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Parkinson Disease: HELP
Articles from Montreal
Based on 453 articles published since 2009
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These are the 453 published articles about Parkinson Disease that originated from Montreal during 2009-2019.
 
+ Citations + Abstracts
Pages: 1 · 2 · 3 · 4 · 5 · 6 · 7 · 8 · 9 · 10 · 11 · 12 · 13 · 14 · 15 · 16 · 17 · 18 · 19
1 Editorial Editorial: Current State of Postural Research - Beyond Automatic Behavior. 2019

Keshner, Emily A / Fung, Joyce. ·Department of Health and Rehabilitation Sciences, Temple University, Philadelphia, PA, United States. · School of Physical and Occupational Therapy, McGill University, Montreal, QC, Canada. ·Front Neurol · Pubmed #31736864.

ABSTRACT: -- No abstract --

2 Editorial 5-HT 2018

Huot, Philippe. ·Neurodegenerative Disease Group, Montreal Neurological Institute, Montreal, QC H3A 2B4, Canada. · Department of Neuroscience, McGill University, Montreal, QC H3A 2B4, Canada. · Division of Neurology, McGill University Health Centre, Montreal, QC H3A 2B4, Canada. ·Neurodegener Dis Manag · Pubmed #30451579.

ABSTRACT: -- No abstract --

3 Editorial 5-HT 2018

Huot, Philippe. ·Neurodegenerative Disease Group, Montreal Neurological Institute, Montreal, QC, H3A 2B4, Canada. · Department of Neurology & Neurosurgery, McGill University, Montreal, QC, H3A 2B4, Canada. · Division of Neurology, McGill University Health Centre, Montreal, QC, H3A 2B4, Canada. ·Neurodegener Dis Manag · Pubmed #30040029.

ABSTRACT: -- No abstract --

4 Editorial Sleep Disorders and RBD: What Would James Parkinson Think? 2017

Postuma, Ronald B. ·Department of Neurology, Montreal General Hospital, Montreal, Quebec, Canada. ·Mov Disord · Pubmed #28513080.

ABSTRACT: -- No abstract --

5 Editorial Voice changes in prodromal Parkinson's disease: Is a new biomarker within earshot? 2016

Postuma, Ronald B. ·Department of Neurology, McGill University, Montreal General Hospital, L7-305, 1650 Cedar Ave., Montreal, Quebec, Canada H3G1A4. Electronic address: ron.postuma@mcgill.ca. ·Sleep Med · Pubmed #26825009.

ABSTRACT: -- No abstract --

6 Editorial Serotonin/dopamine transporter ratio as a predictor of L-dopa-induced dyskinesia. 2015

Huot, Philippe / Hutchison, William D. ·From the Department of Pharmacology (P.H.), Faculty of Medicine, University of Montreal, Quebec, Canada · Division of Neurology (P.H.), Centre Hospitalier de l'Université de Montréal, Quebec, Canada · Departments of Surgery and Physiology (W.D.H.), University of Toronto, Ontario, Canada · and Division of Neurosurgery (W.D.H.), Toronto Western Hospital MP11-308 and Toronto Western Research Institute, Ontario, Canada. ·Neurology · Pubmed #26253446.

ABSTRACT: -- No abstract --

7 Editorial Placebo: from belief to movement. 2014

Postuma, Ronald B / Albin, Roger L. ·From the Department of Neurology (R.B.P.), McGill University, Montreal General Hospital, Canada · Neurology Service & GRECC (R.L.A.), VAAAHS · Department of Neurology (R.L.A.), University of Michigan · and Michigan Alzheimer's Disease Center (R.L.A.), Ann Arbor. ·Neurology · Pubmed #24658928.

ABSTRACT: -- No abstract --

8 Editorial Diagnosing REM sleep behavior disorder in Parkinson's disease-can we avoid the polysomnogram? 2014

Postuma, Ronald B. ·Department of Neurology, McGill University, Montreal General Hospital, Montreal, Quebec, Canada; Centre d'Études Avancées en Médecine du Sommeil, Hôpital du Sacré Cœur de Montréal, Montréal, Québec, Canada. ·Mov Disord · Pubmed #24619856.

ABSTRACT: -- No abstract --

9 Review Neuronal vulnerability in Parkinson disease: Should the focus be on axons and synaptic terminals? 2019

Wong, Yvette C / Luk, Kelvin / Purtell, Kerry / Burke Nanni, Samuel / Stoessl, A Jon / Trudeau, Louis-Eric / Yue, Zhenyu / Krainc, Dimitri / Oertel, Wolfgang / Obeso, Jose A / Volpicelli-Daley, Laura A. ·Department of Neurology, Northwestern University Feinberg School of Medicine, Chicago, Illinois, USA. · Department of Pathology and Laboratory Medicine, Center for Neurodegenerative Disease Research, Philadelphia, Pennsylvania, USA. · Department of Neurology, Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, Hess Research Center 9th Floor, New York, New York, USA. · CNS Research Group, Department of Pharmacology and Physiology, Department of Neurosciences, Faculty of Medicine, Université de Montréal, Montreal, QC, Canada. · University of British Columbia and Vancouver Coastal Health, Pacific Parkinson's Research Centre & National Parkinson Foundation Centre of Excellence, Vancouver, BC, Canada. · Department of Neurology, Philipps University Marburg, Marburg, Germany. · HM CINAC, HM Puerta del Sur, Hospitales de Madrid, Mostoles Medical School, CEU-San Pablo University, and CIBERNED, Instituto Carlos III, Madrid, Spain. · Department of Neurology, Center for Neurodegeneration and Experimental Therapeutics, University of Alabama at Birmingham, Birmingham, Alabama, USA. ·Mov Disord · Pubmed #31483900.

