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Parkinson Disease: HELP
Articles from Veterans Health System
Based on 510 articles published since 2008
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These are the 510 published articles about Parkinson Disease that originated from Veterans Health System 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 Mendel and urate: Acid test or random noise? 2018

Brown, Ethan G / Goldman, Samuel M / Tanner, Caroline M. ·Department of Neurology, University of California - San Francisco, San Francisco, CA, USA; Department of Neurology, Weil Institute for Neurosciences, University of California - San Francisco, San Francisco, CA, USA. · Department of Neurology, University of California - San Francisco, San Francisco, CA, USA; Division of Occupational and Environmental Medicine, University of California - San Francisco, San Francisco, CA, USA; Medical Service, San Francisco Veterans Affairs Health Care System, San Francisco, CA, USA. · Department of Neurology, University of California - San Francisco, San Francisco, CA, USA; Department of Neurology, Weil Institute for Neurosciences, University of California - San Francisco, San Francisco, CA, USA; Parkinson's Disease Research, Education and Clinical Center, San Francisco Veterans Affairs Health Care System, San Francisco, CA, USA. Electronic address: Caroline.tanner@ucsf.edu. ·Parkinsonism Relat Disord · Pubmed #30100365.

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? II. Neuroimaging in Parkinson's disease. 2017

Albin, Roger L. ·Department of Neurology, University of Michigan, Ann Arbor, Michigan, USA. · Neurology Service & Geriatrics Research, Education, and Clinical Center, Veterans Affairs Ann Arbor Health System, Ann Arbor, Michigan, USA. · University of Michigan Morris K. Udall Center of Excellence for Parkinson's Disease Research, Ann Arbor, Michigan, USA. · University of Michigan Alzheimer Disease Center, Ann Arbor, Michigan, USA. ·Mov Disord · Pubmed #28218459.

ABSTRACT: -- No abstract --

4 Editorial The Clinical Profile of GBA-Related Lewy Body Disorders. 2016

Zabetian, Cyrus P. ·Veterans Affairs Puget Sound Health Care System, Seattle, Washington2Department of Neurology, University of Washington School of Medicine, Seattle. ·JAMA Neurol · Pubmed #27723881.

ABSTRACT: -- No abstract --

5 Editorial Role of Neuroinflammation in Parkinson Disease: The Enigma Continues. 2016

Mehta, Shyamal H / Tanner, Caroline M. ·Department of Neurology, Mayo Clinic, Scottsdale, AZ. Electronic address: mehta.shyamal@mayo.edu. · San Francisco Veterans Affairs Medical Center and Department of Neurology, University of California, San Francisco, CA. ·Mayo Clin Proc · Pubmed #27712631.

ABSTRACT: -- No abstract --

6 Editorial Serum vitamin D and risk of Parkinson's disease. 2016

Ross, G Webster / Petrovitch, Helen / Abbott, Robert D. ·Veterans Affairs Pacific Islands Health Care System, Honolulu, Hawaii, USA. · Pacific Health Research and Education Institute, Honolulu, Hawaii, USA. · Department of Medicine, University of Hawaii John A. Burns School of Medicine, Honolulu, Hawaii, USA. · Department of Geriatric Medicine, University of Hawaii John A. Burns School of Medicine, Honolulu, Hawaii, USA. · Center for Epidemiologic Research in Asia, Shiga University of Medical Science, Otsu, Shiga, Japan. ·Mov Disord · Pubmed #27091700.

ABSTRACT: -- No abstract --

7 Editorial Parkinson Disease Risk in Patients With Rosacea. 2016

Wingo, Thomas S. ·Department of Neurology, Emory University, Atlanta, Georgia2Department of Human Genetics, Emory University, Atlanta, Georgia3Division of Neurology, Atlanta Veterans Affairs Medical Center, Atlanta, Georgia. ·JAMA Neurol · Pubmed #26998584.

