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Parkinson Disease: HELP
Articles from Johns Hopkins University
Based on 204 articles published since 2008
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These are the 204 published articles about Parkinson Disease that originated from Johns Hopkins University during 2008-2019.
 
+ Citations + Abstracts
Pages: 1 · 2 · 3 · 4 · 5 · 6 · 7 · 8 · 9
1 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 --

2 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 --

3 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 --

4 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 [

5 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.

6 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.

7 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.

8 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

9 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,

10 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.

11 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.

12 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.

13 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.

14 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.

15 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.

16 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.

17 Review Sterile cyst formation after intrathecal stem cell transplant for Parkinson's disease: A case presentation and literature review. 2015

Al-Tawfiq, Jaffar A / Banda, Ramzi W / Ghandour, Jihad. ·Specialty Internal Medicine Unit, Johns Hopkins Aramco Healthcare, Dhahran, Saudi Arabia. Electronic address: jaffar.tawfiq@jhah.com. · Specialty Internal Medicine Unit, Johns Hopkins Aramco Healthcare, Dhahran, Saudi Arabia. ·J Infect Public Health · Pubmed #25676545.

ABSTRACT: In recent years, fetal or autologous stem cell transplant for the treatment of Parkinson's disease (PD) has been practiced in a few medical organizations. However, the potential complications related to the growth of allograft tissue have not yet been well described apart from case reports. Here, we present a 42-year-old Saudi male who suffered from early onset Parkinson's disease. He sought medical care in China and received autologous intrathecal stem cell transplantation. He did not demonstrate any significant improvement. A few months later, the patient went back to China and underwent fetal cell transplantation into the left hemisphere and a second stem cell transplantation intrathecally. He presented with seizures and had a left frontal brain cyst. The cyst was drained and contained clear fluid. All cultures were negative. He had an uneventful recovery.

18 Review Molecular imaging of neuropsychiatric symptoms in Alzheimer's and Parkinson's disease. 2015

Hirao, Kentaro / Pontone, Gregory M / Smith, Gwenn S. ·Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, USA; Department of Geriatric Medicine, Tokyo Medical University, Tokyo, Japan. · Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, USA. · Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, USA. Electronic address: gsmith95@jhmi.edu. ·Neurosci Biobehav Rev · Pubmed #25446948.

ABSTRACT: Neuropsychiatric symptoms (NPS) are very common in neurodegenerative diseases and are a major contributor to disability and caregiver burden. There is accumulating evidence that NPS may be a prodrome and/or a "risk factor" of neurodegenerative diseases. The medications used to treat these symptoms in younger patients are not very effective in patients with neurodegenerative disease and may have serious side effects. An understanding of the neurobiology of NPS is critical for the development of more effective intervention strategies. Targeting these symptoms may also have implications for prevention of cognitive or motor decline. Molecular brain imaging represents a bridge between basic and clinical observations and provides many opportunities for translation from animal models and human post-mortem studies to in vivo human studies. Molecular brain imaging studies in Alzheimer's disease (AD) and Parkinson's disease (PD) are reviewed with a primary focus on positron emission tomography studies of NPS. Future directions for the field of molecular imaging in AD and PD to understand the neurobiology of NPS will be discussed.

19 Review Modes of physiologic H2S signaling in the brain and peripheral tissues. 2015

Paul, Bindu D / Snyder, Solomon H. ·1 The Solomon H. Snyder Department of Neuroscience, Johns Hopkins University School of Medicine , Baltimore, Maryland. ·Antioxid Redox Signal · Pubmed #24684551.