ABSTRACT: While current effective therapies are available for the symptomatic control of PD, treatments to halt the progressive neurodegeneration still do not exist. Loss of dopamine neurons in the SNc and dopamine terminals in the striatum drive the motor features of PD. Multiple lines of research point to several pathways which may contribute to dopaminergic neurodegeneration. These pathways include extensive axonal arborization, mitochondrial dysfunction, dopamine's biochemical properties, abnormal protein accumulation of α-synuclein, defective autophagy and lysosomal degradation, and synaptic impairment. Thus, understanding the essential features and mechanisms of dopaminergic neuronal vulnerability is a major scientific challenge and highlights an outstanding need for fostering effective therapies against neurodegeneration in PD. This article, which arose from the Movement Disorders 2018 Conference, discusses and reviews the possible mechanisms underlying neuronal vulnerability and potential therapeutic approaches in PD. © 2019 International Parkinson and Movement Disorder Society.

10 Review Update of the MDS research criteria for prodromal Parkinson's disease. 2019

Heinzel, Sebastian / Berg, Daniela / Gasser, Thomas / Chen, Honglei / Yao, Chun / Postuma, Ronald B / Anonymous3601610. ·Department of Neurology, Christian-Albrechts-University, Kiel, Germany. · Department of Neurodegeneration, Hertie Institute for Clinical Brain Research, University of Tuebingen, Tuebingen, Germany. · Department of Epidemiology and Biostatistics, College of Human Medicine, Michigan State University, East Lansing, Michigan, USA. · Department of Neurology, Montreal General Hospital, Montreal, Quebec, Canada. ·Mov Disord · Pubmed #31412427.

ABSTRACT: The MDS Research Criteria for Prodromal PD allow the diagnosis of prodromal Parkinson's disease using an evidence-based conceptual framework, which was designed to be updated as new evidence becomes available. New prospective evidence of predictive values of risk and prodromal markers published since 2015 was reviewed and integrated into the criteria. Many of the predictive values (likelihood ratios, LR) remain unchanged. The positive likelihood ratio notably increase for olfactory loss and decreased for substantia nigra hyperechogenicity. Negative likelihood ratio remained largely unchanged for all markers. New levels of diagnostic certainty for neurogenic and symptomatic orthostatic hypotension have been added, which substantially differ in positive likelihood ratio from the original publication. For intermediate strength genetic variants, their age-related penetrance is now incorporated in the calculation of the positive likelihood ratio. Moreover, apart from prospective studies, evidence from cross-sectional case-control genome-wide association studies is also considered (given their likely lack of confounding and reverse causation), and to account for the effect of multiple low-penetrance genetic variants polygenic risk scores are added to the model. Diabetes, global cognitive deficit, physical inactivity, and low plasma urate levels in men enter the criteria as new markers. A web-based prodromal PD risk calculator allows the calculation of probabilities of prodromal PD for individuals. Several promising candidate markers may improve the diagnostic accuracy of prodromal PD in the future. © 2019 International Parkinson and Movement Disorder Society.

11 Review Mechanisms of PINK1, ubiquitin and Parkin interactions in mitochondrial quality control and beyond. 2019

Bayne, Andrew N / Trempe, Jean-François. ·Department of Pharmacology and Therapeutics and Centre for Structural Biology, McGill University, 3655 Prom Sir William Osler, Montreal, QC, H3G 1Y6, Canada. · Department of Pharmacology and Therapeutics and Centre for Structural Biology, McGill University, 3655 Prom Sir William Osler, Montreal, QC, H3G 1Y6, Canada. jeanfrancois.trempe@mcgill.ca. ·Cell Mol Life Sci · Pubmed #31254044.

ABSTRACT: Parkinson's disease (PD) is a degenerative movement disorder resulting from the loss of specific neuron types in the midbrain. Early environmental and pathophysiological studies implicated mitochondrial damage and protein aggregation as the main causes of PD. These findings are now vindicated by the characterization of more than 20 genes implicated in rare familial forms of the disease. In particular, two proteins encoded by the Parkin and PINK1 genes, whose mutations cause early-onset autosomal recessive PD, function together in a mitochondrial quality control pathway. In this review, we will describe recent development in our understanding of their mechanisms of action, structure, and function. We explain how PINK1 acts as a mitochondrial damage sensor via the regulated proteolysis of its N-terminus and the phosphorylation of ubiquitin tethered to outer mitochondrial membrane proteins. In turn, phospho-ubiquitin recruits and activates Parkin via conformational changes that increase its ubiquitin ligase activity. We then describe how the formation of polyubiquitin chains on mitochondria triggers the recruitment of the autophagy machinery or the formation of mitochondria-derived vesicles. Finally, we discuss the evidence for the involvement of these mechanisms in physiological processes such as immunity and inflammation, as well as the links to other PD genes.