ABSTRACT: -- No abstract --

8 Editorial More than just a movement disorder: Why cognitive training is needed in Parkinson disease. 2015

Ventura, Maria I / Edwards, Jerri D / Barnes, Deborah E. ·From the Departments of Geriatrics (M.I.V.) and Psychiatry and Epidemiology & Statistics (D.E.B.), University of California, San Francisco · the School of Aging Studies (J.D.E.), University of South Florida, Tampa · and the San Francisco VA Medical Center (D.E.B.), San Francisco, CA. ·Neurology · Pubmed #26519546.

ABSTRACT: -- No abstract --

9 Editorial Living and dying with Parkinson's disease. 2014

Ross, G Webster / Abbott, Robert D. ·Veterans Affairs Pacific Islands Health Care System, Honolulu, Hawaii; Pacific Health Research and Education Institute, Honolulu, Hawaii; Department of Medicine, University of Hawaii John A. Burns School of Medicine, Honolulu, Hawaii; Geriatric Medicine, University of Hawaii John A. Burns School of Medicine, Honolulu, Hawaii. ·Mov Disord · Pubmed #25044188.

ABSTRACT: -- No abstract --

10 Editorial Dopamine-dependent functional connectivity in Parkinson disease: a resting-state diagnosis? 2014

Bohnen, Nicolaas I / Martin, W R Wayne. ·From the Departments of Radiology and Neurology (N.I.B.), University of Michigan, and VA Ann Arbor Healthcare System, MI · and the Movement Disorders Program (W.R.W.M.), Division of Neurology, University of Alberta, Edmonton, Canada. ·Neurology · Pubmed #24920849.

ABSTRACT: -- No abstract --

11 Editorial Freezing of gait in PD has a REM correlate: twice cursed with a shared pathophysiology? 2013

Hershey, Linda A / Lichter, David G. ·From the Department of Neurology (L.A.H.), University of Oklahoma Health Sciences Center, Oklahoma City · Department of Neurology (D.G.L.), University at Buffalo School of Medicine (SUNY), NY · and Veterans Affairs Western New York Healthcare System (D.G.L.), Buffalo. ·Neurology · Pubmed #23946300.

ABSTRACT: -- No abstract --

12 Editorial Neuropsychiatric symptoms in Parkinson disease and dementia with Lewy bodies: what geriatric psychiatry can learn. 2013

Weintraub, Daniel. ·Departments of Psychiatry and Neurology, Perelman School of Medicine at the University of Pennsylvania, and Parkinson's Disease Research, Education and Clinical Center, Philadelphia Veterans Affairs Medical Center, Philadelphia, Pennsylvania. Electronic address: Daniel.Weintraub@uphs.upenn.edu. ·Am J Geriatr Psychiatry · Pubmed #23668226.

ABSTRACT: -- No abstract --

13 Review Immunology of West Nile Virus Infection and the Role of Alpha-Synuclein as a Viral Restriction Factor. 2019

Lesteberg, Kelsey E / Beckham, John David. ·1 Division of Infectious Diseases, Department of Medicine, University of Colorado School of Medicine , Aurora, Colorado. · 2 Division of Neuroimmunology and Neurological Infections, Department of Neurology, University of Colorado School of Medicine , Aurora, Colorado. · 3 Veterans Administration, Eastern Colorado Health System , Denver, Colorado. ·Viral Immunol · Pubmed #30222521.

ABSTRACT: West Nile virus (WNV) is a single-stranded RNA flavivirus and is a major cause of viral encephalitis worldwide. Experimental models of WNV infection in mice are commonly used to define acute neuroinflammatory responses in the brain. Alpha-synuclein (Asyn) is a protein of primarily neuronal origin and is a major cause of Parkinson's disease (PD), a disorder characterized by loss of dopaminergic neurons. Both WNV and PD pathologies are largely mediated by inflammation of the central nervous system (neuroinflammation) and have overlapping inflammatory pathways. In this review, we highlight the roles of the immune system in both diseases while comparing and contrasting both protective and pathogenic roles of immune cells and their effector proteins. Additionally, we review the current literature showing that Asyn is an important mediator of the immune response with diverging roles in PD (pathogenic) and WNV disease (neuroprotective).

