokinetics, pharmacodynamics, and the clinical trials evaluating the efficacy and safety of pimavanserin. Last, the review will address the drug's package insert warning. Expert commentary: Pimavanserin, a 5HT2A receptor inverse agonist, is the first FDA approved drug for the treatment of PDP which has been shown to reduce psychosis in PD through its unique mechanism of action. Pimavanserin, does not worsen PD motor symptoms and has an acceptable safety profile. The development of pimavanserin as an antipsychotic opened a new therapeutic avenue in the treatment of PDP as well as targeting psychosis in other disorders such as Alzheimer's disease.

15 Review Calcium, mitochondrial dysfunction and slowing the progression of Parkinson's disease. 2017

Surmeier, D James / Halliday, Glenda M / Simuni, Tanya. ·Department of Physiology, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA; Department of Neurology, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA. Electronic address: j-surmeier@northwestern.edu. · Brain and Mind Centre, Sydney Medical School, University of Sydney, 2006, Australia; School of Medical Sciences, University of New South Wales, Neuroscience Research Australia, Sydney 2052, Australia. · Department of Neurology, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA. ·Exp Neurol · Pubmed #28780195.

ABSTRACT: Parkinson's disease is characterized by progressively distributed Lewy pathology and neurodegeneration. The motor symptoms of clinical Parkinson's disease (cPD) are unequivocally linked to the degeneration of dopaminergic neurons in the substantia nigra pars compacta (SNc). Several features of these neurons appear to make them selectively vulnerable to factors thought to cause cPD, like aging, genetic mutations and environmental toxins. Among these features, Ca

16 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.

17 Review The Emerging Role of Pimavanserin in the Management of Parkinson's Disease Psychosis. 2017

Hermanowicz, Neal / Alva, Gustavo / Pagan, Fernando / Espay, Alberto J / Patel, Amita / Madrid, Katya Cruz / Kremens, Daniel / Kenney, Jim / Arquette, Sheila / Tereso, Gary / Lopes, Maria / Farnum, Carolyn. ·1 Movement Disorders Program and Department of Neurology, University of California Irvine Health, Irvine, California. · 2 Chapman Global Medical Center, Orange, California; ATP Clinical Research, Costa Mesa, California; and University of California, Riverside, Orange, California. · 3 Department of Neurology; Movement Disorders Program; Georgetown University Hospital National Parkinsonism Foundation Center of Excellence; and Translational Neurotherapeutics Program, Georgetown University, Washington, DC. · 4 Department of Neurology and Rehabilitation Medicine, University of Cincinnati Gardner Neuroscience Institute, Cincinnati, Ohio. · 5 Institute for Psychiatric Education, Dayton Psychiatric Association, Dayton, Ohio. · 6 Academic Internal Medicine and Geriatrics, University of Illinois, and Jesse Brown Veterans' Center, Chicago, Illinois. · 7 Movement Disorders Program and Department of Neurology, Jefferson University, Philadelphia, Pennsylvania. · 8 Specialty and Pharmacy Contracts, Harvard Pilgrim Health Care, Quincy, Massachusetts. · 9 Pharmacy Services, Independent Health, Buffalo, New York. · 10 Health New England, Springfield, Massachusetts. · 11 Magellan Rx Management, Newport, Rhode Island. ·J Manag Care Spec Pharm · Pubmed #28636480.