12 Review Prodromal Parkinson's Disease: The Decade Past, the Decade to Come. 2019

Postuma, Ronald B / Berg, Daniela. ·Department of Neurology, Montreal General Hospital, Montreal, Quebec, Canada. · Department of Neurology, Christian-Albrechts-University of Kiel, Kiel, Germany. ·Mov Disord · Pubmed #30919499.

ABSTRACT: The past decade has seen a dramatic expansion of the field of prodromal PD. Ten years ago, there were only six known prodromal markers of disease, none of which had more than two studies documenting diagnostic value. We now have at least 16 markers, with as many as 10 prospective studies for a single marker. This review summarizes the major advances over the last decade and speculates about the advances we will see in the decade to come. The most notable advances over the last decade came through the study of high-risk cohorts (REM sleep behavior disorder and later genetic and autonomic cohorts), the generation of more representative population-based cohorts for studying prodromal PD, major advances in neuroimaging of early disease stages, the emerging likelihood that tissue biopsy will be able to diagnose prodromal PD, and the coalescence of prodromal markers into discrete criteria. As the next decade dawns, we await increasing precision of sensitivity and specificity estimates of known markers, the discovery of new biomarkers of prodromal disease, improvements in diagnosis using combined methods/criteria (with increasing recognition of prodromal PD as one stage of the full PD spectrum), and ultimately the development of neuroprotective therapy that can be provided at the earliest stages of disease. © 2019 International Parkinson and Movement Disorder Society.

13 Review Revisiting protein aggregation as pathogenic in sporadic Parkinson and Alzheimer diseases. 2019

Espay, Alberto J / Vizcarra, Joaquin A / Marsili, Luca / Lang, Anthony E / Simon, David K / Merola, Aristide / Josephs, Keith A / Fasano, Alfonso / Morgante, Francesca / Savica, Rodolfo / Greenamyre, J Timothy / Cambi, Franca / Yamasaki, Tritia R / Tanner, Caroline M / Gan-Or, Ziv / Litvan, Irene / Mata, Ignacio F / Zabetian, Cyrus P / Brundin, Patrik / Fernandez, Hubert H / Standaert, David G / Kauffman, Marcelo A / Schwarzschild, Michael A / Sardi, S Pablo / Sherer, Todd / Perry, George / Leverenz, James B. ·From the UC Gardner Neuroscience Institute and Gardner Family Center for Parkinson's Disease and Movement Disorders (A.J.E., J.A.V., L.M., A.M.), Department of Neurology, University of Cincinnati, OH · Edmond J. Safra Program in Parkinson's Disease and the Morton and Gloria Shulman Movement Disorders Clinic (A.E.L., A.F.), Toronto Western Hospital, University of Toronto · Krembil Research Institute (A.E.L., A.F.), Toronto, Canada · Parkinson's Disease and Movement Disorders Center (D.K.S.), Department of Neurology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA · College of Medicine (K.A.J.), Mayo Clinic, Rochester, MN · Institute of Molecular and Clinical Sciences (F.M.), St George's University of London, UK · Division of Movement Disorders (R.S.), Department of Neurology and Department of Health Science Research, Mayo Clinic College of Medicine, Rochester, MN · Department of Neurology and the Pittsburgh Institute for Neurodegenerative Diseases (J.T.G., F.C.), University of Pittsburgh, PA · Department of Neurology (T.R.Y.), University of Kentucky, Lexington · Parkinson's Disease Research, Education and Clinical Center (C.M.T.), Neurology, San Francisco Veterans Affairs Medical Center · Department of Neurology (C.M.T.), University of California-San Francisco · Department of Neurology & Neurosurgery, Montreal Neurological Institute, and Department of Human Genetics (Z.G.-O.), McGill University, Canada · Parkinson & Other Movement Disorders Center UC San Diego (I.L.), Department of Neurosciences, Altman Clinical Translational Research Institute, La Jolla, CA · VA Puget Sound Health Care System and Department of Neurology (I.F.M., CP.Z.), University of Washington, Seattle · Department of Neurology (I.F.M.), University of Washington School of Medicine, Seattle · Center for Neurodegenerative Science (P.B.), Van Andel Research Institute, Grand Rapids, MI · Center for Neurological Restoration (H.H.F.) and Lou Ruvo Center for Brain Health, Neurological Institute (J.B.L.), Cleveland Clinic, OH · Department of Neurology (D.G.S.), University of Alabama at Birmingham · Consultorio y Laboratorio de Neurogenética (M.A.K.), Centro Universitario de Neurología "José María Ramos Mejía" y División Neurología, Hospital JM Ramos Mejía, Facultad de Medicina, UBA · Programa de Medicina de Precision y Genomica Clinica (M.A.K.), Instituto de Investigaciones en Medicina Traslacional, Facultad de Ciencias Biomédicas, Universidad Austral-CONICET, Buenos Aires, Argentina · Department of Neurology (M.A.S.), Massachusetts General Hospital, Boston · Division of Neuroscience (S.P.S.), Sanofi-Genzyme, Framingham, MA · Michael J. Fox Foundation for Parkinson's Research (T.S.), New York, NY · and College of Sciences (G.P.), University of Texas at San Antonio. ·Neurology · Pubmed #30745444.