14 Review Molecular Imaging of the Cholinergic System in Parkinson's Disease. 2018

Bohnen, Nicolaas I / Kanel, Prabesh / Müller, Martijn L T M. ·Department of Radiology, University of Michigan, Ann Arbor, MI, United States; Department of Neurology, University of Michigan, Ann Arbor, MI, United States; Veterans Administration Ann Arbor Healthcare System, Ann Arbor, MI, United States; Morris K. Udall Center of Excellence for Parkinson's Disease Research, University of Michigan, Ann Arbor, MI, United States. Electronic address: nbohnen@umich.edu. · Department of Radiology, University of Michigan, Ann Arbor, MI, United States; Morris K. Udall Center of Excellence for Parkinson's Disease Research, University of Michigan, Ann Arbor, MI, United States. ·Int Rev Neurobiol · Pubmed #30314597.

ABSTRACT: One of the first identified neurotransmitters in the brain, acetylcholine, is an important modulator that drives changes in neuronal and glial activity. For more than two decades, the main focus of molecular imaging of the cholinergic system in Parkinson's disease (PD) has been on cognitive changes. Imaging studies have confirmed that degeneration of the cholinergic system is a major determinant of dementia in PD. Within the last decade, the focus is expanding to studying cholinergic correlates of mobility impairments, dyskinesias, olfaction, sleep, visual hallucinations and risk taking behavior in this disorder. These studies increasingly recognize that the regional topography of cholinergic brain areas associates with specific functions. In parallel with this trend, more recent molecular cholinergic imaging approaches are investigating cholinergic modulatory functions and contributions to large-scale brain network functions. A novel area of research is imaging cholinergic innervation functions of peripheral autonomic organs that may have the potential of future prodromal diagnosis of PD. Finally, emerging evidence of hypercholinergic activity in prodromal and symptomatic leucine-rich repeat kinase 2 PD may reflect neuronal cholinergic compensation versus a response to neuro-inflammation. Molecular imaging of the cholinergic system has led to many new insights in the etiology of dopamine non-responsive symptoms of PD (more "malignant" hypocholinergic disease phenotype) and is poised to guide and evaluate future cholinergic drug development in this disorder.

15 Review To bee or not to bee: The potential efficacy and safety of bee venom acupuncture in humans. 2018

Cherniack, E Paul / Govorushko, Sergey. ·Division of Geriatrics and Palliative Medicine, University of Miami Miller School of Medicine, Miami VA Medical Center, Miami, USA. Electronic address: evan.cherniack@va.gov. · Pacific Geographic Institute, Russian Academy of Sciences, Vladivostok, Russia; Far Eastern Federal University, Vladivostok, Russia. ·Toxicon · Pubmed #30268393.

ABSTRACT: Bee venom acupuncture is a form of acupuncture in which bee venom is applied to the tips of acupuncture needles, stingers are extracted from bees, or bees are held with an instrument exposing the stinger, and applied to acupoints on the skin. Bee venom is a complex substance consisting of multiple anti-inflammatory compounds such as melittin, adolapin, apamin. Other substances such as phospholipase A2 can be anti-inflammatory in low concentrations and pro-inflammatory in others. However, bee venom also contains proinflammatory substances, melittin, mast cell degranulation peptide 401, and histamine. Nevertheless, in small studies, bee venom acupuncture has been used in man to successfully treat a number of musculoskeletal diseases such as lumbar disc disease, osteoarthritis of the knee, rheumatoid arthritis, adhesive capsulitis, and lateral epicondylitis. Bee venom acupuncture can also alleviate neurological conditions, including peripheral neuropathies, stroke and Parkinson's Disease. The treatment has even been piloted in one series to alleviate depression. An important concern is the safety of bee venom. Bee venom can cause anaphylaxis, and several deaths have been reported in patients who successfully received the therapy prior to the adverse event. While the incidence of adverse events is unknown, the number of published reports of toxicity is small. Refining bee venom to remove harmful substances may potentially limit its toxicity. New uses for bee venom acupuncture may also be considered.

