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Parkinson Disease: HELP
Articles from Baltimore
Based on 309 articles published since 2008
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These are the 309 published articles about Parkinson Disease that originated from Baltimore during 2008-2019.
 
+ Citations + Abstracts
Pages: 1 · 2 · 3 · 4 · 5 · 6 · 7 · 8 · 9 · 10 · 11 · 12 · 13
1 Editorial Are Alzheimer's disease and other neurodegenerative disorders caused by impaired signalling of insulin and other hormones? 2018

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

ABSTRACT: -- No abstract --

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

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

ABSTRACT: -- No abstract --

3 Editorial Editorial overview: Neurobiology of disease. 2016

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

ABSTRACT: -- No abstract --

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

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

ABSTRACT: -- No abstract --

5 Review Essential Tremor. 2019

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

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

6 Review Parkinson's Disease. 2019

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

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

7 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 [

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

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

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

9 Review The Promise of Telemedicine for Movement Disorders: an Interdisciplinary Approach. 2018

Ben-Pazi, H / Browne, P / Chan, P / Cubo, E / Guttman, M / Hassan, A / Hatcher-Martin, J / Mari, Z / Moukheiber, E / Okubadejo, N U / Shalash, A / Anonymous1401121. ·Neuropediatric unit, Shaare Zedek Medical Center, Jerusalem, Israel. · Neurology Department, University Hospital Galway, Newcastle Road, Galway, Ireland. · School of Medicine, National University of Ireland Galway, Galway, Ireland. · Department of Neurobiology, Neurology and Geriatrics, Xuanwu Hospital of Capital Medical University Beijing, Beijing, China. · Neurology Department, University Hospital, Burgos, Spain. mcubo@saludcastillayleon.es. · University of Toronto, Toronto, ON, Canada. · Department of Neurology, Mayo Clinic, Rochester, MN, USA. · Movement Disorders Program, Department of Neurology, Emory University School of Medicine, Atlanta, GA, USA. · Parkinson's Disease and Movement Disorders Program, Cleveland Clinic Lou Ruvo Center for Brain Health, Las Vegas, USA. · Department of Neurology, Johns Hopkins Medicine, Baltimore, MD, USA. · Neurology Unit, Department of Medicine, College of Medicine, University of Lagos, Lagos State, Nigeria. · Department of Neurology, Faculty of Medicine, Ain Shams University, Cairo, Egypt. ·Curr Neurol Neurosci Rep · Pubmed #29654523.

ABSTRACT: PURPOSE OF REVIEW: Advances in technology have expanded telemedicine opportunities covering medical practice, research, and education. This is of particular importance in movement disorders (MDs), where the combination of disease progression, mobility limitations, and the sparse distribution of MD specialists increase the difficulty to access. In this review, we discuss the prospects, challenges, and strategies for telemedicine in MDs. RECENT FINDINGS: Telemedicine for MDs has been mainly evaluated in Parkinson's disease (PD) and compared to in-office care is cost-effective with similar clinical care, despite the barriers to engagement. However, particular groups including pediatric patients, rare MDs, and the use of telemedicine in underserved areas need further research. Interdisciplinary telemedicine and tele-education for MDs are feasible, provide similar care, and reduce travel costs and travel time compared to in-person visits. These benefits have been mainly demonstrated for PD but serve as a model for further validation in other movement disorders.

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

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

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

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

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

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

12 Review NAD 2017

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

ABSTRACT: The coenzyme NAD

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

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

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

14 Review Trumping neurodegeneration: Targeting common pathways regulated by autosomal recessive Parkinson's disease genes. 2017

Scott, Laura / Dawson, Valina L / Dawson, Ted M. ·Neuroregeneration and Stem Cell Programs, Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA; Cellular and Molecular Medicine Program, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA; Adrienne Helis Malvin Medical Research Foundation, New Orleans, LA 70130-2685, USA. · Neuroregeneration and Stem Cell Programs, Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA; Cellular and Molecular Medicine Program, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA; Department of Physiology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA; Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA; Adrienne Helis Malvin Medical Research Foundation, New Orleans, LA 70130-2685, USA. · Neuroregeneration and Stem Cell Programs, Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA; Cellular and Molecular Medicine Program, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA; Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA; Department of Pharmacology and Molecular Sciences, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA; Adrienne Helis Malvin Medical Research Foundation, New Orleans, LA 70130-2685, USA. Electronic address: tdawson2@jhmi.edu. ·Exp Neurol · Pubmed #28445716.

