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Parkinson Disease: HELP
Articles from Illinois
Based on 729 articles published since 2010
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These are the 729 published articles about Parkinson Disease that originated from Illinois during 2010-2020.
 
+ 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 Diet to beat the odds of prodromal Parkinson's disease? 2019

Tangney, Christy C. ·Professor, Departments of Clinical Nutrition & Preventive Medicine and Associate Dean for Research, College of Health Sciences, Rush University Medical Center, Chicago, Illinois, USA. ·Mov Disord · Pubmed #30397942.

ABSTRACT: -- No abstract --

2 Editorial Biomedical devices go wild. 2018

Rogers, John / Malliaras, George / Someya, Takao. ·John Rogers, Northwestern University, Evanston, IL 60208, USA. Email: jrogers@northwestern.edu. · George Malliaras, University of Cambridge, Cambridge, UK. Email: gm603@cam.ac.uk. · Takao Someya, University of Tokyo, Tokyo, Japan. Email: someya@ee.t.u-tokyo.ac.jp. ·Sci Adv · Pubmed #30255157.

ABSTRACT: -- No abstract --

3 Editorial Cerebrospinal fluid levels of alpha-synuclein in PARKINSON'S disease: Another long and winding road. 2018

Markopoulou, Katerina / Compta, Yaroslau. ·Movement Disorders Section, Department of Neurology, NorthShore University HealthSystem, Chicago, Evanston, USA; University of Chicago, Pritzker School of Medicine, Chicago, IL, USA. · Parkinson's Disease and Movement Disorders Unit, Neurology Service, ICN, Hospital Clínic, IDIBAPS, CIBERNED, Barcelona, Catalonia, Spain; Physiology Unit, Department of Biomedicine, Institut de Neurociències, University of Barcelona, Barcelona, Catalonia, Spain. Electronic address: ycompta@clinic.cat. ·Parkinsonism Relat Disord · Pubmed #29548634.

ABSTRACT: -- No abstract --

4 Editorial Closing the celebration of 200 years of Parkinson's Essay on the Shaking Palsy: Where do we go in the next 200 years? 2017

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

ABSTRACT: -- No abstract --

5 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 --

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

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

ABSTRACT: -- No abstract --

7 Editorial Editorial: Molecular Diagnostics in the Detection of Neurodegenerative Disorders. 2017

Agrawal, Megha / Cho, William C. ·Department of Bioengineering, University of Illinois at Chicago Chicago, IL, USA. · Department of Clinical Oncology, Queen Elizabeth Hospital Kowloon, Hong Kong. ·Front Mol Biosci · Pubmed #28303242.

ABSTRACT: -- No abstract --

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

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

ABSTRACT: -- No abstract --

9 Editorial Preface. 2015

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

ABSTRACT: -- No abstract --

10 Review Chronic stress-induced gut dysfunction exacerbates Parkinson's disease phenotype and pathology in a rotenone-induced mouse model of Parkinson's disease. 2020

Dodiya, Hemraj B / Forsyth, Christopher B / Voigt, Robin M / Engen, Phillip A / Patel, Jinal / Shaikh, Maliha / Green, Stefan J / Naqib, Ankur / Roy, Avik / Kordower, Jeffrey H / Pahan, Kalipada / Shannon, Kathleen M / Keshavarzian, Ali. ·Department of Neurobiology, the University of Chicago, Chicago, IL, USA; Department of Internal Medicine, Division of Digestive Diseases, Rush University Medical Center, Chicago, IL, USA. · Department of Internal Medicine, Division of Digestive Diseases, Rush University Medical Center, Chicago, IL, USA. · Department of Biological Sciences, University of Illinois at Chicago, Chicago, IL, USA. · Department of Neurology, Rush University Medical Center, Chicago, IL, USA. · Department of Neurology, University of Wisconsin School of Public Health, Madison, WI, USA. · Department of Internal Medicine, Division of Digestive Diseases, Rush University Medical Center, Chicago, IL, USA; Division of Pharmacology, Utrecht Institute for Pharmaceutical Sciences, Utrecht University, Utrecht, Netherlands. Electronic address: Ali_Keshavarzian@rush.edu. ·Neurobiol Dis · Pubmed #30579705.