16 Review Adenosine role in brain functions: Pathophysiological influence on Parkinson's disease and other brain disorders. 2018

Soliman, Amira M / Fathalla, Ahmed M / Moustafa, Ahmed A. ·Department of Pharmacology, Faculty of Medicine, Suez Canal University, Ismailia, Egypt. Electronic address: amiram.soliman_pgs@med.suez.edu.eg. · Department of Pharmacology, Faculty of Medicine, Suez Canal University, Ismailia, Egypt. · Department of Veterans Affairs, New Jersey Health Care System, East Orange, NJ, USA; School of Social Sciences and Psychology and Marcs Institute for Brain and Behaviour, Western Sydney University, Sydney, New South Wales, Australia. Electronic address: a.moustafa@westernsydney.edu.au. ·Pharmacol Rep · Pubmed #29909246.

ABSTRACT: Although adenosine plays a key role in multiple motor, affective, and cognitive processes, it has received less attention in the neuroscience field compared to other neurotransmitters (e.g., dopamine). In this review, we highlight the role of adenosine in behavior as well as its interaction with other neurotransmitters, such as dopamine. We also discuss brain disorders impacted by alterations to adenosine, and how targeting adenosine can ameliorate Parkinson's disease motor symptoms. We also discuss the role of caffeine (as an adenosine antagonist) on cognition as well as a neuroprotective agent against Parkinson's disease (PD).

17 Review Motor learning in people with Parkinson's disease: Implications for fall prevention across the disease spectrum. 2018

Paul, Serene S / Dibble, Leland E / Peterson, Daniel S. ·Faculty of Health Sciences, University of Sydney. 75 East St, Lidcombe NSW 2141, Australia. Electronic address: serene.paul@sydney.edu.au. · Department of Physical Therapy and Athletic Training, University of Utah. 520 Wakara Way, Salt Lake City, UT 84108, USA. Electronic address: lee.dibble@hsc.utah.edu. · School of Nutrition and Health Promotion, Arizona State University. 550 N 3rd St, Phoenix, AZ 85004, USA; Phoenix Department of Veterans Affairs, 215 E Indian School Rd, Phoenix, AZ 85012, USA. Electronic address: Daniel.Peterson1@asu.edu. ·Gait Posture · Pubmed #29413803.

ABSTRACT: BACKGROUND: Falls are a significant burden for people with Parkinson's disease (PD), however, individuals across the spectrum of disease severity respond differently to fall prevention interventions. Despite the multifactorial causes of falls in people with PD, recent work has provided insight into interventions that hold promise for fall prevention. Further, studies have begun to identify patient characteristics that may predict responsiveness to such interventions. RESEARCH QUESTION: We discuss (i) the postural motor learning abilities of people with mild versus severe PD that could affect their ability to benefit from fall prevention interventions, (ii) how people with different severity of PD respond to such interventions, and (iii) the practical considerations of providing effective fall prevention interventions for people with PD across the spectrum of disease severity. METHODS: This narrative review consolidates recent work on postural motor learning and fall prevention rehabilitation involving exercise in people with PD. RESULTS: People with PD are able to improve postural motor control through practice, enabling them to benefit from exercise which challenges their gait and balance to reduce falling. Worsening of axial and cognitive symptoms may result in diminished learning, and those with more severe PD may require fully supervised, high intensity programs to reduce falls. SIGNIFICANCE: Understanding how people with PD across the spectrum of disease severity differ in their postural motor learning ability and response to different fall prevention interventions will enable researchers and clinicians to refine such interventions and their delivery to minimize falls and their negative sequelae in people with PD.