ABSTRACT: Parkinson's disease (PD) is a neurodegenerative movement disorder characterized by the progressive loss of dopaminergic (DA) neurons. Most PD cases are sporadic; however, rare familial forms have been identified. Autosomal recessive PD (ARPD) results from mutations in Parkin, PINK1, DJ-1, and ATP13A2, while rare, atypical juvenile ARPD result from mutations in FBXO7, DNAJC6, SYNJ1, and PLA2G6. Studying these genes and their function has revealed mitochondrial quality control, protein degradation processes, and oxidative stress responses as common pathways underlying PD pathogenesis. Understanding how aberrancy in these common processes leads to neurodegeneration has provided the field with numerous targets that may be therapeutically relevant to the development of disease-modifying treatments.

15 Review Models of LRRK2-Associated Parkinson's Disease. 2017

Xiong, Yulan / Dawson, Ted M / Dawson, Valina L. ·Neuroregeneration and Stem Cell Programs, Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, MD, 21205, USA. yulanxiong@ksu.edu. · Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, 21205, USA. yulanxiong@ksu.edu. · Department of Anatomy and Physiology, Kansas State University College of Veterinary Medicine, Manhattan, KS, 66506, USA. yulanxiong@ksu.edu. · Neuroregeneration and Stem Cell Programs, Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, MD, 21205, USA. vdawson@jhmi.edu. · Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, 21205, USA. vdawson@jhmi.edu. · Department of Pharmacology and Molecular Sciences, Johns Hopkins University School of Medicine, Baltimore, MD, 21205, USA. vdawson@jhmi.edu. · Solomon H. Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD, 21205, USA. vdawson@jhmi.edu. · Adrienne Helis Malvin Medical Research Foundation, New Orleans, LA, 70130-2685, USA. vdawson@jhmi.edu. · Neuroregeneration and Stem Cell Programs, Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, MD, 21205, USA. tdawson@jhmi.edu. · Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, 21205, USA. tdawson@jhmi.edu. · Solomon H. Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD, 21205, USA. tdawson@jhmi.edu. · Adrienne Helis Malvin Medical Research Foundation, New Orleans, LA, 70130-2685, USA. tdawson@jhmi.edu. · Department of Physiology, Johns Hopkins University School of Medicine, Baltimore, MD, 21205, USA. tdawson@jhmi.edu. ·Adv Neurobiol · Pubmed #28353284.

ABSTRACT: Mutations in the leucine-rich repeat kinase 2 (LRRK2) gene are the most common genetic causes of Parkinson's disease (PD) and also one of the strongest genetic risk factors in sporadic PD. The LRRK2 protein contains a GTPase and a kinase domain and several protein-protein interaction domains. Both in vitro and in vivo assays in different model systems have provided tremendous insights into the molecular mechanisms underlying LRRK2-induced dopaminergic neurodegeneration. Among all the model systems, animal models are crucial tools to study the pathogenesis of human disease. How do the animal models recapitulate LRRK2-induced dopaminergic neuronal loss in human PD? To answer this question, this review focuses on the discussion of the animal models of LRRK2-associated PD including genetic- and viral-based models.

16 Review Interventions in Parkinson's disease: Role of executive function. 2017

Mahajan, Abhimanyu / Deal, Jennifer A / Carlson, Michelle. ·Department of Neurology, Henry Ford Hospital, Detroit, MI, amahaja1@hfhs.org. · Bloomberg School of Public Health, Johns Hopkins University, Baltimore, MD. ·Front Biosci (Landmark Ed) · Pubmed #27814622.

ABSTRACT: The cortico-striatal network plays a major role in executive functions (EF), and is believed to play a role in the pathophysiology of Parkinson's disease (PD). However, the tools to assess EF are limited. This review assesses the impact of all PD interventions, namely, pharmacotherapy, physical exercise and Deep Brain Stimulation (DBS) surgery on EF. The effect of PD pharmacotherapy varies with the drug class, neuropsychological test used and the affected dopamine receptor family. There appears to be a benefit of aerobic exercise on EF, including judgment and attention. The effect of Deep Brain Stimulation on EF might vary with site of brain stimulation, the neuropsychological test performed and the pre-operative cognitive state. The effect of EF on underlying manifestations and as a factor in the pathway to the motor benefit needs to be better assessed with more accurate tests that focus on motor component of EF.