ABSTRACT: Recent evidence provides support for involvement of the microbiota-gut-brain axis in Parkinson's disease (PD) pathogenesis. We propose that a pro-inflammatory intestinal milieu, due to intestinal hyper-permeability and/or microbial dysbiosis, initiates or exacerbates PD pathogenesis. One factor that can cause intestinal hyper-permeability and dysbiosis is chronic stress which has been shown to accelerate neuronal degeneration and motor deficits in Parkinsonism rodent models. We hypothesized that stress-induced intestinal barrier dysfunction and microbial dysbiosis lead to a pro-inflammatory milieu that exacerbates the PD phenotype in the low-dose oral rotenone PD mice model. To test this hypothesis, mice received unpredictable restraint stress (RS) for 12 weeks, and during the last six weeks mice also received a daily administration of low-dose rotenone (10 mg/kg/day) orally. The initial six weeks of RS caused significantly higher urinary cortisol, intestinal hyperpermeability, and decreased abundance of putative "anti-inflammatory" bacteria (Lactobacillus) compared to non-stressed mice. Rotenone alone (i.e., without RS) disrupted the colonic expression of the tight junction protein ZO-1, increased oxidative stress (N-tyrosine), increased myenteric plexus enteric glial cell GFAP expression and increased α-synuclein (α-syn) protein levels in the colon compared to controls. Restraint stress exacerbated these rotenone-induced changes. Specifically, RS potentiated rotenone-induced effects in the colon including: 1) intestinal hyper-permeability, 2) disruption of tight junction proteins (ZO-1, Occludin, Claudin1), 3) oxidative stress (N-tyrosine), 4) inflammation in glial cells (GFAP + enteric glia cells), 5) α-syn, 6) increased relative abundance of fecal Akkermansia (mucin-degrading Gram-negative bacteria), and 7) endotoxemia. In addition, RS promoted a number of rotenone-induced effects in the brain including: 1) reduced number of resting microglia and a higher number of dystrophic/phagocytic microglia as well as (FJ-C+) dying cells in the substantia nigra (SN), 2) increased lipopolysaccharide (LPS) reactivity in the SN, and 3) reduced dopamine (DA) and DA metabolites (DOPAC, HVA) in the striatum compared to control mice. Our findings support a model in which chronic stress-induced, gut-derived, pro-inflammatory milieu exacerbates the PD phenotype via a dysfunctional microbiota-gut-brain axis.

11 Review Diet in Parkinson's Disease: Critical Role for the Microbiome. 2019

Jackson, Aeja / Forsyth, Christopher B / Shaikh, Maliha / Voigt, Robin M / Engen, Phillip A / Ramirez, Vivian / Keshavarzian, Ali. ·Division of Digestive Diseases, Department of Internal Medicine, Rush University Medical Center, Chicago, IL, United States. · Graduate College of Rush University, Chicago, IL, United States. ·Front Neurol · Pubmed #31920905.

ABSTRACT:

12 Review Advance care planning in Parkinson's disease: ethical challenges and future directions. 2019

Sokol, Leonard L / Young, Michael J / Paparian, Jack / Kluger, Benzi M / Lum, Hillary D / Besbris, Jessica / Kramer, Neha M / Lang, Anthony E / Espay, Alberto J / Dubaz, Ornella M / Miyasaki, Janis M / Matlock, Daniel D / Simuni, Tanya / Cerf, Moran. ·1The Ken and Ruth Davee Department of Neurology, Northwestern University Feinberg School of Medicine, Chicago, IL USA. · 0000 0001 2299 3507 · grid.16753.36 · 2McGaw Bioethics Scholars Program, Center for Bioethics and Humanities, Northwestern University Feinberg School of Medicine, Chicago, IL USA. · 3Department of Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL USA. · Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Boston, MA USA. · Independent Researcher, San Francisco, CA USA. · 6Division of Neuropallaitive Care, Department of Neurology, University of Colorado School of Medicine, Aurora, CO USA. · 0000 0001 0703 675X · grid.430503.1 · 7Eastern Colorado VA Geriatric Research Education and Clinical Center and the Division of Geriatric Medicine, Department of Medicine, University of Colorado School of Medicine, Aurora, CO USA. · 8Departments of Neurology and Supportive Care Medicine, Cedars-Sinai Medical Center, Los Angeles, CA USA. · 0000 0001 2152 9905 · grid.50956.3f · 9Departments of Medicine (Section of Palliative Medicine) and Neurology, Rush University School of Medicine, Chicago, IL USA. · 0000000107058297 · grid.262743.6 · 10The Edmond J. Safra Program in Parkinson's Disease and the Morton and Gloria Shulman Movement Disorders Clinic, University Health Network, University of Toronto, Toronto, ON Canada. · 0000 0001 2157 2938 · grid.17063.33 · 11Gardner Family Center for Parkinson's Disease and Movement Disorders, Department of Neurology, University of Cincinnati College of Medicine, Cincinnati, OH USA. · 0000 0001 2179 9593 · grid.24827.3b · Department of Neurology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA USA. · 13Department of Medicine, Division of Neurology, Parkinson and Movement Disorders Program and the Complex Neurologic Symptoms Clinic, Kaye Edmonton Clinic, University of Alberta, Edmonton, AL Canada. · grid.17089.37 · 14Interdepartmental Neuroscience Program, Northwestern University, Evanston, IL USA. · 15Kellogg School of Management, Northwestern University, Evanston, IL USA. ·NPJ Parkinsons Dis · Pubmed #31799376.