ABSTRACT: The gold standard for a definitive diagnosis of Parkinson disease (PD) is the pathologic finding of aggregated α-synuclein into Lewy bodies and for Alzheimer disease (AD) aggregated amyloid into plaques and hyperphosphorylated tau into tangles. Implicit in this clinicopathologic-based nosology is the assumption that pathologic protein aggregation at autopsy reflects pathogenesis at disease onset. While these aggregates may in exceptional cases be on a causal pathway in humans (e.g., aggregated α-synuclein in

14 Review Therapeutic trial design for frontotemporal dementia and related disorders. 2019

Desmarais, Philippe / Rohrer, Jonathan D / Nguyen, Quoc Dinh / Herrmann, Nathan / Stuss, Donald T / Lang, Anthony E / Boxer, Adam L / Dickerson, Bradford C / Rosen, Howie / van Swieten, John Cornelis / Meeter, Lieke H / Borroni, Barbara / Tartaglia, Maria Carmela / Feldman, Howard H / Black, Sandra E / Masellis, Mario. ·Cognitive & Movement Disorders Clinic, Sunnybrook Health Sciences Centre, Toronto, Ontario, Canada. · LC Campbell Cognitive Neurology Research Unit, Sunnybrook Health Sciences Centre, Toronto, Ontario, Canada. · Hurvitz Brain Sciences Program, Sunnybrook Research Institute, Toronto, Ontario, Canada. · Division of Neurology, Department of Medicine, University of Toronto, Toronto, Ontario, Canada. · Dementia Research Centre, Department of Neurodegenerative Disease, UCL Queen Square Institute of Neurology, London, UK. · Division of Geriatric Medicine, Department of Medicine, Centre Hospitalier de l'Université de Montréal, Montréal, Québec, Canada. · Department of Psychiatry, University of Toronto, Toronto, Ontario, Canada. · Rotman Research Institute, Baycrest Centre for Geriatric Care, Toronto, Ontario, Canada. · Department of Psychology, University of Toronto, Toronto, Ontario, Canada. · Tanz Centre for Research in Neurodegenerative Diseases, University of Toronto, Toronto, Ontario, Canada. · Memory and Aging Center, Department of Neurology, University of California, San Francisco, California, USA. · Department of Neurology, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts, USA. · Department of Neurology, Erasmus Medical Centre, Rotterdam, The Netherlands. · Centre for Neurodegenerative Disorders, Neurology Clinic, Department of Clinical and Experimental Sciences, University of Brescia, Brescia, Italy. · Institute of Medical Science, University of Toronto, Toronto, Ontario, Canada. · Department of Neurosciences, University of California, San Diego, California, USA. · Division of Neurology, Department of Medicine, University of British Columbia, Vancouver, British Columbia, Canada. · Cognitive & Movement Disorders Clinic, Sunnybrook Health Sciences Centre, Toronto, Ontario, Canada Mario.Masellis@sunnybrook.ca. ·J Neurol Neurosurg Psychiatry · Pubmed #30361298.

ABSTRACT: The frontotemporal dementia (FTD) spectrum is a heterogeneous group of neurodegenerative syndromes with overlapping clinical, molecular and pathological features, all of which challenge the design of clinical trials in these conditions. To date, no pharmacological interventions have been proven effective in significantly modifying the course of these disorders. This study critically reviews the construct and methodology of previously published randomised controlled trials (RCTs) in FTD spectrum disorders in order to identify limitations and potential reasons for negative results. Moreover, recommendations based on the identified gaps are elaborated in order to guide future clinical trial design. A systematic literature review was carried out and presented in conformity with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses criteria. A total of 23 RCTs in cohorts with diagnoses of behavioural and language variants of FTD, corticobasal syndrome and progressive supranuclear palsy syndrome were identified out of the 943 citations retrieved and were included in the qualitative review. Most studies identified were early-phase clinical trials that were small in size, short in duration and frequently underpowered. Diagnoses of populations enrolled in clinical trials were based on clinical presentation and rarely included precision-medicine tools, such as genetic and molecular testing. Uniformity and standardisation of research outcomes in the FTD spectrum are essential. Several elements should be carefully considered and planned in future clinical trials. We anticipate that precision-medicine approaches will be crucial to adequately address heterogeneity in the FTD spectrum research.

15 Review The sinister face of heme oxygenase-1 in brain aging and disease. 2019

Schipper, Hyman M / Song, Wei / Tavitian, Ayda / Cressatti, Marisa. ·Lady Davis Institute for Medical Research, Jewish General Hospital, Montreal, Quebec, Canada; Department of Neurology and Neurosurgery McGill University, Montreal, Quebec, Canada; Department of Medicine, McGill University, Montreal, Quebec, Canada. Electronic address: hyman.schipper@mcgill.ca. · Lady Davis Institute for Medical Research, Jewish General Hospital, Montreal, Quebec, Canada. · Lady Davis Institute for Medical Research, Jewish General Hospital, Montreal, Quebec, Canada; Department of Neurology and Neurosurgery McGill University, Montreal, Quebec, Canada. ·Prog Neurobiol · Pubmed #30009872.