17 Review Clinical subtypes and genetic heterogeneity: of lumping and splitting in Parkinson disease. 2016

von Coelln, Rainer / Shulman, Lisa M. ·Department of Neurology, University of Maryland School of Medicine, Baltimore, Maryland, USA. ·Curr Opin Neurol · Pubmed #27749396.

ABSTRACT: PURPOSE OF REVIEW: Recent studies on clinical, genetic and pathological heterogeneity of Parkinson disease have renewed the old debate whether we should think of Parkinson disease as one disease with variations, or as a group of independent diseases that happen to present with similar phenotypes. Here, we provide an overview of where the debate is coming from, and how recent findings in clinical subtyping, genetics and clinico-pathological correlation have shaped this controversy over the last few years. RECENT FINDINGS: New and innovative clinical diagnostic criteria for Parkinson disease have been proposed and await validation. Studies using functional imaging or wearable biosensors, as well as biomarker studies, provide new support for the validity of the traditional clinical subtypes of Parkinson disease (tremor-dominant versus akinetic-rigid or postural instability/gait difficulty). A recent cluster analysis (as unbiased data-driven approach to subtyping) included a wide spectrum of nonmotor variables, and showed correlation of the proposed subtypes with disease progression in a longitudinal analysis. New genetic factors contributing to Parkinson disease susceptibility continue to be identified, including rare mutations causing monogenetic disease, common variants with small effect size and risk factors (like mutations in the gene for glucocerebrosidase) that fall in between the two other categories. Recent studies show some limited correlation between genetic factors and clinical heterogeneity. Despite some variations in patterns of pathology, Lewy bodies are still the hallmark of Parkinson disease, including the vast majority of genetic subgroups. SUMMARY: Evidence of clinical, genetic and pathological heterogeneity of Parkinson disease continues to emerge, but clearly defined subtypes that hold up in more than one of these domains remain elusive. For research to identify such subtypes, splitting is likely the way forward; until then, for clinical practice, lumping remains the more pragmatic approach.

18 Review Update on the Management of Parkinson's Disease: Focus on Psychosis. 2016

Brandt, Nicole J / Chen, Jack J / Menza, Matthew. ·Peter Lamy Center on Drug Therapy and Aging, University of Maryland School of Pharmacy, Baltimore, Maryland, USA. ·Consult Pharm · Pubmed #27629061.

ABSTRACT: -- No abstract --

19 Review Disability Rating Scales in Parkinson's Disease: Critique and Recommendations. 2016

Shulman, Lisa M / Armstrong, Melissa / Ellis, Terry / Gruber-Baldini, Ann / Horak, Fay / Nieuwboer, Alice / Parashos, Sotirios / Post, Bart / Rogers, Mark / Siderowf, Andrew / Goetz, Christopher G / Schrag, Anette / Stebbins, Glenn T / Martinez-Martin, Pablo. ·Department of Neurology, University of Maryland School of Medicine, Baltimore, Maryland, USA. lshulman@som.umaryland.edu. · Department of Neurology, University of Maryland School of Medicine, Baltimore, Maryland, USA. · Department of Physical Therapy & Athletic Training, Boston University, Boston, Massachusetts, USA. · Department of Epidemiology and Public Health, University of Maryland School of Medicine, Baltimore, Maryland, USA. · Department of Neurology, Oregon Health and Science University and Portland VA Medical System, Portland, Oregon, USA. · Department of Rehabilitation Science, KU Leuven-University of Leuven, Heverlee, Belgium. · Struthers Parkinson's Center, Golden Valley, Minnesota, USA. · Department of Neurology, Radboud University Medical Center, Nijmegen, The Netherlands. · Department of Physical Therapy & Rehabilitation, University of Maryland School of Medicine, Baltimore, Maryland, USA. · Avid Radiopharmaceuticals, Philadelphia, PA, USA. · Department of Neurology, Rush University Medical Center, Chicago, USA. · UCL Institute of Neurology, University College London, UK. · National Center of Epidemiology and CIBERNED, Carlos III Institute of Health, Madrid, Spain. ·Mov Disord · Pubmed #27193358.