ABSTRACT: Recent discoveries support the principle that palliative care may improve the quality of life of patients with Parkinson's disease and those who care for them. Advance care planning, a component of palliative care, provides a vehicle through which patients, families, and clinicians can collaborate to identify values, goals, and preferences early, as well as throughout the disease trajectory, to facilitate care concordant with patient wishes. While research on this topic is abundant in other life-limiting disorders, particularly in oncology, there is a paucity of data in Parkinson's disease and related neurological disorders. We review and critically evaluate current practices on advance care planning through the analyses of three bioethical challenges pertinent to Parkinson's disease and propose recommendations for each.

13 Review Immunotherapy in Parkinson's disease: Current status and future directions. 2019

Chatterjee, Diptaman / Kordower, Jeffrey H. ·Department of Neurological Sciences, Rush University Medical Center, Chicago, IL 60612, USA. · Department of Neurological Sciences, Rush University Medical Center, Chicago, IL 60612, USA. Electronic address: jkordowe@rush.edu. ·Neurobiol Dis · Pubmed #31454546.

ABSTRACT: Immunotherapeutic approaches for the treatment of Parkinson's disease (PD) and related synucleinopathies have steadily developed over the last two decades with several iterations currently being tested in clinical trials. Although classically characterized as a movement disorder, PD is also defined clinically by numerous non-motor features that can precede the motor manifestations and span across several decades of disease progression. Pathologically, PD is characterized by proteinaceous inclusions that largely consist of misfolded and aggregated forms of the protein, alpha-synuclein. Recent research has proposed that alpha-synuclein pathology is capable of propagating from cell-to-cell, and thus, may cause the clinical progression of the disease. Antibody-based therapies are ideal drugs to theoretically target pathological proteins, especially those located in the extracellular space. Several other targeting strategies have been developed to indirectly mitigate the propagation of alpha-synuclein and are in various stages of pre-clinical and clinical development. In this review, we discuss the current status of development for immunotherapies in PD as well as the primary challenges that must be hurdled to bring an effective immunotherapeutic drug to market.

14 Review RANTES-induced invasion of Th17 cells into substantia nigra potentiates dopaminergic cell loss in MPTP mouse model of Parkinson's disease. 2019

Dutta, Debashis / Kundu, Madhuchhanda / Mondal, Susanta / Roy, Avik / Ruehl, Samantha / Hall, Deborah A / Pahan, Kalipada. ·Department of Neurological Sciences, Rush University Medical Center, Chicago, USA. · Department of Neurological Sciences, Rush University Medical Center, Chicago, USA; Division of Research and Development, Jesse Brown Veterans Affairs Medical Center, Chicago, USA. · Department of Neurological Sciences, Rush University Medical Center, Chicago, USA; Division of Research and Development, Jesse Brown Veterans Affairs Medical Center, Chicago, USA. Electronic address: Kalipada_Pahan@rush.edu. ·Neurobiol Dis · Pubmed #31445159.

ABSTRACT: Although Parkinson's disease (PD) is a progressive neurodegenerative disease, the disease does not progress or persist in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model, the most common animal model of PD. Recently, we have described that supplementation of regulated on activation, normal T cell expressed and secreted (RANTES), a chemokine known to drive infiltration of T cells, induces persistent nigrostriatal pathology in MPTP mouse model. However, which particular T cell subsets are recruited to the substantia nigra (SN) by RANTES is not known. Here, by adoptive transfer of different subset of T cells from tomato red transgenic mice to MPTP-intoxicated immunodeficient Rag1

15 Review The role of dopamine in the pathogenesis of GBA1-linked Parkinson's disease. 2019

Burbulla, Lena F / Krainc, Dimitri. ·Department of Neurology, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA. · Department of Neurology, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA. Electronic address: dkrainc@nm.org. ·Neurobiol Dis · Pubmed #31351996.

ABSTRACT: Our understanding of the molecular mechanisms underlying differential vulnerability of substantia nigra dopamine neurons in Parkinson's disease (PD) remains limited, and previous therapeutic efforts targeting rodent nigral neurons have not been successfully translated to humans. However, recent emergence of induced pluripotent stem cell technology has highlighted some fundamental differences between human and rodent midbrain dopamine neurons that may at least in part explain relative resistance of rodent neurons to degeneration in genetic models of PD. Using GBA1-linked PD as an example, we discuss cellular pathways that may predispose human neurons to degeneration in PD, including mitochondrial oxidant stress, elevated intracellular calcium, altered synaptic vesicle endocytosis, accumulation of oxidized dopamine and neuromelanin. Recent studies have suggested that a combination of mitochondrial oxidant stress and accumulation of oxidized dopamine contribute to dysfunction of nigral neurons in various genetic and sporadic forms of PD. We also briefly summarize the development of targeted therapies for GBA1-associated synucleinopathies and highlight that modulation of wild-type GCase activity serves as an important target for the treatment of genetic and idiopathic forms of PD and dementia with Lewy bodies.