18 Review Constipation in Parkinson's Disease: a Nuisance or Nuanced Answer to the Pathophysiological Puzzle? 2018

Sharma, Amol / Kurek, Julie / Morgan, John C / Wakade, Chandramohan / Rao, Satish S C. ·Division of Gastroenterology/Hepatology, Medical College of Georgia, Augusta University Medical Center, 1120 15th Street, AD-2226, Augusta, GA, 30912, USA. amosharma@augusta.edu. · Parkinson's Foundation Center of Excellence, Movement Disorders Program, Department of Neurology, Medical College of Georgia, Augusta University, Augusta, GA, USA. · Department of Physical Therapy, College of Allied Health Sciences, Augusta University & Charlie Norwood VAMC, Augusta, GA, USA. · Division of Gastroenterology/Hepatology, Medical College of Georgia, Augusta University Medical Center, 1120 15th Street, AD-2226, Augusta, GA, 30912, USA. ·Curr Gastroenterol Rep · Pubmed #29350301.

ABSTRACT: PURPOSE OF REVIEW: Chronic constipation is a common, nonmotor, and prodromal symptom in Parkinson's disease (PD). Its underlying neuropathology may provide pathophysiological insight into PD. Here, we critically review what is currently known about the neuroanatomical and brain-gut interactions, and the origin and progression of Lewy pathology (LP) at three levels-brain/brainstem, spinal cord, and enteric nervous system. RECENT FINDINGS: Many recent studies have illustrated the challenges of examining LP in tissues obtained from colon biopsies of PD patients. Large-scale epidemiological studies have not confirmed the widely accepted Braakpostula. In this review, we propose an alternative origin and route of spread of LP in PD. We describe novel, noninvasive neurophysiological testing that could advance the understanding of LP and complex bidirectional brain-pelvic floor neural pathways in PD-a true disease model of a neurogastrointestinal disorder. This review may provide the impetus for future studies investigating gut and brain interaction and constipation in PD.

19 Review Mitochondrial function and autophagy: integrating proteotoxic, redox, and metabolic stress in Parkinson's disease. 2018

Zhang, Jianhua / Culp, Matilda Lillian / Craver, Jason G / Darley-Usmar, Victor. ·Center for Free Radical Biology, Birmingham, Alabama, USA. · Department of Pathology, University of Alabama at Birmingham, Birmingham, Alabama, USA. · Department of Veterans Affairs, Birmingham VA Medical Center, Birmingham, Alabama, USA. ·J Neurochem · Pubmed #29341130.

ABSTRACT: Parkinson's disease (PD) is a movement disorder with widespread neurodegeneration in the brain. Significant oxidative, reductive, metabolic, and proteotoxic alterations have been observed in PD postmortem brains. The alterations of mitochondrial function resulting in decreased bioenergetic health is important and needs to be further examined to help develop biomarkers for PD severity and prognosis. It is now becoming clear that multiple hits on metabolic and signaling pathways are likely to exacerbate PD pathogenesis. Indeed, data obtained from genetic and genome association studies have implicated interactive contributions of genes controlling protein quality control and metabolism. For example, loss of key proteins that are responsible for clearance of dysfunctional mitochondria through a process called mitophagy has been found to cause PD, and a significant proportion of genes associated with PD encode proteins involved in the autophagy-lysosomal pathway. In this review, we highlight the evidence for the targeting of mitochondria by proteotoxic, redox and metabolic stress, and the role autophagic surveillance in maintenance of mitochondrial quality. Furthermore, we summarize the role of α-synuclein, leucine-rich repeat kinase 2, and tau in modulating mitochondrial function and autophagy. Among the stressors that can overwhelm the mitochondrial quality control mechanisms, we will discuss 4-hydroxynonenal and nitric oxide. The impact of autophagy is context depend and as such can have both beneficial and detrimental effects. Furthermore, we highlight the potential of targeting mitochondria and autophagic function as an integrated therapeutic strategy and the emerging contribution of the microbiome to PD susceptibility.