ABSTRACT: SIGNIFICANCE: Hydrogen sulfide (H2S), once associated with rotten eggs and sewers, is now recognized as a gasotransmitter that is synthesized in vivo in a regulated fashion. This ancient gaseous molecule has been retained throughout evolution to perform various roles in different life forms. H2S modulates important signaling functions in diverse cellular processes ranging from regulation of blood pressure to redox homeostasis. RECENT ADVANCES: One of the modes by which H2S signals is by post-translational modification of reactive cysteine residues in a process designated as sulfhydration, resulting in conversion of the -SH groups of target cysteine residues to -SSH. Using the modified biotin-switch assay and a fluorescent maleimide-based analysis, sulfhydration of several proteins has been detected in various cell types. Aberrant sulfhydration patterns occur in neurodegenerative conditions such as Parkinson's disease. CRITICAL ISSUES: The exact concentration, source of H2S, and conditions under which various stores of H2S are utilized have not been fully elucidated. Currently, available inhibitors of the biosynthetic enzymes of H2S lack sufficient specificity to shed light on detailed mechanisms of H2S action. Probes with a higher sensitivity that can reliably detect cellular and tissue H2S levels are yet to be developed. FUTURE DIRECTIONS: Availability of advanced probes and biosynthesis inhibitors would help in the measurement of real-time changes of endogenous H2S levels in an in vivo context. The study of the dynamics of sulfhydration and nitrosylation of critical cysteine residues of regulatory proteins involved in physiology and pathophysiology is an area of interest for the future.

20 Review LRRK2 pathobiology in Parkinson's disease. 2014

Martin, Ian / Kim, Jungwoo Wren / Dawson, Valina L / Dawson, Ted M. ·Neuroregeneration and Stem Cell Programs, Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA; Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. ·J Neurochem · Pubmed #25251388.

ABSTRACT: Mutations in the catalytic Roc-COR and kinase domains of leucine-rich repeat kinase 2 (LRRK2) are a common cause of familial Parkinson's disease (PD). LRRK2 mutations cause PD with age-related penetrance and clinical features identical to late-onset sporadic PD. Biochemical studies support an increase in LRRK2 kinase activity and a decrease in GTPase activity for kinase domain and Roc-COR mutations, respectively. Strong evidence exists that LRRK2 toxicity is kinase dependent leading to extensive efforts to identify selective and brain-permeable LRRK2 kinase inhibitors for clinical development. Cell and animal models of PD indicate that LRRK2 mutations affect vesicular trafficking, autophagy, protein synthesis, and cytoskeletal function. Although some of these biological functions are affected consistently by most disease-linked mutations, others are not and it remains currently unclear how mutations that produce variable effects on LRRK2 biochemistry and function all commonly result in the degeneration and death of dopamine neurons. LRRK2 is typically present in Lewy bodies and its toxicity in mammalian models appears to be dependent on the presence of α-synuclein, which is elevated in human iPS-derived dopamine neurons from patients harboring LRRK2 mutations. Here, we summarize biochemical and functional studies of LRRK2 and its mutations and focus on aberrant vesicular trafficking and protein synthesis as two leading mechanisms underlying LRRK2-linked disease.

21 Review Multiple system atrophy as emerging template for accelerated drug discovery in α-synucleinopathies. 2014

Krismer, Florian / Jellinger, Kurt A / Scholz, Sonja W / Seppi, Klaus / Stefanova, Nadia / Antonini, Angelo / Poewe, Werner / Wenning, Gregor K. ·Department of Neurology, Innsbruck Medical University, Innsbruck, Austria. Electronic address: florian.krismer@i-med.ac.at. · Institute of Clinical Neurobiology, Vienna, Austria. Electronic address: kurt.jellinger@univie.ac.at. · Department of Neurology, The Johns Hopkins Hospital, Baltimore, MD 21287, USA. Electronic address: sonja.w.scholz@googlemail.com. · Department of Neurology, Innsbruck Medical University, Innsbruck, Austria. Electronic address: klaus.seppi@uki.at. · Department of Neurology, Innsbruck Medical University, Innsbruck, Austria. Electronic address: nadia.stefanova@i-med.ac.at. · Department of Parkinson's Disease and Movement Disorders, IRCCS San Camillo, Venice, Italy. Electronic address: angelo3000@yahoo.com. · Department of Neurology, Innsbruck Medical University, Innsbruck, Austria. Electronic address: werner.poewe@i-med.ac.at. · Department of Neurology, Innsbruck Medical University, Innsbruck, Austria. Electronic address: Gregor.Wenning@i-med.ac.at. ·Parkinsonism Relat Disord · Pubmed #24894118.