16 Review Scales to assess impulsive and compulsive behaviors in Parkinson's disease: Critique and recommendations. 2019

Evans, Andrew H / Okai, David / Weintraub, Daniel / Lim, Shen-Yang / O'Sullivan, Sean S / Voon, Valerie / Krack, Paul / Sampaio, Cristina / Post, Bart / Leentjens, Albert F G / Martinez-Martin, Pablo / Stebbins, Glenn T / Goetz, Christopher G / Schrag, Anette / Anonymous7760991. ·Department of Neurology, the Royal Melbourne Hospital, Parkville, Australia. · Kings College London, Institute of Psychiatry, Section of Cognitive Neuropsychiatry, London, UK. · Department of Psychiatry, University of Pennsylvania, Philadelphia, Pennsylvania, USA. · Parkinson's Disease and Mental Illness Research, Education and Clinical Centers (Philadelphia Parkinson's Disease Research, Education and Clinical Center (PADRECC) and Mental Illness Research Education Clinical, Centers of Excellence (MIRECC)), Philadelphia Veterans Affairs Medical Center, Philadelphia, Pennsylvania, USA. · Division of Neurology, Department of Medicine, University of Malaya, Kuala Lumpur, Malaysia. · Department of Neurology, Bon Secours Hospital, Cork, Ireland. · Department of Psychiatry, University of Cambridge, Cambridge, UK. · Movement Disorders Center, Department of Neurology, University Hospital (Inselspital) and University of Bern, Bern Switzerland. · Cure Huntington's Disease InitiativeEl (CHDI) Management/CHDI Foundation, Princeton, New Jersey, USA. · Department of Neurology, Radboud University Nijmegen Medical Center, Nijmegen, The Netherlands. · Department of Psychiatry, Maastricht University Medical Center, Maastricht, The Netherlands. · National Center of Epidemiology and Centro de Investigacion Biomedica en Red sobre Enfermedades Neurodegenerativas (CIBERNED), Carlos III Institute of Health, Madrid, Spain. · Department of Neurological Sciences, Rush University Medical Center, Chicago, Illinois, USA. · Department of Clinical Neurosciences, Institute of Neurology, University College London, London, UK. ·Mov Disord · Pubmed #31136681.

ABSTRACT: Impulse control disorders (ICDs) and related impulsive and compulsive behaviors (together called ICBs) have been increasingly recognized in the context of Parkinson's disease (PD) and treatment. The International Parkinson's and Movement Disorder Society commissioned a task force to assess available clinical screening instruments and rating scales, including their clinimetric properties, make recommendations regarding their utility, and suggest future directions in scale development and validation. The literature was systematically searched for scales measuring a range of reported ICBs in PD. A scale was designated "recommended" if the scale had been employed in PD studies, been used beyond the group that developed it, and had adequate clinimetric data published for PD. Numerous diagnostic screening tools and severity rating scales were identified for a range of ICBs, including compulsive medication use, punding/hobbyism, walkabout, pathological gambling, hypersexuality, compulsive or binge eating, compulsive buying, reckless driving, compulsive exercise, pyromania, trichotillomania, hoarding, kleptomania, intermittent explosive disorder, and internet addiction. For screening across the range of ICBs (except compulsive medication use), the Questionnaire for Impulsive-Compulsive Disorders in Parkinson's disease (QUIP) and QUIP-Rating Scale (QUIP-RS) are recommended, and for severity rating across the range of ICBs the QUIP-RS and the Ardouin Scale of Behavior in Parkinson's Disease are recommended. The Scale for Outcomes in Parkinson's Disease-Psychiatric Complications is recommended for rating of hypersexuality and the compulsive behaviors gambling/shopping. Further testing of established scales against gold standard diagnostic criteria is urgently required for all other individual ICBs in PD. © 2019 International Parkinson and Movement Disorder Society © 2019 International Parkinson and Movement Disorder Society.

17 Review Using wearables to assess bradykinesia and rigidity in patients with Parkinson's disease: a focused, narrative review of the literature. 2019

Teshuva, Itay / Hillel, Inbar / Gazit, Eran / Giladi, Nir / Mirelman, Anat / Hausdorff, Jeffrey M. ·Center for the Study of Movement, Cognition and Mobility, Neurological Institute, Tel Aviv Sourasky Medical Center, Tel Aviv, Israel. · Sagol School of Neuroscience, Tel Aviv University, Tel Aviv, Israel. · Department of Neurology and Neurosurgery, Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel. · Center for the Study of Movement, Cognition and Mobility, Neurological Institute, Tel Aviv Sourasky Medical Center, Tel Aviv, Israel. jhausdor@tlvmc.gov.il. · Sagol School of Neuroscience, Tel Aviv University, Tel Aviv, Israel. jhausdor@tlvmc.gov.il. · Department of Physical Therapy, Sackler Faculty of Medicine, Tel Aviv, Israel. jhausdor@tlvmc.gov.il. · Rush Alzheimer's Disease Center, Chicago, USA. jhausdor@tlvmc.gov.il. · Department of Orthopedic Surgery, Rush University Medical Center, Chicago, USA. jhausdor@tlvmc.gov.il. ·J Neural Transm (Vienna) · Pubmed #31115669.