ABSTRACT: Under stressful conditions, cellular heme catabolism to carbon monoxide, iron and biliverdin is mediated by the 32 kDa enzyme, heme oxygenase-1 (HO-1). A wide range of pro-oxidant and inflammatory stimuli act on diverse consensus sequences within the Hmox1 promoter to rapidly induce the gene. There is ample evidence attesting to the beneficial effects of HO-1 upregulation in brain. By converting pro-oxidant heme to the antioxidants, biliverdin and bilirubin, HO-1/biliverdin reductase may help restore a more favorable tissue redox microenvironment. Contrariwise, in some cell types and under certain circumstances, heme-derived carbon monoxide and iron may amplify intracellular oxidative stress and exacerbate the disease process. This inimical side of neural HO-1 has often been ignored in biomedical literature promulgating interventions aimed at boosting central HO-1 expression for the management of diverse CNS conditions and is the focus of the current review. A comprehensive model of astroglial stress is presented wherein sustained Hmox1 induction promotes oxidative mitochondrial membrane damage, iron sequestration and mitophagy (macroautophagy). The HO-1 mediated gliopathy renders nearby neuronal constituents vulnerable to oxidative injury and recapitulates 'core' neuropathological features of many aging-related neurodegenerative and some neurodevelopmental brain disorders. A balanced literature should acknowledge that, in a host of chronic human CNS afflictions, the glial HO-1 response may serve as a robust transducer of noxious stimuli, an important driver of relevant neuropathology and a potentially disease-modifying therapeutic target.

16 Review A clinical-anatomical signature of Parkinson's disease identified with partial least squares and magnetic resonance imaging. 2019

Zeighami, Yashar / Fereshtehnejad, Seyed-Mohammad / Dadar, Mahsa / Collins, D Louis / Postuma, Ronald B / Mišić, Bratislav / Dagher, Alain. ·Montreal Neurological Institute, McGill University, Montreal, Quebec, Canada. · Montreal Neurological Institute, McGill University, Montreal, Quebec, Canada. Electronic address: alain.dagher@mcgill.ca. ·Neuroimage · Pubmed #29277406.

ABSTRACT: Parkinson's disease (PD) is a neurodegenerative disorder characterized by a wide array of motor and non-motor symptoms. It remains unclear whether neurodegeneration in discrete loci gives rise to discrete symptoms, or whether network-wide atrophy gives rise to the unique behavioural and clinical profile associated with PD. Here we apply a data-driven strategy to isolate large-scale, multivariate associations between distributed atrophy patterns and clinical phenotypes in PD. In a sample of N = 229 de novo PD patients, we estimate disease-related atrophy using deformation based morphometry (DBM) of T1 weighted MR images. Using partial least squares (PLS), we identify a network of subcortical and cortical regions whose collective atrophy is associated with a clinical phenotype encompassing motor and non-motor features. Despite the relatively early stage of the disease in the sample, the atrophy pattern encompassed lower brainstem, substantia nigra, basal ganglia and cortical areas, consistent with the Braak hypothesis. In addition, individual variation in this putative atrophy network predicted longitudinal clinical progression in both motor and non-motor symptoms. Altogether, these results demonstrate a pleiotropic mapping between neurodegeneration and the clinical manifestations of PD, and that this mapping can be detected even in de novo patients.

17 Review From Prodromal to Overt Parkinson's Disease: Towards a New Definition in the Year 2040. 2018

Berg, Daniela / Postuma, Ronald B. ·Department of Neurology, Christian-Albrechts-University of Kiel, Kiel, Germany. · Department of Neurodegeneration, Hertie-Institute for Clinical Brain Research Tuebingen, Germany. · Department of Neurology, Montreal General Hospital, Montreal, Quebec, Canada. ·J Parkinsons Dis · Pubmed #30584153.

ABSTRACT: The field of prodromal PD is still in its infancy, and at the cusp of major advances. This article summarizes where we are, and most importantly where we need to go in order for the promise of prodromal PD to be realized. In the immediate future, the criteria need to be updated with additional markers and disseminated broadly. In the near future, they need to better incorporate changes in likelihood ratio with age and sex, combine markers in novel ways using big data approaches, identify subtypes, and incorporate better higher-specificity markers as they are discovered. Integration of smartphone/wearable markers and biomarkers of progression from the prodromal phase will allow development of neuroprotective trials in early stages. By 2040, it is hoped that prodromal criteria will be incorporated into active neuroprotective treatment programs, allowing a program of population-based screening followed by early treatment and ultimately the prevention of clinical PD from ever becoming manifest.