20 Review Global scales for cognitive screening in Parkinson's disease: Critique and recommendations. 2018

Skorvanek, Matej / Goldman, Jennifer G / Jahanshahi, Marjan / Marras, Connie / Rektorova, Irena / Schmand, Ben / van Duijn, Erik / Goetz, Christopher G / Weintraub, Daniel / Stebbins, Glenn T / Martinez-Martin, Pablo / Anonymous2421195. ·Department of Neurology, Safarik University, Kosice, Slovakia. · Department of Neurology, University Hospital of L. Pasteur, Kosice, Slovakia. · Rush University Medical Center, Department of Neurological Sciences, Section of Parkinson Disease and Movement Disorders, Chicago, Illinois, USA. · Sobell Department of Motor Neuroscience & Movement Disorders and the National Hospital for Neurology & Neurosurgery, London, UK. · Morton and Gloria Shulman Movement Disorders Centre and the Edmond J. Safra Program in Parkinson's Disease, Toronto Western Hospital, Toronto, Ontario, Canada. · Applied Neuroscience Research Group, Central European Institute of Technology, CEITEC, Masaryk University, Brno, Czech Republic. · Department of Psychology, University of Amsterdam, Amsterdam, The Netherlands. · Department of Psychiatry, Leiden University Medical Centre, Leiden, and Centre of Mental Health Care Delfland, Delft, Netherlands. · Department of Psychiatry, Perelman School of Medicine at the University of Pennsylvania and Parkinson's Disease and Mental Health Research, Education and Clinical Centers (PADRECC and MIRECC), Philadelphia Veterans Affairs Medical Center, Philadelphia, Pennsylvania, USA. · National Centre of Epidemiology and CIBERNED, Carlos III Institute of Health, Madrid, Spain. ·Mov Disord · Pubmed #29168899.

ABSTRACT: BACKGROUND: Cognitive impairment is a common nonmotor manifestation of Parkinson's disease, with deficits ranging from mild cognitive difficulties in 1 or more of the cognitive domains to severe dementia. The International Parkinson and Movement Disorder Society commissioned the assessment of the clinimetric properties of cognitive rating scales measuring global cognitive performance in PD to make recommendations regarding their use. METHODS: A systematic literature search was conducted to identify the scales used to assess global cognitive performance in PD, and the identified scales were reviewed and rated as "recommended," "recommended with caveats," "suggested," or "listed" by the panel using previously established criteria. RESULTS: A total of 12 cognitive scales were included in this review. Three scales, the Montreal Cognitive Assessment, the Mattis Dementia Rating Scale Second Edition, and the Parkinson's Disease-Cognitive Rating Scale, were classified as "recommended." Two scales were classified as "recommended with caveats": the Mini-Mental Parkinson, because of limited coverage of executive abilities, and the Scales for Outcomes in Parkinson's Disease-Cognition, which has limited data on sensitivity to change. Six other scales were classified as "suggested" and 1 scale as "listed." CONCLUSIONS: Because of the existence of "recommended" scales for assessment of global cognitive performance in PD, this task force suggests that the development of a new scale for this purpose is not needed at this time. However, global cognitive scales are not a substitute for comprehensive neuropsychological testing. © 2017 International Parkinson and Movement Disorder Society.

21 Review Sex differences in Parkinson's disease: Features on clinical symptoms, treatment outcome, sexual hormones and genetics. 2018

Jurado-Coronel, Juan Camilo / Cabezas, Ricardo / Ávila Rodríguez, Marco Fidel / Echeverria, Valentina / García-Segura, Luis Miguel / Barreto, George E. ·Departamento de Nutrición y Bioquímica, Facultad de Ciencias, Pontificia Universidad Javeriana, Bogotá D.C., Colombia. · Facultad de Ciencias de la Salud, Universidad del Tolima, Ibagué, Colombia. · Universidad San Sebastián, Fac. Cs de la Salud, Lientur 1457, Concepción, 4080871, Chile; Research & Development Service, Bay Pines VA Healthcare System, Bay Pines, FL 33744, USA. · Instituto Cajal, CSIC, Madrid, Spain; CIBER de Investigación Biomédica en Red de Fragilidad y Envejecimiento Saludable (CIBERFES), Instituto de Salud Carlos III, Madrid, Spain. · Departamento de Nutrición y Bioquímica, Facultad de Ciencias, Pontificia Universidad Javeriana, Bogotá D.C., Colombia; Instituto de Ciencias Biomédicas, Universidad Autónoma de Chile, Santiago, Chile. Electronic address: gsampaio@javeriana.edu.co. ·Front Neuroendocrinol · Pubmed #28974386.