ABSTRACT: The potential of using wearable technologies for the objective assessment of motor symptoms in Parkinson's disease (PD) has gained prominence recently. Nonetheless, compared to tremor and gait impairment, less emphasis has been placed on the quantification of bradykinesia and rigidity. This review aimed to consolidate the existing research on objective measurement of bradykinesia and rigidity in PD through the use of wearables, focusing on the continuous monitoring of these two symptoms in free-living environments. A search of PubMed was conducted through a combination of keyword and MeSH searches. We also searched the IEEE, Google Scholar, Embase, and Scopus databases to ensure thorough results and to minimize the chances of missing relevant studies. Papers published after the year 2000 with sample sizes greater than five were included. Studies were assessed for quality and information was extracted regarding the devices used and their location on the body, the setting and duration of the study, the "gold standard" used as a reference for validation, the metrics used, and the results of each paper. Thirty-one and eight studies met the search criteria and evaluated bradykinesia and rigidity, respectively. Several studies reported strong associations between wearable-based measures and the gold-standard references for bradykinesia, and, to a lesser extent, rigidity. Only a few, pilot studies investigated the measurement of bradykinesia and rigidity in the home and free-living settings. While the current results are promising for the future of wearables, additional work is needed on their validation and adaptation in ecological, free-living settings. Doing so has the potential to improve the assessment and treatment of motor fluctuations and symptoms of PD more generally through real-time objective monitoring of bradykinesia and rigidity.

18 Review Dopaminergic modulation of striatal function and Parkinson's disease. 2019

Zhai, Shenyu / Shen, Weixing / Graves, Steven M / Surmeier, D James. ·Department of Physiology, Feinberg School of Medicine, Northwestern University, Chicago, IL, 60611, USA. · Department of Pharmacology, University of Minnesota Medical School, Minneapolis, MN, 55455, USA. · Department of Physiology, Feinberg School of Medicine, Northwestern University, Chicago, IL, 60611, USA. j-surmeier@northwestern.edu. ·J Neural Transm (Vienna) · Pubmed #30937538.

ABSTRACT: The striatum is richly innervated by mesencephalic dopaminergic neurons that modulate a diverse array of cellular and synaptic functions that control goal-directed actions and habits. The loss of this innervation has long been thought to be the principal cause of the cardinal motor symptoms of Parkinson's disease (PD). Moreover, chronic, pharmacological overstimulation of striatal dopamine (DA) receptors is generally viewed as the trigger for levodopa-induced dyskinesia (LID) in late-stage PD patients. Here, we discuss recent advances in our understanding of the relationship between the striatum and DA, particularly as it relates to PD and LID. First, it has become clear that chronic perturbations of DA levels in PD and LID bring about cell type-specific, homeostatic changes in spiny projection neurons (SPNs) that tend to normalize striatal activity. Second, perturbations in DA signaling also bring about non-homeostatic aberrations in synaptic plasticity that contribute to disease symptoms. Third, it has become evident that striatal interneurons are major determinants of network activity and behavior in PD and LID. Finally, recent work examining the activity of SPNs in freely moving animals has revealed that the pathophysiology induced by altered DA signaling is not limited to imbalance in the average spiking in direct and indirect pathways, but involves more nuanced disruptions of neuronal ensemble activity.

19 Review A roadmap for implementation of patient-centered digital outcome measures in Parkinson's disease obtained using mobile health technologies. 2019