18 Review Interaction Between Neuropsychiatric Symptoms and Cognitive Performance in Parkinson's Disease: What Do Clinical and Neuroimaging Studies Tell Us? 2018

Hanganu, Alexandru / Monchi, Oury. ·Department of Clinical Neurosciences and Department of Radiology, University of Calgary, 3330 Hospital DR NW, Calgary, Alberta, T2N 4N1, Canada. · Cumming School of Medicine, Hotchkiss Brain Institute, Calgary, Alberta, Canada. · Centre de Recherche, Institut Universitaire de Gériatrie de Montréal, Montréal, Québec, Canada. · Department of Psychology, University of Montréal, Montréal, Québec, Canada. · Department of Clinical Neurosciences and Department of Radiology, University of Calgary, 3330 Hospital DR NW, Calgary, Alberta, T2N 4N1, Canada. oury.monchi@ucalgary.ca. · Cumming School of Medicine, Hotchkiss Brain Institute, Calgary, Alberta, Canada. oury.monchi@ucalgary.ca. · Centre de Recherche, Institut Universitaire de Gériatrie de Montréal, Montréal, Québec, Canada. oury.monchi@ucalgary.ca. · Department of Radiology, Faculty of Medicine, University of Montréal, Montréal, Québec, Canada. oury.monchi@ucalgary.ca. ·Curr Neurol Neurosci Rep · Pubmed #30324260.

ABSTRACT: PURPOSE OF REVIEW: Parkinson's disease was studied for a long time from the prism of a motor impairment. Recent advances have outlined the importance of cognitive and neuropsychiatric symptoms (NPS) in the PD equation. This review concentrates on the present possibilities of using neuroimaging techniques in order to quantify the cognitive performance and NPS in PD patients. RECENT FINDINGS: Mild cognitive impairment as well as many NPS have been acknowledged as important criteria for assessing the quality of life in patients with Parkinson's disease and have been shown as potential factors in predicting further evolution of PD from a clinical perspective. Some NPS strongly influence cognition (depression, REM sleep behavior disorder), while others are less specifically associated with it (impulse control disorders). Neuroimaging techniques reported specific structural, functional, and metabolic brain changes that might be specific for each NPS type. Recent neuroimaging advances report a strong interrelation between NPS and cognitive performance in PD. A special place for consideration is given to REM sleep behavior disorder, depression, and hallucinations. Nevertheless, some studies report distinct results, outlining that the neuroimaging acquisition and analysis techniques still have limitations and also likely represent the complexity of the manifestation of NPS in PD.

19 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 [

20 Review The effects of exercise on cognition and gait in Parkinson's disease: A scoping review. 2018

Intzandt, Brittany / Beck, Eric N / Silveira, Carolina R A. ·PERFORM Centre, Concordia University, 7200 rue Sherbrooke O, Montreal, H4B 1R6, Canada. Electronic address: brittany.intzandt@mail.concordia.ca. · School of Medicine, Trinity College Dublin, University of Dublin, College Green, Dublin, 2, Ireland. Electronic address: becke@tcd.ie. · Lawson Health Research Institute, 750 Base Line Rd E, London, N6C 2R5, Canada. Electronic address: carolina.silveira@sjhc.london.on.ca. ·Neurosci Biobehav Rev · Pubmed #30291852.

ABSTRACT: Cognitive and gait deficits are two debilitating symptoms that occur in Parkinson's disease (PD). Importantly, a relationship between cognitive and gait deficits exists in PD, suggesting reliance on cognition is increased to compensate for gait deficits and/or deterioration of cognition and gait may share common mechanisms. Rehabilitation strategies targeting one factor could lead to the improvement of the other, presenting a unique opportunity to treat both simultaneously. Gold-standard pharmaceuticals partially alleviate these deficits with significant side effects, highlighting the importance of investigating adjunct therapies like exercise. We critically reviewed the influence of three exercise modalities (aerobic, resistance, and goal-based) on cognition and/or gait in PD. Most studies showed improvements in cognition or gait, yet, a limited number investigated them concurrently. This is the first review examining exercise for cognition and gait in PD. Key gaps in the literature are identified; potential exercise-driven mechanisms for enhancements in cognition and gait proposed, and suggestions for the design of future studies investigating the effects of exercise on cognition and gait in PD.

21 Review New insights into the structure of PINK1 and the mechanism of ubiquitin phosphorylation. 2018

Rasool, Shafqat / Trempe, Jean-François. ·a Department of Biochemistry , McGill University , Montréal , Canada. · b Groupe de Recherche Axé sur la Structure des Protéines (GRASP) , Montréal , Canada. · c Department of Pharmacology & Therapeutics , McGill University , Montréal , Canada. ·Crit Rev Biochem Mol Biol · Pubmed #30238821.

ABSTRACT: Mutations in PINK1 cause early-onset recessive Parkinson's disease. This gene encodes a protein kinase implicated in mitochondrial quality control via ubiquitin phosphorylation and activation of the E3 ubiquitin ligase Parkin. Here, we review and analyze functional features emerging from recent crystallographic, nuclear magnetic resonance (NMR) and mass spectrometry studies of PINK1. We compare the apo and ubiquitin-bound PINK1 structures and reveal an allosteric switch, regulated by autophosphorylation, which modulates substrate recognition. We critically assess the conformational changes taking place in ubiquitin and the Parkin ubiquitin-like domain in relation to its binding to PINK1. Finally, we discuss the implications of these biophysical findings in our understanding of the role of PINK1 in mitochondrial function, and analyze the potential for structure-based drug design.

