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Parkinson Disease: HELP
Articles from Alabama
Based on 235 articles published since 2010
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These are the 235 published articles about Parkinson Disease that originated from Alabama during 2010-2020.
 
+ Citations + Abstracts
Pages: 1 · 2 · 3 · 4 · 5 · 6 · 7 · 8 · 9 · 10
1 Editorial Editorial: Mitochondria and Endoplasmic Reticulum Dysfunction in Parkinson's Disease. 2019

Barodia, Sandeep Kumar / Prabhakaran, Krishnan / Karunakaran, Smitha / Mishra, Vikas / Tapias, Victor. ·Center for Neurodegeneration and Experimental Therapeutics, Birmingham, AL, United States. · Department of Biology, Norfolk State University, Norfolk, VA, United States. · Centre for Brain Research, Indian Institute of Science, Bangalore, India. · Department of Pharmaceutical Sciences, Basanaheb Bhirao Ambedkar University, Lucknow, India. · Feil Family Brain and Mind Research Institute, Weill Cornell Medicine, New York, NY, United States. ·Front Neurosci · Pubmed #31780882.

ABSTRACT: -- No abstract --

2 Editorial What would Dr. James parkinson think today? Mutations in beta-glucocerebrosidase and risk of Parkinson's disease. 2017

Standaert, David G. ·Department of Neurology, University of Alabama at Birmingham, Birmingham, Alabama, USA. ·Mov Disord · Pubmed #29068500.

ABSTRACT: -- No abstract --

3 Editorial Editorial: Pathophysiology of the Basal Ganglia and Movement Disorders: Gaining New Insights from Modeling and Experimentation, to Influence the Clinic. 2017

Andres, Daniela S / Merello, Marcelo / Darbin, Olivier. ·Laboratory of Neuroengineering, Science and Technology School, National University of San MartínSan Martín, Argentina. · Movement Disorders Section, Neuroscience Department, Raul Carrea Institute for Neurological Research, Fundación para la Lucha contra las Enfermedades Neurológicas de la Infancia (FLENI)Buenos Aires, Argentina. · Department of Neurology, University South AlabamaMobile, AL, United States. · Division of System Neurophysiology, National Institute for Physiological SciencesOkazaki, Japan. ·Front Hum Neurosci · Pubmed #28979200.

ABSTRACT: -- No abstract --

4 Editorial Biomarkers in Parkinson's disease: From pathophysiology to early diagnosis. 2016

Calabresi, Paolo / Standaert, David G / Chiasserini, Davide / Parnetti, Lucilla. ·Clinica Neurologica, Università degli Studi di Perugia, Ospedale S. Maria della Misericordia, Perugia, Italy. · IRCCS Fondazione Santa Lucia, Rome, Italy. · Department of Neurology, University of Alabama at Birmingham, Birmingham, Alabama, USA. ·Mov Disord · Pubmed #27245116.

ABSTRACT: -- No abstract --

5 Editorial Identification of bona-fide LRRK2 kinase substrates. 2016

West, Andrew B / Cookson, Mark R. ·Center for Neurodegeneration and Experimental Therapeutics, Department of Neurology, The University of Alabama at Birmingham, Birmingham, Alabama, USA. · Cell Biology and Gene Expression Section, Laboratory of Neurogenetics, National Institute on Aging, Bethesda, Maryland, USA. ·Mov Disord · Pubmed #27126091.

ABSTRACT: -- No abstract --

6 Editorial Reaping what you sow: Cross-seeding between aggregation-prone proteins in neurodegeneration. 2014

Yacoubian, Talene A / Standaert, David G. ·Center for Neurodegeneration and Experimental Therapeutics, Department of Neurology, University of Alabama at Birmingham, Birmingham, Alabama, USA. ·Mov Disord · Pubmed #24395732.