Espay, Alberto J / Hausdorff, Jeffrey M / Sánchez-Ferro, Álvaro / Klucken, Jochen / Merola, Aristide / Bonato, Paolo / Paul, Serene S / Horak, Fay B / Vizcarra, Joaquin A / Mestre, Tiago A / Reilmann, Ralf / Nieuwboer, Alice / Dorsey, E Ray / Rochester, Lynn / Bloem, Bastiaan R / Maetzler, Walter / Anonymous2170984. ·James J. and Joan A. Gardner Family Center for Parkinson's Disease and Movement Disorders, University of Cincinnati, Cincinnati, Ohio, USA. · Center for the Study of Movement, Cognition, and Mobility, Department of Neurology, Tel Aviv Sourasky Medical Center, Tel Aviv, Israel. · Department of Physical Therapy, Sackler Faculty of Medicine and Sagol School of Neuroscience, Tel Aviv University, Tel Aviv, Israel. · Rush Alzheimer's Disease Center and Department of Orthopedic Surgery, Rush University, Chicago, Illinois, USA. · HM CINAC, Hospital Universitario HM Puerta del Sur, Móstoles, Madrid, Spain. · Department of Molecular Neurology, University Hospital Erlangen, Friedrich-Alexander University Erlangen-Nürnberg, Erlangen, Germany. · Fraunhofer Institut for Integrated Circuits, Digital Health Pathway Research Group, Erlangen, Germany. · Department of Physical Medicine and Rehabilitation, Harvard Medical School, Boston, Massachusetts, USA. · Discipline of Physiotherapy, Faculty of Health Sciences, The University of Sydney, Sydney, New South Wales, Australia. · Department of Neurology, Oregon Health & Science University, Portland Veterans Affairs Medical System, Portland, Oregon, USA. · APDM, Inc, Portland, Oregon, USA. · Parkinson's Disease and Movement Disorders Center, Division of Neurology, Department of Medicine, The Ottawa Hospital Research Institute, University of Ottawa, Ottawa, ON, Canada. · George-Huntington-Institute, Technology Park, Muenster, Germany. · Department of Radiology, University of Muenster, Muenster, Germany. · Department of Neurodegenerative Diseases and Hertie-Institute for Clinical Brain Research, University of Tuebingen, Tuebingen, Germany. · Neuromotor Rehabilitation Research Group, Department of Rehabilitation Sciences, KU Leuven, Leuven, Belgium. · Department of Neurology, University of Rochester Medical Center, Rochester, New York, USA. · Institute of Neuroscience, Newcastle University, Newcastle Upon Tyne NE4 5PL, UK. · Newcastle upon Tyne Hospitals National Health Service Foundation Trust, Newcastle upon Tyne, UK. · Radboud University Medical Center, Donders Institute for Brain, Cognition and Behaviour, Department of Neurology, Nijmegen, The Netherlands. · Department of Neurology, Christian-Albrechts University, Kiel, Germany. ·Mov Disord · Pubmed #30901495.

ABSTRACT: Obtaining reliable longitudinal information about everyday functioning from individuals with Parkinson's disease (PD) in natural environments is critical for clinical care and research. Despite advances in mobile health technologies, the implementation of digital outcome measures is hindered by a lack of consensus on the type and scope of measures, the most appropriate approach for data capture (eg, in clinic or at home), and the extraction of timely information that meets the needs of patients, clinicians, caregivers, and health care regulators. The Movement Disorder Society Task Force on Technology proposes the following objectives to facilitate the adoption of mobile health technologies: (1) identification of patient-centered and clinically relevant digital outcomes; (2) selection criteria for device combinations that offer an acceptable benefit-to-burden ratio to patients and that deliver reliable, clinically relevant insights; (3) development of an accessible, scalable, and secure platform for data integration and data analytics; and (4) agreement on a pathway for approval by regulators, adoption into e-health systems and implementation by health care organizations. We have developed a tentative roadmap that addresses these needs by providing the following deliverables: (1) results and interpretation of an online survey to define patient-relevant endpoints, (2) agreement on the selection criteria for use of device combinations, (3) an example of an open-source platform for integrating mobile health technology output, and (4) recommendations for assessing readiness for deployment of promising devices and algorithms suitable for regulatory approval. This concrete implementation guidance, harmonizing the collaborative endeavor among stakeholders, can improve assessments of individuals with PD, tailor symptomatic therapy, and enhance health care outcomes. © 2019 International Parkinson and Movement Disorder Society.

20 Review Emerging links between pediatric lysosomal storage diseases and adult parkinsonism. 2019

Ysselstein, Daniel / Shulman, Joshua M / Krainc, Dimitri. ·Ken and Ruth Davee Department of Neurology, Northwestern University Feinberg School of Medicine, Chicago, Illinois, USA. · Departments of Neurology, Neuroscience, and Molecular and Human Genetics, Baylor College of Medicine, Houston, Texas, USA. · Jan and Dan Duncan Neurologic Research Institute, Texas Children's Hospital, Houston, Texas, USA. ·Mov Disord · Pubmed #30726573.

ABSTRACT: Lysosomal storage disorders comprise a clinically heterogeneous group of autosomal-recessive or X-linked genetic syndromes caused by disruption of lysosomal biogenesis or function resulting in accumulation of nondegraded substrates. Although lysosomal storage disorders are diagnosed predominantly in children, many show variable expressivity with clinical presentations possible later in life. Given the important role of lysosomes in neuronal homeostasis, neurological manifestations, including movement disorders, can accompany many lysosomal storage disorders. Over the last decade, evidence from genetics, clinical epidemiology, cell biology, and biochemistry have converged to implicate links between lysosomal storage disorders and adult-onset movement disorders. The strongest evidence comes from mutations in Glucocerebrosidase, which cause Gaucher's disease and are among the most common and potent risk factors for PD. However, recently, many additional lysosomal storage disorder genes have been similarly implicated, including SMPD1, ATP13A2, GALC, and others. Examination of these links can offer insight into pathogenesis of PD and guide development of new therapeutic strategies. We systematically review the emerging genetic links between lysosomal storage disorders and PD. © 2019 International Parkinson and Movement Disorder Society.