ABSTRACT: A panel of experts drawn from neurology, psychiatry, geropsychiatry, geriatrics, and pharmacy representatives of 3 health plans convened in New York City on July 30, 2016, with the objective of sharing opinions, ideas, and information regarding the optimal management of Parkinson's disease psychosis (PDP). Three key points emerged from the discussion: (1) Because of the nature of Parkinson's disease and PDP, finding appropriate treatment can prove challenging; (2) emerging therapies may present an opportunity for effective disease management; and (3) moving forward, provider and patient education regarding PDP and available treatment options is essential for well-managed symptoms and better quality of life. The panel reviewed current practices and formulated recommendations on moving forward in the treatment of PDP. DISCLOSURES: This project and manuscript was funded by ACADIA Pharmaceuticals and developed by Magellan Rx Management. Lopes and Farnum are employees of Magellan Rx Management. Kremens has received consulting/speaker fees from Teva Pharmaceuticals, UCB, Sunovion, Impax, Lundbeck, ACADIA, USWorldMeds, Merz, Acorda, Kyowa, Neurocrine, and GE Healthcare. Pagan reports consulting/speaker fees from Teva Nanoscience, AbbVie, Impax, ACADIA, Medtronic, USWorldMeds, Merz, and Cynapsus and research and educational grants from USWorldMeds, Teva, and Medtronic. Patel has received consultant/speaker fees from ACADIA, Allergen, and Avanir. Alva reports research support from Accera, Allergan, Axovant, Eisai, Neurotrope, Genentech, Intra Cellular, Janssen, Lundbeck, Neurim, Novartis, Otsuka, Roche, Suven, and Trans Tech and consultant/speaker fees from ACADIA, Alkermes, Allergan, Avanir, Janssen, Lundbeck, Merck, Nestle, Otsuka, Sunovion, Takeda, and Vanda. The other authors report no potential conflicts of interest, financial or otherwise.

18 Review The gut-brain axis in Parkinson's disease: Possibilities for food-based therapies. 2017

Perez-Pardo, Paula / Kliest, Tessa / Dodiya, Hemraj B / Broersen, Laus M / Garssen, Johan / Keshavarzian, Ali / Kraneveld, Aletta D. ·Division of Pharmacology, Utrecht Institute for Pharmaceutical Sciences, Faculty of Science, Utrecht University, Universiteitsweg 99, 3584 CG Utrecht, The Netherlands. · Department of Internal Medicine, Division of Gastroenterology, Rush University Medical Center, 1725 West Harrison Street Chicago, IL 60612, USA. · Division of Pharmacology, Utrecht Institute for Pharmaceutical Sciences, Faculty of Science, Utrecht University, Universiteitsweg 99, 3584 CG Utrecht, The Netherlands; Nutricia Research, Uppsalalaan 12, 3584 CT Utrecht, The Netherlands. · Division of Pharmacology, Utrecht Institute for Pharmaceutical Sciences, Faculty of Science, Utrecht University, Universiteitsweg 99, 3584 CG Utrecht, The Netherlands; Department of Internal Medicine, Division of Gastroenterology, Rush University Medical Center, 1725 West Harrison Street Chicago, IL 60612, USA. · Division of Pharmacology, Utrecht Institute for Pharmaceutical Sciences, Faculty of Science, Utrecht University, Universiteitsweg 99, 3584 CG Utrecht, The Netherlands. Electronic address: A.D.Kraneveld@uu.nl. ·Eur J Pharmacol · Pubmed #28549787.

ABSTRACT: Parkinson's disease (PD) is usually characterized by cardinal motor impairments. However, a range of non-motor symptoms precede the motor-phase and are major determinants for the quality of life. To date, no disease modifying treatment is available for PD patients. The gold standard therapy of levodopa is based on restoring dopaminergic neurotransmission, thereby alleviating motor symptoms, whereas non-motor symptoms remain undertreated. One of the most common non-motor symptoms is gastrointestinal dysfunction usually associated with alpha-synuclein accumulations and low-grade mucosal inflammation in the enteric nervous system. Accumulating evidence suggest that the enteric nervous system is involved in PD pathological progression towards the central nervous system. Moreover, different components of the gut could provide a central role in the gut-brain axis, which is as a bidirectional communicational system between the gastrointestinal tract and central nervous system. Dietary components might influence the gut-brain axis by altering microbiota composition or by affecting neuronal functioning in both the ENS and the CNS. This review gives a comprehensive overview of the evidences supporting the hypothesis that PD could initiate in the gut. We also consider how food-based therapies might then have an impact on PD pathology and/or improve non-motor as well as motor symptoms in PD.