ABSTRACT: -- No abstract --

7 Editorial Metabolomics and the search for biomarkers in Parkinson's disease. 2013

Amara, Amy W / Standaert, David G. ·Department of Neurology, University of Alabama at Birmingham, Birmingham, Alabama, USA. ·Mov Disord · Pubmed #24105981.

ABSTRACT: -- No abstract --

8 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.

9 Review Patient Satisfaction in Surgery for Parkinson's Disease: A Systematic Review of the Literature. 2019

Elsayed, Galal A / Menendez, Joshua Y / Tabibian, Borna E / Chagoya, Gustavo / Omar, Nidal B / Zeiger, Evan / Walters, Beverly C / Walker, Harrison / Guthrie, Barton L. ·Neurological Surgery, University of Alabama at Birmingham, Birmingham, USA. · Neurological Surgery, University of Alabama at Birmimgham, Birmingham, USA. · Neurology, University of Alabama at Birmingham, Birmingham, USA. ·Cureus · Pubmed #31183296.

ABSTRACT: The objective of the study was to establish how patient satisfaction with surgical treatment of Parkinson's disease (PD) has been previously measured, determine whether an ideal patient satisfaction instrument exists, and to define the dimensions of care that determine patient satisfaction with the surgical treatment of PD. A systematic search of four online databases, unpublished sources, and citations was undertaken to identify 15 studies reporting patient satisfaction with the surgical treatment of PD. Manuscripts were reviewed and instruments were categorized by content and method axes. One study was found to utilize two distinct patient satisfaction instruments, which brought the total number of satisfaction instruments assessed to 16. Major factors influencing patient satisfaction were identified and served as a structure to define the dimensions of patient satisfaction in the surgical treatment of PD. Studies used predominantly multidimensional (10/16), rather than global (6/16) satisfaction instruments. Generic (12/16) rather than disease-specific (4/16) instruments were utilized more frequently. Every study reported on satisfaction with outcome and four studies reported on satisfaction with outcome and care. Six dimensions of patient status, outcome and care experience affecting patient satisfaction were identified: motor function, patient-specific health characteristics, programming/long-term care, surgical considerations, device/hardware, and functional independence.  At present, no patient satisfaction instrument exists that is disease-specific and covers all dimensions of patient satisfaction in surgery for PD. For quality improvement, such a disease-specific, comprehensive patient satisfaction instrument should be designed, and, if demonstrated to be reliable and valid, widely implemented.

10 Review Impact of sex differences and gender specificity on behavioral characteristics and pathophysiology of neurodegenerative disorders. 2019

Ullah, Mohammad Fahad / Ahmad, Aamir / Bhat, Showket Hussain / Abu-Duhier, Faisel M / Barreto, George E / Ashraf, Ghulam Md. ·Prince Fahd Research Chair, Department of Medical Laboratory Technology, Faculty of Applied Medical Sciences, University of Tabuk, 71491, Saudi Arabia. Electronic address: m.ullah@ut.edu.sa. · Department of Oncologic Sciences, Mitchell Cancer Institute, University of South Alabama, Mobile, AL, 36604, USA. · Prince Fahd Research Chair, Department of Medical Laboratory Technology, Faculty of Applied Medical Sciences, University of Tabuk, 71491, Saudi Arabia. · Departamento de Nutrición y Bioquímica, Facultad de Ciencias, Pontificia Universidad Javeriana, Bogotá, D.C., Colombia; Instituto de Ciencias Biomédicas, Universidad Autónoma de Chile, Santiago, Chile. · King Fahd Medical Research Center, King Abdulaziz University, Jeddah, Saudi Arabia; Department of Medical Laboratory Technology, Faculty of Applied Medical Sciences, King Abdulaziz University, Jeddah, Saudi Arabia. Electronic address: gashraf@kau.edu.sa. ·Neurosci Biobehav Rev · Pubmed #30959072.