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

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

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

22 Review The pedunclopontine nucleus and Parkinson's disease. 2019

Tubert, Cecilia / Galtieri, Daniel / Surmeier, D James. ·Department of Physiology, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA. · Department of Physiology, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA. Electronic address: j-surmeier@northwestern.edu. ·Neurobiol Dis · Pubmed #30171892.

ABSTRACT: In the last decade, scientific and clinical interest in the pedunculopontine nucleus (PPN) has grown dramatically. This growth is largely a consequence of experimental work demonstrating its connection to the control of gait and of clinical work implicating PPN pathology in levodopa-insensitive gait symptoms of Parkinson's disease (PD). In addition, the development of optogenetic and chemogenetic approaches has made experimental analysis of PPN circuitry and function more tractable. In this brief review, recent findings in the field linking PPN to the basal ganglia and PD are summarized; in addition, an attempt is made to identify key gaps in our understanding and challenges this field faces in moving forward.

23 Review Dysregulation of the autophagic-lysosomal pathway in Gaucher and Parkinson's disease. 2019

Pitcairn, Caleb / Wani, Willayat Yousuf / Mazzulli, Joseph R. ·The Ken and Ruth Davee Department of Neurology, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA. · The Ken and Ruth Davee Department of Neurology, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA. Electronic address: jmazzulli@northwestern.edu. ·Neurobiol Dis · Pubmed #29550539.

ABSTRACT: The finding that mutations in the Gaucher's Disease (GD) gene GBA1 are a strong risk factor for Parkinson's Disease (PD) has allowed for unique insights into pathophysiology centered on disruption of the autophagic-lysosomal pathway. Protein aggregations in the form of Lewy bodies and the effects of canonical PD mutations that converge on the lysosomal degradation system suggest that neurodegeneration in PD is mediated by dysregulation of protein homeostasis. The well-characterized clinical and pathological relationship between PD and the lysosomal storage disorder GD emphasizes the importance of dysregulated protein metabolism in neurodegeneration, and one intriguing piece of this relationship is a shared phenotype of autophagic-lysosomal dysfunction in both diseases. Translational application of these findings may be accelerated by the use of midbrain dopamine neuronal models derived from induced pluripotent stem cells (iPSCs) that recapitulate several pathological features of GD and PD. In this review, we discuss evidence linking autophagic dysfunction to the pathophysiology of GD and GBA1-linked parkinsonism and focus more specifically on studies performed recently in iPSC-derived neurons.

24 Review Guidance for switching from off-label antipsychotics to pimavanserin for Parkinson's disease psychosis: an expert consensus. 2018

Black, Kevin J / Nasrallah, Henry / Isaacson, Stuart / Stacy, Mark / Pahwa, Rajesh / Adler, Charles H / Alva, Gustavo / Cooney, Jeffrey W / Kremens, Daniel / Menza, Matthew A / Meyer, Jonathan M / Patkar, Ashwin A / Simuni, Tanya / Morrissette, Debbi A / Stahl, Stephen M. ·1Departments of Psychiatry,Neurology,Radiology,and Neuroscience,Washington University School of Medicine in St. Louis,St. Louis,Missouri,USA. · 2Department of Psychiatry and Behavioral Neuroscience,Saint Louis University School of Medicine,St. Louis,Missouri,USA. · 3Parkinson's Disease and Movement Disorders Center of Boca Raton,Boca Raton,Florida,USA. · 4Brody School of Medicine,East Carolina University,Greenville,North Carolina,USA. · 5Department of Neurology,University of Kansas Medical Center,Kansas City,Kansas,USA. · 6Department of Neurology, Mayo Clinic College of Medicine, Scottsdale, Arizona,USA. · 7Department of Psychiatry and Neuroscience,University of California,Riverside,Riverside,California,USA. · 9Department of Neurology,Duke University School of Medicine,Durham,North Carolina,USA. · 10Comprehensive Parkinson's Disease and Movement Disorders Center at the Vickie and Jack Farber Center for Neurosciences at the Sidney Kimmel Medical School at Jefferson University,Philadelphia,Philadelphia,USA. · 11Department of Psychiatry,Robert Wood Johnson Medical School,New Brunswick,New Jersey,USA. · 12California Department of State Hospitals,Sacramento,California,USA. · 14Department of Psychiatry & Community and Family Medicine,Duke University Medical Center,Durham,North Carolina,USA. · 15Department of Neurology,Northwestern University Feinberg School of Medicine,Chicago,Illinois,USA. · 16Neuroscience Education Institute,Carlsbad,California,USA. · 13Department of Psychiatry,University of California,San Diego,La Jolla,California,USA. ·CNS Spectr · Pubmed #30588905.