ABSTRACT: Parkinson's disease (PD) is the second most frequent age-related neurodegenerative disorder. Sex is an important factor in the development of PD, as reflected by the fact that it is more common in men than in women by an approximate ratio of 2:1. Our hypothesis is that differences in PD among men and women are highly determined by sex-dependent differences in the nigrostriatal dopaminergic system, which arise from environmental, hormonal and genetic influences. Sex hormones, specifically estrogens, influence PD pathogenesis and might play an important role in PD differences between men and women. The objective of this review was to discuss the PD physiopathology and point out sex differences in nigrostriatal degeneration, symptoms, genetics, responsiveness to treatments and biochemical and molecular mechanisms among patients suffering from this disease. Finally, we discuss the role estrogens may have on PD sex differences.

22 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.

23 Review Olfactory Dysfunction as an Early Biomarker in Parkinson's Disease. 2017

Fullard, Michelle E / Morley, James F / Duda, John E. ·Parkinson's Disease Research, Education and Clinical Center, Corporal Michael J. Crescenz VA Medical Center, Philadelphia, PA, 19104, USA. Michelle.Fullard@uphs.upenn.edu. · Department of Neurology, University of Pennsylvania School of Medicine, Philadelphia, PA, 19104, USA. Michelle.Fullard@uphs.upenn.edu. · Parkinson's Disease Research, Education and Clinical Center, Corporal Michael J. Crescenz VA Medical Center, Philadelphia, PA, 19104, USA. · Department of Neurology, University of Pennsylvania School of Medicine, Philadelphia, PA, 19104, USA. ·Neurosci Bull · Pubmed #28831680.

ABSTRACT: Olfactory dysfunction is common in Parkinson's disease (PD) and often predates the diagnosis by years, reflecting early deposition of Lewy pathology, the histologic hallmark of PD, in the olfactory bulb. Clinical tests are available that allow for the rapid characterization of olfactory dysfunction, including tests of odor identification, discrimination, detection, and recognition thresholds, memory, and tests assessing the build-up of odor intensity across increasing suprathreshold stimulus concentrations. The high prevalence of olfactory impairment, along with the ease and low cost of assessment, has fostered great interest in olfaction as a potential biomarker for PD. Hyposmia may help differentiate PD from other causes of parkinsonism, and may also aid in the identification of "pre-motor" PD due to the early pathologic involvement of olfactory pathways. Olfactory function is also correlated with other non-motor features of PD and may serve as a predictor of cognitive decline. In this article, we summarize the existing literature on olfaction in PD, focusing on the potential for olfaction as a biomarker for early or differential diagnosis and prognosis.

24 Review Molecular Imaging and Updated Diagnostic Criteria in Lewy Body Dementias. 2017

Bohnen, Nicolaas I / Müller, Martijn L T M / Frey, Kirk A. ·Departments of Radiology and Neurology, University of Michigan, and Neurology service and GRECC, VA Ann Arbor Healthcare System, Ann Arbor, MI, USA. nbohnen@umich.edu. · Departments of Radiology and Neurology, University of Michigan, and Neurology service and GRECC, VA Ann Arbor Healthcare System, Ann Arbor, MI, USA. · Functional Neuroimaging, Cognitive and Mobility Laboratory, Domino's Farms, University of Michigan, Lobby B, Suite 1000, Level I; 24 Frank Lloyd Wright Drive, Box 362, Ann Arbor, MI, 48105-9755, USA. · Department of Radiology, Division of Nuclear Medicine, 1500 East Medical Center Drive, Room B1-G505 UH, Ann Arbor, MI, 48109-5028, USA. ·Curr Neurol Neurosci Rep · Pubmed #28808912.