22 Review Structural neuroimaging as clinical predictor: A review of machine learning applications. 2018

Mateos-Pérez, José María / Dadar, Mahsa / Lacalle-Aurioles, María / Iturria-Medina, Yasser / Zeighami, Yashar / Evans, Alan C. ·Montreal Neurological Institute, McGill University, Montreal, Quebec, Canada. Electronic address: chema@rinzewind.org. · Montreal Neurological Institute, McGill University, Montreal, Quebec, Canada. ·Neuroimage Clin · Pubmed #30167371.

ABSTRACT: In this paper, we provide an extensive overview of machine learning techniques applied to structural magnetic resonance imaging (MRI) data to obtain clinical classifiers. We specifically address practical problems commonly encountered in the literature, with the aim of helping researchers improve the application of these techniques in future works. Additionally, we survey how these algorithms are applied to a wide range of diseases and disorders (e.g. Alzheimer's disease (AD), Parkinson's disease (PD), autism, multiple sclerosis, traumatic brain injury, etc.) in order to provide a comprehensive view of the state of the art in different fields.

23 Review REM sleep behaviour disorder. 2018

Dauvilliers, Yves / Schenck, Carlos H / Postuma, Ronald B / Iranzo, Alex / Luppi, Pierre-Herve / Plazzi, Giuseppe / Montplaisir, Jacques / Boeve, Bradley. ·Centre National de Référence Narcolepsie Hypersomnies, Unité des Troubles du Sommeil, Service de Neurologie, Hôpital Gui-de-Chauliac Montpellier, Montpellier, France. ydauvilliers@yahoo.fr. · INSERM, U1061, Montpellier, France, Université Montpellier, Montpellier, France. ydauvilliers@yahoo.fr. · Minnesota Regional Sleep Disorders Center, and Departments of Psychiatry, Hennepin County Medical Center and University of Minnesota Medical School, Minneapolis, MN, USA. · Department of Neurology, Montreal General Hospital, Montreal, Quebec, Canada. · Neurology Service, Multidisciplinary Sleep Unit, Hospital Clinic de Barcelona, IDIBAPS, CIBERNED, Barcelona, Spain. · UMR 5292 CNRS/U1028 INSERM, Center of Research in Neuroscience of Lyon (CRNL), SLEEP Team, Université Claude Bernard Lyon I, Faculté de Médecine RTH Laennec, Lyon, France. · Department of Biomedical and Neuromotor Sciences (DIBINEM), University of Bologna, Bologna, Italy. · IRCCS, Istituto delle Scienze Neurologiche, Bologna, Italy. · Department of Psychiatry, Université de Montréal, Québec, Canada and Center for Advanced Research in Sleep Medicine (CARSM), Hôpital du Sacré-Coeur de Montréal, Quebec, Canada. · Department of Neurology and Center for Sleep Medicine, Mayo Clinic, Rochester, MN, USA. ·Nat Rev Dis Primers · Pubmed #30166532.

ABSTRACT: Rapid eye movement (REM) sleep behaviour disorder (RBD) is a parasomnia that is characterized by loss of muscle atonia during REM sleep (known as REM sleep without atonia, or RSWA) and abnormal behaviours occurring during REM sleep, often as dream enactments that can cause injury. RBD is categorized as either idiopathic RBD or symptomatic (also known as secondary) RBD; the latter is associated with antidepressant use or with neurological diseases, especially α-synucleinopathies (such as Parkinson disease, dementia with Lewy bodies and multiple system atrophy) but also narcolepsy type 1. A clinical history of dream enactment or complex motor behaviours together with the presence of muscle activity during REM sleep confirmed by video polysomnography are mandatory for a definite RBD diagnosis. Management involves clonazepam and/or melatonin and counselling and aims to suppress unpleasant dreams and behaviours and improve bedpartner quality of life. RSWA and RBD are now recognized as manifestations of an α-synucleinopathy; most older adults with idiopathic RBD will eventually develop an overt neurodegenerative syndrome. In the future, studies will likely evaluate neuroprotective therapies in patients with idiopathic RBD to prevent or delay α-synucleinopathy-related motor and cognitive decline.