ABSTRACT: INTRODUCTION: PD is associated with impairments that progress over time to disability. A large number of disability scales exist with little information on the best choice in PD. METHODS: Following methodology adopted by the International Parkinson and Movement Disorder Society Task Force, a review of disability scales used in PD was completed. Based on prespecified criteria, the review categorized scales into: "Recommended"; "Recommended with Further Validation in PD Required" when well-validated scales have not been specifically tested for clinimetric properties in PD; "Suggested"; and "Listed." RESULTS: Twenty-nine disability instruments were identified with nine scales fulfilling criteria for "Recommended" and 7 "Recommended with Further Validation in PD Required." Eight scales are "Suggested" and five scales are "Listed" for use in PD. The nine Recommended scales (Functional Status Questionnaire, Lawton-Brody Activities of Daily Living, Nottingham Activities of Daily Living, Schwab and England Activities of Daily Living, Self-Assessment PD Disability, Short Parkinson's Evaluation Scale/Scales for Outcomes in PD, Unified PD Rating Scale-II: Activities of Daily Living, Movement Disorders Society UPDRS Motor Experiences of Daily Living, PROMIS CONCLUSION: Many disability measures are available and recommended for application in PD. The Task Force does not recommend the development of a new scale. Selection of the most appropriate instrument for a particular objective requires consideration of the characteristics of each scale and the goals of the assessment. © 2016 International Parkinson and Movement Disorder Society.

20 Review Phosphatidylethanolamine Metabolism in Health and Disease. 2016

Calzada, Elizabeth / Onguka, Ouma / Claypool, Steven M. ·Department of Physiology, Johns Hopkins University School of Medicine, Baltimore, MD, USA. ·Int Rev Cell Mol Biol · Pubmed #26811286.

ABSTRACT: Phosphatidylethanolamine (PE) is the second most abundant glycerophospholipid in eukaryotic cells. The existence of four only partially redundant biochemical pathways that produce PE, highlights the importance of this essential phospholipid. The CDP-ethanolamine and phosphatidylserine decarboxylase pathways occur in different subcellular compartments and are the main sources of PE in cells. Mammalian development fails upon ablation of either pathway. Once made, PE has diverse cellular functions that include serving as a precursor for phosphatidylcholine and a substrate for important posttranslational modifications, influencing membrane topology, and promoting cell and organelle membrane fusion, oxidative phosphorylation, mitochondrial biogenesis, and autophagy. The importance of PE metabolism in mammalian health has recently emerged following its association with Alzheimer's disease, Parkinson's disease, nonalcoholic liver disease, and the virulence of certain pathogenic organisms.

21 Review miRNAs as Circulating Biomarkers for Alzheimer's Disease and Parkinson's Disease. 2016

Mushtaq, Gohar / Greig, Nigel H / Anwar, Firoz / Zamzami, Mazin A / Choudhry, Hani / Shaik, Munvar M / Tamargo, Ian A / Kamal, Mohammad A. ·Drug Design and Development Section, Translational Gerontology Branch, Intramural Research Program, National Institute on Aging, National Institutes of Health, Baltimore, MD 21224, USA. greign@mail.nih.gov. ·Med Chem · Pubmed #26527155.

ABSTRACT: Detection of biomarkers for neurodegenerative disorders (NDDs) within brain tissues of Alzheimer's disease (AD) and Parkinson's disease (PD) patients has always been hampered by our inability to access and biopsy tissue of key brain regions implicated in disease occurrence and progression. Currently, diagnosis of NDDs is principally based on clinical observations of symptoms that present at later stages of disease progression, followed by neuroimaging and, possibly, CSF evaluation. One way to potentially detect and diagnose NDDs at a far earlier stage is to screen for abnormal levels of specific disease markers within the peripheral circulation of patients with NDDs. Increasing evidence suggests that there is dysregulation of microRNAs (miRNAs) in NDDs. Peripheral blood mononuclear cells, as well as biofluids, such as plasma, serum, urine and cerebrospinal fluid, contain miRNAs that can be identified and quantified. Circulating miRNAs within blood and other biofluids may thus be characterized and used as non-invasive, diagnostic biomarkers that facilitate the early detection of disease and potentially the continual monitoring of disease progression for NDDs such as AD and PD. Plainly, such a screen is only possible with a clear understanding of which miRNAs change with disease, and when these changes occur during the progression of AD and PD. Such information is becoming increasingly available and, in the near future, may not only support disease diagnosis, but provide the opportunity to evaluate therapeutic interventions earlier in the disease process.