ABSTRACT: PURPOSE OF REVIEW: The aims of the study were to review recent advances in molecular imaging in the Lewy body dementias (LBD) and determine if these may support the clinical but contested temporal profile distinction between Parkinson disease (PD) with dementia (PDD) versus dementia with Lewy bodies (DLB). RECENT FINDINGS: There do not appear to be major regional cerebral metabolic or neurotransmitter distinctions between PDD and DLB. However, recent studies highlight the relative discriminating roles of Alzheimer proteinopathies. PDD patients have lower cortical β-amyloid deposition than DLB. Preliminary tau PET studies suggest a gradient of increasing tau binding from cognitively normal PD (absent to lowest) to cognitively impaired PD (low) to DLB (intermediate) to Alzheimer disease (AD; highest). However, tau binding in DLB, including the medial temporal lobe, is substantially lower than in AD. Alzheimer-type proteinopathies appear to be more common in DLB compared to PDD with relative but no absolute differences. Given the spectrum of overlapping pathologies, future α-synuclein ligands are expected to have the best potential to distinguish the LBD from pure AD.

25 Review Impulse Control and Related Disorders in Parkinson's Disease. 2017

Weintraub, Daniel / Claassen, Daniel O. ·Perelman School of Medicine at the University of Pennsylvania, Philadelphia, PA, United States; Parkinson's Disease and Mental Illness Research, Education and Clinical Centers, Corporal Michael J. Crescenz Veterans Affairs Medical Center, Philadelphia, PA, United States. Electronic address: daniel.weintraub@uphs.upenn.edu. · Vanderbilt University School of Medicine, Nashville, TN, United States. ·Int Rev Neurobiol · Pubmed #28802938.

ABSTRACT: Impulse control disorders (ICDs), such as compulsive gambling, buying, sexual, and eating behaviors, are a serious and increasingly recognized complication in Parkinson's disease (PD), occurring in up to 20% of PD patients over the course of their illness. Related behaviors include punding (stereotyped, repetitive, purposeless behaviors), dopamine dysregulation syndrome (DDS) (compulsive medication overuse), and hobbyism (e.g., compulsive internet use, artistic endeavors, and writing). These disorders have a significant impact on quality of life and function, strain interpersonal relationships, and worsen caregiver burden, and are associated with significant psychiatric comorbidity. ICDs have been most closely related to the use of dopamine agonists (DAs), while DDS is primarily associated with shorter acting, higher potency dopamine replacement therapy (DRT), such as levodopa. However, in preliminary research ICDs have also been reported to occur with monoamine oxidase inhibitor-B and amantadine treatment, and after deep brain stimulation (DBS) surgery. Other risk factors for ICDs may include sex (e.g., male sex for compulsive sexual behavior, and female sex for compulsive buying behavior); younger age overall at PD onset; a pre-PD history of an ICD; personal or family history of substance abuse, bipolar disorder, or gambling problems; and impulsive personality traits. Dysregulation of the mesocorticolimbic dopamine system is thought to be the major neurobiological substrate for ICDs in PD, but there is preliminary evidence for alterations in opiate and serotonin systems too. The primary treatment of ICDs in PD is discontinuation of the offending treatment, but not all patients can tolerate this due to worsening motor symptoms or DA withdrawal syndrome. While psychiatric medications and psychosocial treatments are frequently used to treat ICDs in the general population, there is limited empirical evidence for their use in PD, so it is critical for patients to be monitored closely for ICDs from disease onset and routine throughout its course. In the future, it may be possible to use a precision medicine approach to decrease the incidence of ICDs in PD by avoiding DA use in patients determined to be at highest risk based on their clinical and neurobiological (e.g., motor presentation, behavioral measures of medication response, genetics, dopamine transporter neuroimaging) profile. Additionally, as empirically validated treatments for ICDs and similar disorders (e.g., substance use disorders) emerge, it will also be important to examine their efficacy and tolerability in individuals with comorbid PD.

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