ABSTRACT: Patients with Parkinson's disease psychosis (PDP) are often treated with an atypical antipsychotic, especially quetiapine or clozapine, but side effects, lack of sufficient efficacy, or both may motivate a switch to pimavanserin, the first medication approved for management of PDP. How best to implement a switch to pimavanserin has not been clear, as there are no controlled trials or case series in the literature to provide guidance. An abrupt switch may interrupt partially effective treatment or potentially trigger rebound effects from antipsychotic withdrawal, whereas cross-taper involves potential drug interactions. A panel of experts drew from published data, their experience treating PDP, lessons from switching antipsychotic drugs in other populations, and the pharmacology of the relevant drugs, to establish consensus recommendations. The panel concluded that patients with PDP can be safely and effectively switched from atypical antipsychotics used off label in PDP to the recently approved pimavanserin by considering each agent's pharmacokinetics and pharmacodynamics, receptor interactions, and the clinical reason for switching (efficacy or adverse events). Final recommendations are that such a switch should aim to maintain adequate 5-HT2A antagonism during the switch, thus providing a stable transition so that efficacy is maintained. Specifically, the consensus recommendation is to add pimavanserin at the full recommended daily dose (34 mg) for 2-6 weeks in most patients before beginning to taper and discontinue quetiapine or clozapine over several days to weeks. Further details are provided for this recommendation, as well as for special clinical circumstances where switching may need to proceed more rapidly.

25 Review Clinical Rating Scales for Urinary Symptoms in Parkinson Disease: Critique and Recommendations. 2018

Pavy-Le Traon, Anne / Cotterill, Nikki / Amarenco, Gerard / Duerr, Susanne / Kaufmann, Horacio / Lahrmann, Heinz / Tison, François / Wenning, Gregor K / Goetz, Christopher G / Poewe, Werner / Sampaio, Cristina / Schrag, Anette / Rascol, Olivier / Martinez-Martin, Pablo / Stebbins, Glenn T / Anonymous4550971. ·French Reference Center for MSA, Department of Neurology University Hospital of Toulouse France. · Institute of Cardiovascular and Metabolic Diseases (I2MC-UMR1048) Toulouse France. · Bristol Urological Institute, Southmead Hospital Westbury-on-Trym Bristol United Kingdom. · Neuro-Urology Department Hôpital Tenon, and GRC01 UPMC Paris France. · Department of Neurology University Hospital Innsbruck Austria. · Department of Neurology New York University New York USA. · Private Praxis Vienna Austria. · Institute for Neurodegenerative Diseases, University of Bordeaux University Hospital of Bordeaux Bordeaux France. · Department of Neurological Services Rush University School of Medicine Chicago IL USA. · Laboratory of Clinical Pharmacology and Therapeutics Lisbon School of Medicine Lisbon Portugal. · Department of Clinical Neurosciences, Royal Free Hospital University College London London United Kingdom. · Laboratoire de Pharmacologie Médicale et Clinique Toulouse France. · National Center of Epidemiology and CIBERNED Carlos III Institute of Health Madrid Spain. ·Mov Disord Clin Pract · Pubmed #30515437.

ABSTRACT: Background: The prevalence of lower urinary tract symptoms (LUTS) is high in Parkinson's disease (PD). These problems negatively affect quality of life and include both storage and voiding problems. The International Parkinson and Movement Disorder Society established a task force to review clinical rating scales/questionnaires for the assessment of urinary symptoms in PD. Methods: According to prespecified criteria, these scales/questionnaires were classified as "Recommended" or "Recommended with caveats" when clinimetric properties were satisfactory for Recommended status but had not been assessed specifically in PD, "Suggested" or "Listed." These assessments were applied to rate scales as screening tools for the diagnosis of LUTS and for the rating of symptom severity. Results: Among scales that included LUTS but focused on overall autonomic or non-motor symptoms in PD, no scale reached the clinimetric rigor to be designated as Recommended or Recommended with caveats, but some were Suggested for either diagnostic screening tools or severity measures. Among primary urological scales, most are well validated in urological setting, but none was validated specifically in PD. DAN-PSS (Danish PSS), ICIQ (International Consultation for Incontinence Questionnaire)-MLUTS (Male Lower Urinary Tract Symptoms), OABq, OABq-SF (ICIQ-OABqol), OAB-V8 (as screening tool), and OABSS (OAB Symptom Score) met criteria for Recommended with caveats. Conclusion: The Task Force does not recommend the development of a new scale. However, all above-mentioned questionnaires need to be studied further and specifically validated in PD.

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