22 Review Mechanisms of deep brain stimulation. 2016

Herrington, Todd M / Cheng, Jennifer J / Eskandar, Emad N. ·Nayef Al-Rodhan Laboratories, Department of Neurosurgery, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts; Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts; and therrington@mgh.harvard.edu. · Nayef Al-Rodhan Laboratories, Department of Neurosurgery, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts; Department of Neurosurgery, The Johns Hopkins Hospital, Baltimore, Maryland. · Nayef Al-Rodhan Laboratories, Department of Neurosurgery, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts; ·J Neurophysiol · Pubmed #26510756.

ABSTRACT: Deep brain stimulation (DBS) is widely used for the treatment of movement disorders including Parkinson's disease, essential tremor, and dystonia and, to a lesser extent, certain treatment-resistant neuropsychiatric disorders including obsessive-compulsive disorder. Rather than a single unifying mechanism, DBS likely acts via several, nonexclusive mechanisms including local and network-wide electrical and neurochemical effects of stimulation, modulation of oscillatory activity, synaptic plasticity, and, potentially, neuroprotection and neurogenesis. These different mechanisms vary in importance depending on the condition being treated and the target being stimulated. Here we review each of these in turn and illustrate how an understanding of these mechanisms is inspiring next-generation approaches to DBS.

23 Review Antidepressive treatments for Parkinson's disease: A systematic review and meta-analysis. 2015

Bomasang-Layno, Emily / Fadlon, Iris / Murray, Andrea N / Himelhoch, Seth. ·Department of Psychiatry, University of Maryland School of Medicine, Baltimore, MD, USA. Electronic address: elayno@psych.umaryland.edu. · Department of Psychiatry, University of Maryland School of Medicine, Baltimore, MD, USA. ·Parkinsonism Relat Disord · Pubmed #26037457.

ABSTRACT: CONTEXT: Depression affects 50-70% of patients with Parkinson's disease resulting in significant comorbidity, executive dysfunction, and poorer quality of life. Divergent results from studies of different treatments preclude definite treatment recommendations. OBJECTIVE: To perform a systematic review and meta-analysis of published randomized controlled trials (RCTS) evaluating the efficacy of pharmacologic and behavioral interventions, and repetitive transcranial magnetic stimulation (rTMS) for depression among patients with idiopathic Parkinson's disease. DATA SOURCES: Trial registers and the following databases were searched: PubMed, CINAHL, EMBASE, and PsycInfo. Bibliographies of relevant articles were cross-referenced. STUDY SELECTION AND DATA EXTRACTION: RCTs comparing pharmacologic, behavioral, or rTMS with a placebo/other drugs or methods with no restrictions on participant age, gender, and duration or setting of treatment were included. Eligibility assessment was performed independently. Identified records were sequentially screened according to eligibility criteria. Differences in mean depression score and 95% confidence intervals were calculated. RESULTS: A total of 893 idiopathic Parkinson's disease patients with clinical depression across 20 RCTs were included. The overall standard mean difference for all pharmacologic interventions was 0.30 (95% CI -0.00, 0.61, p = 0.054). On stratification, there was a distinct difference in effect between antidepressants (SMD of 0.54, 95%CI 0.24, 0.83, p = 0.000) and non-antidepressants (SMD of -0.29, 95% CI -0.86, 0.29, p = 0.328). Behavioral interventions demonstrated significant efficacy with an effect size of 0.87 (95% CI 0.41, 1.33, p = 0.000). CONCLUSIONS: This meta-analysis demonstrates that pharmacologic treatment with antidepressant medications, specifically the selective serotonin reuptake inhibitors (SSRIs), and behavioral interventions (CBT) significantly improved depression among Parkinson's disease patients.

24 Review Amyloid deposition in Parkinson's disease and cognitive impairment: a systematic review. 2015

Petrou, Myria / Dwamena, Ben A / Foerster, Bradley R / MacEachern, Mark P / Bohnen, Nicolaas I / Müller, Martijn Ltm / Albin, Roger L / Frey, Kirk A. ·Department of Radiology, University of Michigan, Ann Arbor, Michigan, USA. · Russell H. Morgan Department of Radiology and Radiological Science, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. · Veterans Administration Healthcare System, Ann Arbor, Michigan, USA. · Taubman Health Sciences Library, University of Michigan, Ann Arbor, Michigan, USA. · Department of Neurology, University of Michigan, Ann Arbor, Michigan, USA. · Univerity of Michigan Morris K. Udall Center for Excellence in Parkinson's Disease Research, Ann Arbor, Michigan, USA. ·Mov Disord · Pubmed #25879534.