24 Review Finding useful biomarkers for Parkinson's disease. 2018

Chen-Plotkin, Alice S / Albin, Roger / Alcalay, Roy / Babcock, Debra / Bajaj, Vikram / Bowman, Dubois / Buko, Alex / Cedarbaum, Jesse / Chelsky, Daniel / Cookson, Mark R / Dawson, Ted M / Dewey, Richard / Foroud, Tatiana / Frasier, Mark / German, Dwight / Gwinn, Katrina / Huang, Xuemei / Kopil, Catherine / Kremer, Thomas / Lasch, Shirley / Marek, Ken / Marto, Jarrod A / Merchant, Kalpana / Mollenhauer, Brit / Naito, Anna / Potashkin, Judith / Reimer, Alyssa / Rosenthal, Liana S / Saunders-Pullman, Rachel / Scherzer, Clemens R / Sherer, Todd / Singleton, Andrew / Sutherland, Margaret / Thiele, Ines / van der Brug, Marcel / Van Keuren-Jensen, Kendall / Vaillancourt, David / Walt, David / West, Andrew / Zhang, Jing. ·Department of Neurology, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, PA 19104, USA. chenplot@pennmedicine.upenn.edu. · Neurology Service and GRECC, VAAHS, Ann Arbor, MI 48105, USA. · Department of Neurology, University of Michigan, Ann Arbor, MI 48109, USA. · Department of Neurology, Columbia University Medical Center, New York, NY 10032, USA. · National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20824, USA. · Verily/Google Life Sciences, South San Francisco, CA 94080, USA. · Department of Biostatistics, Mailman School of Public Health, Columbia University, New York, NY 10032, USA. · Human Metabolome Technology-America, Boston, MA 02134, USA. · Biogen, Cambridge, MA 02142, USA. · Caprion Biosciences, Montreal, Quebec H2X 3Y7, Canada. · Cell Biology and Gene Expression Section, Laboratory of Neurogenetics, National Institute of Aging, National Institutes of Health, Bethesda, MD 20892, USA. · Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA. · Department of Neurology and Neurotherapeutics, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA. · Department of Medical and Molecular Genetics, Indiana University School of Medicine, Indianapolis, IN 46202, USA. · The Michael J. Fox Foundation for Parkinson's Research, New York, NY 10163, USA. · Department of Psychiatry, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA. · Department of Neurology, Penn State University-Hershey Medical Center, Hershey, PA 17033, USA. · Pharmaceutical Research and Early Development, NORD Discovery and Translational Area, Roche Innovation Center Basel, F. Hoffmann-La Roche Ltd., 4070 Basel, Switzerland. · Institute for Neurodegenerative Disorders, New Haven, CT 06510, USA. · Departments of Cancer Biology and Pathology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02215, USA. · Blais Proteomics Center, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02215, USA. · Department of Pathology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02215, USA. · Chaperone Therapeutics, Portland, OR 97229, USA. · Paracelsus-Elena-Klinik, 34128 Kassel, Germany. · University Medical Center, 37075 Goettingen, Germany. · Department of Cellular and Molecular Pharmacology, Chicago Medical School, Rosalind Franklin University of Medicine and Science, Chicago, IL 60064, USA. · Department of Neurology, Johns Hopkins School of Medicine, Baltimore, MD 21205, USA. · Department of Neurology, Mount Sinai Beth Israel, Icahn School of Medicine at Mount Sinai, New York, NY 10003, USA. · Center for Advanced Parkinson's Disease Research and Precision Neurology Program, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA. · Laboratory of Neurogenetics, National Institute on Aging, Bethesda, MD 20892, USA. · Luxembourg Centre for Systems Biomedicine, University of Luxembourg, Luxembourg, Luxembourg. · Genentech, San Francisco, CA 94080, USA. · Neurogenomics Division, Translational Genomics Research Institute, Phoenix, AZ 85004, USA. · Department of Applied Physiology, Biomedical Engineering, and Neurology, University of Florida, Gainesville, FL 32611, USA. · Department of Neurology, University of Alabama, Birmingham, AL 35233, USA. · Department of Pathology, University of Washington, Seattle, WA 98195, USA. ·Sci Transl Med · Pubmed #30111645.

ABSTRACT: The recent advent of an "ecosystem" of shared biofluid sample biorepositories and data sets will focus biomarker efforts in Parkinson's disease, boosting the therapeutic development pipeline and enabling translation with real-world impact.

25 Review On Cell Loss and Selective Vulnerability of Neuronal Populations in Parkinson's Disease. 2018

Giguère, Nicolas / Burke Nanni, Samuel / Trudeau, Louis-Eric. ·CNS Research Group, Department of Pharmacology and Physiology, Department of Neurosciences, Faculty of Medicine, Université de Montréal, Montreal, QC, Canada. ·Front Neurol · Pubmed #29971039.

ABSTRACT: Significant advances have been made uncovering the factors that render neurons vulnerable in Parkinson's disease (PD). However, the critical pathogenic events leading to cell loss remain poorly understood, complicating the development of disease-modifying interventions. Given that the cardinal motor symptoms and pathology of PD involve the loss of dopamine (DA) neurons of the substantia nigra pars compacta (SNc), a majority of the work in the PD field has focused on this specific neuronal population. PD however, is not a disease of DA neurons exclusively: pathology, most notably in the form of Lewy bodies and neurites, has been reported in multiple regions of the central and peripheral nervous system, including for example the locus coeruleus, the dorsal raphe nucleus and the dorsal motor nucleus of the vagus. Cell and/or terminal loss of these additional nuclei is likely to contribute to some of the other symptoms of PD and, most notably to the non-motor features. However, exactly which regions show actual, well-documented, cell loss is presently unclear. In this review we will first examine the strength of the evidence describing the regions of cell loss in idiopathic PD, as well as the order in which this loss occurs. Secondly, we will discuss the neurochemical, morphological and physiological characteristics that render SNc DA neurons vulnerable, and will examine the evidence for these characteristics being shared across PD-affected neuronal populations. The insights raised by focusing on the underpinnings of the selective vulnerability of neurons in PD might be helpful to facilitate the development of new disease-modifying strategies and improve animal models of the disease.

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