ABSTRACT: The impact of neurodegenerative disorders in humans has multiple consequences because of the progressive decline in cognitive and physical performances. These disorders have diverse manifestations and are influenced by genetic and lifestyle factors, concurrent health conditions as well as un-modifiable predisposing risk factors, including gender and advanced age. Accumulating evidence indicates a gender-dependent natural bias of neurodegenerative diseases, such as, Alzheimer's disease, Parkinson's disease, Huntington's disease and multiple sclerosis, with the ratio of male to female prevalence as well as the severity of the disease differing significantly between the two sexes. This observation has recently garnered much attention and it is now being realized that understanding the sex as a biological variable in the etiology of the neurodegenerative diseases may advance the status of the pathophysiology and treatment strategies while improving the associated decline in cognitive and functional abilities. This review highlights the influence of gender in neurodegenerative disorders and further discusses the sex-specific pre-determined microenvironments that are critical in predisposing the individuals to such disorders.

11 Review The centromedian nucleus: Anatomy, physiology, and clinical implications. 2019

Ilyas, Adeel / Pizarro, Diana / Romeo, Andrew K / Riley, Kristen O / Pati, Sandipan. ·Department of Neurosurgery, University of Alabama at Birmingham, Birmingham, AL, United States. Electronic address: ailyas@uab.edu. · Department of Neurology, University of Alabama at Birmingham, Birmingham, AL, United States. · Department of Neurosurgery, University of Alabama at Birmingham, Birmingham, AL, United States. ·J Clin Neurosci · Pubmed #30827880.

ABSTRACT: Of all the truncothalamic nuclei, the centromedian-parafascicular nuclei complex (CM-Pf) is the largest and is considered the prototypic thalamic projection system. Located among the caudal intralaminar thalamic nuclei, the CM-Pf been described by Jones as "the forgotten components of the great loop of connections joining the cerebral cortex via the basal ganglia". The CM, located lateral relative to the Pf, is a major source of direct input to the striatum and also has connections to other, distinct region of the basal ganglia as well as the brainstem and cortex. Functionally, the CM participates in sensorimotor coordination, cognition (e.g. attention, arousal), and pain processing. The role of CM as 'gate control' function by propagating only salient stimuli during attention-demanding tasks has been proposed. Given its rich connectivity and diverse physiologic role, recent studies have explored the CM as potential target for neuromodulation therapy for Tourette syndrome, Parkinson's disease, generalized epilepsy, intractable neuropathic pain, and in restoring consciousness. This comprehensive review summarizes the structural and functional anatomy of the CM and its physiologic role with a focus on clinical implications.

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

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

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

13 Review No Country for Old Worms: A Systematic Review of the Application of 2018

Caldwell, Kim A / Thies, Jennifer L / Caldwell, Guy A. ·Department of Biological Sciences, The University of Alabama, Box 870344, Tuscaloosa, AL 35487, USA. kcaldwel@ua.edu. · Departments of Neurology and Neurobiology, Center for Neurodegeneration and Experimental Therapeutics, Nathan Shock Center for Research on the Basic Biology of Aging, University of Alabama at Birmingham School of Medicine, Birmingham, AL 35294, USA. kcaldwel@ua.edu. · Department of Biological Sciences, The University of Alabama, Box 870344, Tuscaloosa, AL 35487, USA. Jthies@crimson.ua.edu. · Department of Biological Sciences, The University of Alabama, Box 870344, Tuscaloosa, AL 35487, USA. gcaldwel@ua.edu. · Departments of Neurology and Neurobiology, Center for Neurodegeneration and Experimental Therapeutics, Nathan Shock Center for Research on the Basic Biology of Aging, University of Alabama at Birmingham School of Medicine, Birmingham, AL 35294, USA. gcaldwel@ua.edu. ·Metabolites · Pubmed #30380609.