ABSTRACT: There is evidence that the α-synucleinopathies Parkinson's disease (PD) and the Parkinson variant of multiple system atrophy (MSA-P) overlap at multiple levels. Both disorders are characterized by deposition of abnormally phosphorylated fibrillar α-synuclein within the central nervous system suggesting shared pathophysiological mechanisms. Despite the considerable clinical overlap in the early disease stages, MSA-P, in contrast to PD, is fatal and rapidly progressive. Moreover recent clinical studies have shown that surrogate markers of disease progression can be quantified easily and may reliably depict the rapid course of MSA. We therefore posit that, MSA-P may be exploited as a filter barrier in the development of disease-modifying therapeutic strategies targeting common pathophysiological mechanisms of α-synucleinopathies. This approach might reduce the number of negative phase III clinical trials, and, in turn, shift the available resources to earlier development stages, thereby increasing the number of candidate compounds validated.

22 Review Poly (ADP-ribose) in the pathogenesis of Parkinson's disease. 2014

Lee, Yunjong / Kang, Ho Chul / Lee, Byoung Dae / Lee, Yun-Il / Kim, Young Pil / Shin, Joo-Ho. ·Neuroregeneration and Stem Cell Programs, Institute for Cell Engineering; Departments of Physiology, and Neurology, the Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA. · Neuroregeneration and Stem Cell Programs, Institute for Cell Engineering; Departments of Neurology, the Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA; Department of Physiology, Ajou University School of Medicine, Suwon 443-721, Korea. · Neurodegeneration Control Research Center, Department of Neuroscience, Kyung Hee University, Seoul 130-701, Korea. · Well Aging Research Center, Samsung Advanced Institute of Technology (SAIT), Suwon 443-803, Korea. · Department of Bio-Engineering, Life Science RD Center, Sinil Pharmaceutical Co., Seoul 462-807, Korea. · Neuroregeneration and Stem Cell Programs, Institute for Cell Engineering; Departments of Neurology, the Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA; Division of Pharmacology, Department of Molecular Cell Biology, Sungkyunkwan University School of Medicine, Samsung Biomedical Research Institute, Suwon 440-746, Korea. ·BMB Rep · Pubmed #24874851.

ABSTRACT: The defining feature of Parkinson's disease is a progressive and selective demise of dopaminergic neurons. A recent report on Parkinson's disease animal model demonstrates that poly (ADP-ribose) (PAR) dependent cell death, also named parthanatos, is accountable for selective dopaminergic neuronal loss. Parthanatos is a programmed necrotic cell death, characterized by PARP1 activation, apoptosis inducing factor (AIF) nuclear translocation, and large scale DNA fragmentation. Besides cell death regulation via interaction with AIF, PAR molecule mediates diverse cellular processes including genomic stability, cell division, transcription, epigenetic regulation, and stress granule formation. In this review, we will discuss the roles of PARP1 activation and PAR molecules in the pathological processes of Parkinson's disease. Potential interaction between PAR molecule and Parkinson's disease protein interactome are briefly introduced. Finally, we suggest promising points of therapeutic intervention in the pathological PAR signaling cascade to halt progression in Parkinson's disease.

23 Review Human-induced pluripotent stem cells: potential for neurodegenerative diseases. 2014

Ross, Christopher A / Akimov, Sergey S. ·Division of Neurobiology, Department of Psychiatry and Departments of Neurology, Neuroscience and Pharmacology, and Program in Cellular and Molecular Medicine, Johns Hopkins University School of Medicine, Baltimore, MA, USA caross@jhu.edu. · Division of Neurobiology, Department of Psychiatry and. ·Hum Mol Genet · Pubmed #24824217.