19 Review Aging and Parkinson's disease: Different sides of the same coin? 2017

Collier, Timothy J / Kanaan, Nicholas M / Kordower, Jeffrey H. ·Department of Translational Science and Molecular Medicine, Michigan State University, Grand Rapids, Michigan, USA. · Mercy Health Hauenstein Neuroscience Center, Grand Rapids, Michigan, USA. · Department of Neurological Sciences, Rush University Medical Center, Chicago, Illinois, USA. · Center for Neurodegenerative Science, Van Andel Research Institute, Grand Rapids, Michigan, USA. ·Mov Disord · Pubmed #28520211.

ABSTRACT: Despite abundant epidemiological evidence in support of aging as the primary risk factor for PD, biological correlates of a connection have been elusive. In this article, we address the following question: does aging represent biology accurately characterized as pre-PD? We present evidence from our work on midbrain dopamine neurons of aging nonhuman primates that demonstrates that markers of known correlates of dopamine neuron degeneration in PD, including impaired proteasome/lysosome function, oxidative/nitrative damage, and inflammation, all increase with advancing age and are exaggerated in the ventral tier substantia nigra dopamine neurons most vulnerable to degeneration in PD. Our findings support the view that aging-related changes in the dopamine system approach the biological threshold for parkinsonism, actively producing a vulnerable pre-parkinsonian state. © 2017 The Authors. Movement Disorders published by Wiley Periodicals, Inc. on behalf of International Parkinson and Movement Disorder Society.

20 Review Characterizing Cognitive Impairment in Parkinson's Disease. 2017

Bailey, Meagan / Goldman, Jennifer G. ·Department of Neurological Sciences, Section of Parkinson Disease and Movement Disorders, Chicago, Illinois. ·Semin Neurol · Pubmed #28511257.

ABSTRACT: Cognitive impairment is a frequent complication in Parkinson's disease (PD), though it can be heterogeneous in its presentation and progression. Cognitive deficits vary among patients with regard to clinical features, severity, and progression to dementia. A growing recognition of cognitive impairment in PD in both the clinical and research settings has led to advances in diagnostic criteria and improved understanding of the clinical phenotypes, associated biomarkers, and underlying pathophysiology of both PD dementia and PD mild cognitive impairment. Therapeutic interventions are geared to improve symptoms and ideally to prevent cognitive decline. Here the authors summarize the current research on the characterization of cognitive impairment in PD, with specific attention focused on its clinical phenotype, associated neuropsychiatric and prodromal features, pathological changes, genetic variations, and imaging and biochemical biomarkers.

21 Review The role of Ca 2017

Zaichick, Sofia V / McGrath, Kaitlyn M / Caraveo, Gabriela. ·Ken and Ruth Davee Department of Neurology, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA. · Ken and Ruth Davee Department of Neurology, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA gabriela.piso@northwestern.edu. ·Dis Model Mech · Pubmed #28468938.

ABSTRACT: Across all kingdoms in the tree of life, calcium (Ca

22 Review Impulse control disorders and levodopa-induced dyskinesias in Parkinson's disease: an update. 2017

Voon, Valerie / Napier, T Celeste / Frank, Michael J / Sgambato-Faure, Veronique / Grace, Anthony A / Rodriguez-Oroz, Maria / Obeso, Jose / Bezard, Erwan / Fernagut, Pierre-Olivier. ·Department of Psychiatry and Behavioural and Clinical Neurosciences Institute, University of Cambridge, Cambridge, UK; Cambridgeshire and Peterborough NHS Foundation Trust, Cambridge, UK. Electronic address: vv247@cam.ac.uk. · Departments of Pharmacology and Psychiatry, Center for Compulsive Behavior and Addiction, Rush University Medical Center, Chicago, IL, USA. · Department of Cognitive, Linguistic and Psychological Sciences and Department of Psychiatry and Human Behavior, Brown Institute for Brain Science, Providence, RI, USA. · Institut des Sciences Cognitives Marc Jeannerod, CNRS, Bron, France; Université Claude Bernard Lyon 1, Villeurbanne, France. · Departments of Neuroscience, Psychiatry and Psychology, University of Pittsburgh, Pittsburgh, PA, USA. · Biodonostia Health Research Institute, University Hospital Donostia, and Basque Center on Cognition, Brain and Language, San Sebastián, Spain; Ikerbasque-Basque Foundation for Science, Bilbao, Spain; Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas, Instituto Carlos III, Spain. · Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas, Instituto Carlos III, Spain; HM Centro Integral de Neurociencias, HM Puerta del Sur, Mostoles and Centro de Estudios Universitarios-San Pablo University, Madrid, Spain. · Université de Bordeaux, Institut des Maladies Neurodégénératives, Bordeaux, France; Centre National de la Recherche Scientifique, Institut des Maladies Neurodégénératives, Bordeaux, France. ·Lancet Neurol · Pubmed #28229895.