ABSTRACT: While progress has been made in discerning genetic associations with Parkinson's disease (PD), identifying elusive environmental contributors necessitates the application of unconventional hypotheses and experimental strategies. Here, we provide an overview of studies that we conducted on a neurotoxic metabolite produced by a species of common soil bacteria,

14 Review Implementing Levodopa-Carbidopa Intestinal Gel for Parkinson Disease: Insights from US Practitioners. 2018

Burack, Michelle / Aldred, Jason / Zadikoff, Cindy / Vanagunas, Arvydas / Klos, Kevin / Bilir, Bahri / Fernandez, Hubert H / Standaert, David G. ·University of Rochester Medical Center Rochester New York USA. · Northwest Neurological Spokane Washington USA. · Northwestern University Feinberg School of Medicine Northwestern Memorial Hospital Chicago Illinois USA. · Movement Disorder Center of Oklahoma Tulsa Oklahoma USA. · Rocky Mountain Gastroenterology Littleton Colorado USA. · Cleveland Clinic Cleveland Ohio USA. · University of Alabama at Birmingham Birmingham Alabama USA. ·Mov Disord Clin Pract · Pubmed #30363427.

ABSTRACT: Background: Levodopa-carbidopa intestinal gel (LCIG, designated in the United States as carbidopa-levodopa enteral suspension, CLES) was approved in the United States in 2015 for the treatment of refractory motor fluctuations in individuals with Parkinson disease (PD). Many neurologists in the United States have not had personal experience with implementation and management of the unique delivery system for this treatment. Methods and Findings: This educational review was developed to provide practitioners with an understanding of LCIG use from the clinician's point of view. Practical recommendations for the use of LCIG from the early planning stages through long-term patient management were compiled from the published literature, regulatory guidance, and clinical experience. Among the topics reviewed were: assembling a multidisciplinary treatment team, identifying treatment candidates, patient/care partner education, procedural considerations, post-procedural care, LCIG initiation and titration, troubleshooting issues, and ongoing monitoring. For most of these steps, a considerable amount of individualization is possible, which allows clinicians to tailor protocols based on the needs of their teams, the healthcare system, and the patient and care partner. Although clinical practices are heterogeneous, themes of early planning, ongoing education, and a team-based approach to management are universal. Conclusions: By using established protocols and insights gleaned from experienced practitioners, clinicians who are unfamiliar with LCIG can more feasibly incorporate this treatment option into their armamentarium for treating PD motor fluctuations.

15 Review Deep Brain Stimulation and Sleep-Wake Disturbances in Parkinson Disease: A Review. 2018

Sharma, Vibhash D / Sengupta, Samarpita / Chitnis, Shilpa / Amara, Amy W. ·Department of Neurology, University of Kansas Medical Center, Kansas City, KS, United States. · Department of Neurology, University of Southwestern Medical Center, Dallas, TX, United States. · Department of Neurology, University of Alabama at Birmingham, Birmingham, AL, United States. ·Front Neurol · Pubmed #30210429.

ABSTRACT: Sleep-wake disturbances are common non-motor manifestations in Parkinson Disease (PD). Complex pathophysiological changes secondary to neurodegeneration in combination with motor symptoms and dopaminergic medications contribute to development of sleep-wake disturbances. The management of sleep complaints in PD is important as this symptom can affect daily activities and impair quality of life. Deep brain stimulation (DBS) is an effective adjunctive therapy for management of motor symptoms in PD. However, its effect on non-motor symptoms including sleep-wake disturbances is not widely understood. In this article, we reviewed studies assessing the effect of DBS at various therapeutic targets on sleep-wake disturbances. Of the studies examining the role of DBS in sleep-wake disturbances, the effect of subthalamic nucleus stimulation is most widely studied and has shown improvement in sleep quality, sleep efficiency, and sleep duration. Although, studies investigating changes in sleep with stimulation of thalamus, globus pallidus interna, and pedunculopontine nucleus are limited, they support the potential for modulation of sleep-wake centers with DBS at these sites. The mechanism by which DBS at different anatomical targets affects sleep-wake disturbances in PD is unclear and may involves multiple factors, including improved motor symptoms, medication adjustment, and direct modulation of sleep-wake centers.