ABSTRACT: BACKGROUND: Varying degrees of cortical amyloid deposition are reported in the setting of Parkinsonism with cognitive impairment. We performed a systematic review to estimate the prevalence of Alzheimer disease (AD) range cortical amyloid deposition among patients with Parkinson's disease with dementia (PDD), Parkinson's disease with mild cognitive impairment (PD-MCI) and dementia with Lewy bodies (DLB). We included amyloid positron emission tomography (PET) imaging studies using Pittsburgh Compound B (PiB). METHODS: We searched the databases Ovid MEDLINE, PubMed, Embase, Scopus, and Web of Science for articles pertaining to amyloid imaging in Parkinsonism and impaired cognition. We identified 11 articles using PiB imaging to quantify cortical amyloid. We used the metan module in Stata, version 11.0, to calculate point prevalence estimates of patients with "PiB-positive" studies, that is, patients showing AD range cortical Aβ-amyloid deposition. Heterogeneity was assessed. A scatterplot was used to assess publication bias. RESULTS: Overall pooled prevalence of "PiB-positive" studies across all three entities along the spectrum of Parkinson's disease and impaired cognition (specifically PDD, PD-MCI, and DLB) was 0.41 (95% confidence interval [CI], 0.24-0.57). Prevalence of "PiB-positive" studies was 0.68 (95% CI, 0.55-0.82) in the DLB group, 0.34 (95% CI, 0.13-0.56) in the PDD group, and 0.05 (95% CI, -0.07-0.17) in the PD-MCI group. CONCLUSIONS: Substantial variability occurs in the prevalence of "PiB-positive" studies in subjects with Parkinsonism and cognitive impairment. Higher prevalence of PiB-positive studies was encountered among subjects with DLB as opposed to subjects with PDD. The PD-MCI subjects showed overall lower prevalence of PiB-positive studies than reported findings in non-PD-related MCI. © 2015 International Parkinson and Movement Disorder Society.

25 Review Apathy in Neurodegenerative Diseases: Recommendations on the Design of Clinical Trials. 2015

Cummings, Jeffrey / Friedman, Joseph H / Garibaldi, George / Jones, Martin / Macfadden, Wayne / Marsh, Laura / Robert, Philippe H. ·Cleveland Clinic Lou Ruvo Center for Brain Health, Las Vegas, NV, USA cumminj@ccf.org. · Department of Neurology, Movement Disorders Program, Butler Hospital, Alpert Medical School of Brown University, Providence, RI, USA. · Clinical Development, Neurosciences, F. Hoffman-La Roche AG, Basel, Switzerland. · Bridge Medical Consulting Ltd, London, United Kingdom. · Mental Health Care Line, Michael E. DeBakey Veterans Affairs Medical Center, Houston, TX, USA Menninger Department of Psychiatry, Baylor College of Medicine, Houston, TX, USA Department of Psychiatry, Johns Hopkins University School of Medicine, Baltimore, MD, USA. · CoBTeK, Research Memory Center CMRR CHU, University of Sophia Antipolis, Nice, France. ·J Geriatr Psychiatry Neurol · Pubmed #25809634.

ABSTRACT: Apathy is a common feature of neurodegenerative disorders but is difficult to study in a clinical trial setting due to practical and conceptual barriers. Principal challenges include a paucity of data regarding apathy in these disorders, an absence of established diagnostic criteria, the presence of confounding factors (eg, coexisting depression), use of concomitant medications, and an absence of a gold-standard apathy assessment scale. Based on a literature search and ongoing collaboration among the authors, we present recommendations for the design of future clinical trials of apathy, suggesting Alzheimer disease and Parkinson disease as models with relevance across a wider array of neuropsychiatric disorders. Recommendations address clarification of the targeted study population (apathy diagnosis and severity at baseline), confounding factors (mood/cognition, behavior, and treatment), outcome measures, study duration, use of comparators and considerations around environment, and the role of the caregiver and patient assent. This review contributes to the search for an optimal approach to study treatment of apathy in neuropsychiatric disorders.

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