ABSTRACT: Dopaminergic medications used in the treatment of patients with Parkinson's disease are associated with motor and non-motor behavioural side-effects, such as dyskinesias and impulse control disorders also known as behavioural addictions. Levodopa-induced dyskinesias occur in up to 80% of patients with Parkinson's after a few years of chronic treatment. Impulse control disorders, including gambling disorder, binge eating disorder, compulsive sexual behaviour, and compulsive shopping occur in about 17% of patients with Parkinson's disease on dopamine agonists. These behaviours reflect the interactions of the dopaminergic medications with the individual's susceptibility, and the underlying neurobiology of Parkinson's disease. Parkinsonian rodent models show enhanced reinforcing effects of chronic dopaminergic medication, and a potential role for individual susceptibility. In patients with Parkinson's disease and impulse control disorders, impairments are observed across subtypes of decisional impulsivity, possibly reflecting uncertainty and the relative balance of rewards and losses. Impairments appear to be more specific to decisional than motor impulsivity, which might reflect differences in ventral and dorsal striatal engagement. Emerging evidence suggests impulse control disorder subtypes have dissociable correlates, which indicate that individual susceptibility predisposes towards the expression of different behavioural subtypes and neurobiological substrates. Therapeutic interventions to treat patients with Parkinson's disease and impulse control disorders have shown efficacy in randomised controlled trials. Large-scale studies are warranted to identify individual risk factors and novel therapeutic targets for these diseases. Mechanisms underlying impulse control disorders and dyskinesias could provide crucial insights into other behavioural symptoms in Parkinson's disease and addictions in the general population.

23 Review α-synuclein toxicity in neurodegeneration: mechanism and therapeutic strategies. 2017

Wong, Yvette C / Krainc, Dimitri. ·Department of Neurology, Northwestern University Feinberg School of Medicine, Chicago, Illinois, USA. ·Nat Med · Pubmed #28170377.

ABSTRACT: Alterations in α-synuclein dosage lead to familial Parkinson's disease (PD), and its accumulation results in synucleinopathies that include PD, dementia with Lewy bodies (DLB) and multiple system atrophy (MSA). Furthermore, α-synuclein contributes to the fibrilization of amyloid-b and tau, two key proteins in Alzheimer's disease, which suggests a central role for α-synuclein toxicity in neurodegeneration. Recent studies of factors contributing to α-synuclein toxicity and its disruption of downstream cellular pathways have expanded our understanding of disease pathogenesis in synucleinopathies. In this Review, we discuss these emerging themes, including the contributions of aging, selective vulnerability and non-cell-autonomous factors such as α-synuclein cell-to-cell propagation and neuroinflammation. Finally, we summarize recent efforts toward the development of targeted therapies for PD and related synucleinopathies.

24 Review Selective neuronal vulnerability in Parkinson disease. 2017

Surmeier, D James / Obeso, José A / Halliday, Glenda M. ·Department of Physiology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois 60611, USA. · Centro Integral de Neurociencias A.C. (CINAC), HM Puerta del Sur, Hospitales de Madrid, Mostoles and CEU San Pablo University, 28938 Madrid, Spain. · Network Center for Biomedical Research on Neurodegenerative Diseases (CIBERNED), Instituto Carlos III, 28031 Madrid, Spain. · Brain and Mind Centre, Sydney Medical School, The University of Sydney, Sydney 2006, Australia. · School of Medical Sciences, University of New South Wales and Neuroscience Research Australia, Sydney 2052, Australia. ·Nat Rev Neurosci · Pubmed #28104909.