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

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

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

17 Review Prion-like propagation of pathology in Parkinson disease. 2018

Volpicelli-Daley, Laura / Brundin, Patrik. ·Center for Neurodegeneration and Experimental Therapeutics, Department of Neurology, University of Alabama at Birmingham, Birmingham, AL, United States. · Van Andel Research Institute, Center for Neurodegenerative Science, Grand Rapids, MI, United States. Electronic address: Patrik.Brundin@vai.org. ·Handb Clin Neurol · Pubmed #29887143.

ABSTRACT: Over 100 years ago, Lewy bodies and Lewy neurites were defined as a pathologic hallmark of Parkinson disease. Eighty years later, α-synuclein was found to be the primary component of these inclusions. Emerging evidence suggests that α-synuclein pathology propagates across interconnected networks throughout the nervous system in a prion-like manner. Pathologic α-synuclein seeds aggregation of native α-synuclein, resulting in the formation of insoluble inclusions. These seeds can propagate within the neuron and to interconnected neurons, resulting in the spread of pathology throughout the brain. Here, we discuss how the findings that α-synuclein pathology spreads throughout the nervous system has revolutionized our understanding about Parkinson disease pathogenesis and resulted in the development of novel therapeutic strategies to halt disease progression.

18 Review New Developments in Genetic rat models of Parkinson's Disease. 2018

Creed, Rose B / Goldberg, Matthew S. ·Center for Neurodegeneration and Experimental Therapeutics, Department of Neurology, The University of Alabama at Birmingham, Birmingham, Alabama, USA. ·Mov Disord · Pubmed #29418019.

ABSTRACT: Preclinical research on Parkinson's disease has relied heavily on mouse and rat animal models. Initially, PD animal models were generated primarily by chemical neurotoxins that induce acute loss of dopaminergic neurons in the substantia nigra. On the discovery of genetic mutations causally linked to PD, mice were used more than rats to generate laboratory animals bearing PD-linked mutations because mutagenesis was more difficult in rats. Recent advances in technology for mammalian genome engineering and optimization of viral expression vectors have increased the use of genetic rat models of PD. Emerging research tools include "knockout" rats with disruption of genes in which mutations have been causally linked to PD, including LRRK2, α-synuclein, Parkin, PINK1, and DJ-1. Rats have also been increasingly used for transgenic and viral-mediated overexpression of genes relevant to PD, particularly α-synuclein. It may not be realistic to obtain a single animal model that completely reproduces every feature of a human disease as complex as PD. Nevertheless, compared with mice with the same mutations, many genetic rat animal models of PD better reproduce key aspects of PD including progressive loss of dopaminergic neurons in the substantia nigra, locomotor behavior deficits, and age-dependent formation of abnormal α-synuclein protein aggregates. Here we briefly review new developments in genetic rat models of PD that may have greater potential for identifying underlying mechanisms, for discovering novel therapeutic targets, and for developing greatly needed treatments to slow or halt disease progression. © 2018 International Parkinson and Movement Disorder Society.

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

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

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

20 Review Complex Dynamics in the Basal Ganglia: Health and Disease Beyond the Motor System. 2018

Andres, Daniela S / Darbin, Olivier. ·From the Science and Technology School, National University of San Martin, Buenos Aires, Argentina (DSA) · the Department of Neurology, University of South Alabama, Mobile, Ala. (OD) · and the Division of System Neurophysiology, National Institute for Physiological Sciences, Okazaki, Japan (OD). ·J Neuropsychiatry Clin Neurosci · Pubmed #29183233.