ABSTRACT: The cell biology of human neurodegenerative diseases has been difficult to study till recently. The development of human induced pluripotent stem cell (iPSC) models has greatly enhanced our ability to model disease in human cells. Methods have recently been improved, including increasing reprogramming efficiency, introducing non-viral and non-integrating methods of cell reprogramming, and using novel gene editing techniques for generating genetically corrected lines from patient-derived iPSCs, or for generating mutations in control cell lines. In this review, we highlight accomplishments made using iPSC models to study neurodegenerative disorders such as Huntington's disease, Parkinson's disease, Amyotrophic Lateral Sclerosis, Fronto-Temporal Dementia, Alzheimer's disease, Spinomuscular Atrophy and other polyglutamine diseases. We review disease-related phenotypes shown in patient-derived iPSCs differentiated to relevant neural subtypes, often with stressors or cell "aging", to enhance disease-specific phenotypes. We also discuss prospects for the future of using of iPSC models of neurodegenerative disorders, including screening and testing of therapeutic compounds, and possibly of cell transplantation in regenerative medicine. The new iPSC models have the potential to greatly enhance our understanding of pathogenesis and to facilitate the development of novel therapeutics.

24 Review Systematic review of factors associated with depression and anxiety disorders among older adults with Parkinson's disease. 2014

Sagna, Atami / Gallo, Joseph J / Pontone, Gregory M. ·Department of Mental Health, Johns Hopkins University Bloomberg School of Public Health, Baltimore, MD, USA. · Department of Mental Health, Johns Hopkins University Bloomberg School of Public Health, Baltimore, MD, USA. Electronic address: jgallo@jhsph.edu. · Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, MD, USA. ·Parkinsonism Relat Disord · Pubmed #24780824.

ABSTRACT: Depression and anxiety disorders have a substantial impact on the quality of life, the functioning and mortality of older adults with Parkinson's disease (PD). The purpose of this systematic review was to examine the factors associated with the prevalence of depression and anxiety disorders among individuals with PD aged 60 years and older. Following a literature search in PubMed, PsycINFO, CINAHL, and EMBASE, 5 articles met the inclusion criteria (adults aged 60 years and older, individuals with PD, and with depression and anxiety disorders, and English-language peer reviewed articles) and were included in this review. These studies were conducted in the U.S (n = 3), in Italy (n = 1) and the U.K (n = 1). Findings indicated that autonomic symptoms, motor fluctuations, severity and frequency of symptoms, staging of the disease, and PD onset and duration were associated with the prevalence of depression and anxiety disorders among older adults suffering from PD. Despite the limited number of studies included in the review, depression and anxiety disorders are often unrecognized and untreated and the comorbidity greatly exacerbates PD symptoms. The identification of factors associated with the development of depression and anxiety disorders could help in designing preventive interventions that would decrease the risk and burden of depression and anxiety disorders among older adults with PD.

25 Review Parkin and PINK1: much more than mitophagy. 2014

Scarffe, Leslie A / Stevens, Daniel A / 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; Solomon H. Snyder Department of Neuroscience, 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; Solomon H. Snyder Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA. · Neuroregeneration and Stem Cell Programs, Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA; Solomon H. Snyder Department of Neuroscience, 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. Electronic address: vdawson@jhmi.edu. · Neuroregeneration and Stem Cell Programs, Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA; Solomon H. Snyder Department of Neuroscience, 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: tdawson@jhmi.edu. ·Trends Neurosci · Pubmed #24735649.

ABSTRACT: Parkinson's disease (PD) is a progressive neurodegenerative disease that causes a debilitating movement disorder. Although most cases of PD appear to be sporadic, rare Mendelian forms have provided tremendous insight into disease pathogenesis. Accumulating evidence suggests that impaired mitochondria underpin PD pathology. In support of this theory, data from multiple PD models have linked Phosphatase and tensin homolog (PTEN)-induced putative kinase 1 (PINK1) and parkin, two recessive PD genes, in a common pathway impacting mitochondrial health, prompting a flurry of research to identify their mitochondrial targets. Recent work has focused on the role of PINK1 and parkin in mediating mitochondrial autophagy (mitophagy); however, emerging evidence casts parkin and PINK1 as key players in multiple domains of mitochondrial health and quality control.

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