ABSTRACT: Intracellular α-synuclein (α-syn)-rich protein aggregates called Lewy pathology (LP) and neuronal death are commonly found in the brains of patients with clinical Parkinson disease (cPD). It is widely believed that LP appears early in the disease and spreads in synaptically coupled brain networks, driving neuronal dysfunction and death. However, post-mortem analysis of human brains and connectome-mapping studies show that the pattern of LP in cPD is not consistent with this simple model, arguing that, if LP propagates in cPD, it must be gated by cell- or region-autonomous mechanisms. Moreover, the correlation between LP and neuronal death is weak. In this Review, we briefly discuss the evidence for and against the spreading LP model, as well as evidence that cell-autonomous factors govern both α-syn pathology and neuronal death.

25 Review The Search for a Peripheral Biopsy Indicator of α-Synuclein Pathology for Parkinson Disease. 2017

Lee, John M / Derkinderen, Pascal / Kordower, Jeffrey H / Freeman, Roy / Munoz, David G / Kremer, Thomas / Zago, Wagner / Hutten, Samantha J / Adler, Charles H / Serrano, Geidy E / Beach, Thomas G. ·Department of Pathology, NorthShore University Health System, University of Chicago, Pritzker School of Medicine, Evanston, Illinois, USA. · Inserm, U913, Nantes F-44035; Nantes University, Nantes F-44035; Department of Neurology, CHU Nantes, Nantes F-44093, France. · Center for Brain Repair, Department of Pathology, Rush Medical College, Chicago, Illinois, USA. · Harvard Medical School; Center for Autonomic and Peripheral Nerve Disorders, Department of Neurology, Beth Israel Deaconess Medical Center, Boston, Massachusetts, USA. · Laboratory Medicine and Keenan Research Centre for Biomedical Research of the Li Ka Shing Knowledge Institute, St. Michael's Hospital, University of Toronto, Toronto, Ontario, Canada. · Roche Pharmaceutical Research and Early Development, Nord DTA, Biomarker and Clinical Imaging, Roche Innovation Center, F Hoffman-La Roche, Ltd., Basel, Switzerland. · Prothena Biosciences, Inc., South San Francisco, California · Prothena Biosciences, Inc., South San Francisco, California (WZ); Michael J. Fox Foundation for Parkinson's Research, New York, New York, USA. · Department of Neurology, Mayo Clinic College of Medicine, Mayo Clinic Arizona, Scottsdale, Arizona, USA. · Civin Laboratory for Neuropathology, Banner Sun Health Research Institute, Sun City, Arizona, USA. ·J Neuropathol Exp Neurol · Pubmed #28069931.

ABSTRACT: The neuropathological hallmark of Parkinson disease (PD) is abnormal accumulation of α-synuclein (α-syn). Demonstrating pathological α-syn in live patients would be useful for identifying and monitoring PD patients. To date, however, imaging and biofluid approaches have not permitted premortem assessment of pathological α-syn. α-syn pathology in the peripheral nervous system of patients with PD has been demonstrated in studies dating back more than 40 years. More recent work suggests that colon, submandibular gland and skin biopsies could be useful as expedient biomarkers but histological differentiation of pathological and normal peripheral α-syn has been challenging and multiple research groups have reported variable results. A variety of immunohistochemical methods have been employed but almost all studies to date originated at single centers with no independent, blinded replication. To address these issues, the Michael J. Fox Foundation for Parkinson's Research sponsored a series of meetings and investigations by several research groups with relevant experience. The major finding reported herein was that biopsies can be used to distinguish PD patients from normal subjects. However, full assessment of the clinical potential of biopsy will only be achieved through large, multicenter trials in which both the initial detection methodology and histology have been assessed by blinded panels of pathologists.

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