ABSTRACT: The rate and oscillatory hypotheses are the two main current frameworks of basal ganglia pathophysiology. Both hypotheses have emerged from research on movement disorders sharing similar conceptualizations. These pathological conditions are classified either as hypokinetic or hyperkinetic, and the electrophysiological hallmarks of basal ganglia dysfunction are categorized as prokinetic or antikinetic. Although nonmotor symptoms, including neurobehavioral symptoms, are a key manifestation of basal ganglia dysfunction, they are uncommonly accounted for in these models. In patients with Parkinson's disease, the broad spectrum of motor symptoms and neurobehavioral symptoms challenges the concept that basal ganglia disorders can be classified into two categories. The profile of symptoms of basal ganglia dysfunction is best characterized by a breakdown of information processing, accompanied at an electrophysiological level by complex alterations of spiking activity from basal ganglia neurons. The authors argue that the dynamics of the basal ganglia circuit cannot be fully characterized by linear properties such as the firing rate or oscillatory activity. In fact, the neuronal spiking stream of the basal ganglia circuit is irregular but has temporal structure. In this context, entropy was introduced as a measure of probabilistic irregularity in the temporal organization of neuronal activity of the basal ganglia, giving place to the entropy hypothesis of basal ganglia pathology. Obtaining a quantitative characterization of irregularity of spike trains from basal ganglia neurons is key to elaborating a new framework of basal ganglia pathophysiology.

21 Review Review of cardiovascular imaging in the Journal of Nuclear Cardiology 2017. Part 1 of 2: Positron emission tomography, computed tomography, and magnetic resonance. 2018

AlJaroudi, Wael A / Hage, Fadi G. ·Division of Cardiovascular Medicine, Clemenceau Medical Center, Beirut, Lebanon. · Division of Cardiovascular Disease, Department of Medicine, University of Alabama at Birmingham, 306 Lyons-Harrison Research Building, 701 19th Street South, Birmingham, AL, 35294-0007, USA. fadihage@uab.edu. · Section of Cardiology, Birmingham Veterans Affairs Medical Center, Birmingham, AL, USA. fadihage@uab.edu. ·J Nucl Cardiol · Pubmed #29119374.

ABSTRACT: Several original articles and editorials have been published in the Journal of Nuclear Cardiology in 2017. It has become a tradition at the beginning of each year to summarize some of these key articles in 2 sister reviews. In this first part one, we will discuss some of the progress made in the field of heart failure (cardio-oncology, myocardial blood flow, viability, dyssynchrony, and risk stratification), inflammation, molecular and hybrid imaging using advancement in positron emission tomography, computed tomography, and magnetic resonance imaging.

22 Review Role of the JAK/STAT signaling pathway in regulation of innate immunity in neuroinflammatory diseases. 2018

Yan, Zhaoqi / Gibson, Sara A / Buckley, Jessica A / Qin, Hongwei / Benveniste, Etty N. ·Department of Cell, Developmental and Integrative Biology, University of Alabama at Birmingham, Birmingham, AL 35294, United States. · Department of Cell, Developmental and Integrative Biology, University of Alabama at Birmingham, Birmingham, AL 35294, United States. Electronic address: hqin@uab.edu. · Department of Cell, Developmental and Integrative Biology, University of Alabama at Birmingham, Birmingham, AL 35294, United States. Electronic address: tika@uab.edu. ·Clin Immunol · Pubmed #27713030.

ABSTRACT: The Janus Kinase/Signal Transducers and Activators of Transcription (JAK/STAT) signaling pathway is utilized by numerous cytokines and interferons, and is essential for the development and function of both innate and adaptive immunity. Aberrant activation of the JAK/STAT pathway is evident in neuroinflammatory diseases such as Multiple Sclerosis and Parkinson's Disease. Innate immunity is the front line defender of the immune system and is composed of various cell types, including microglia, macrophages and neutrophils. Innate immune responses have both pathogenic and protective roles in neuroinflammation, depending on disease context and the microenvironment in the central nervous system. In this review, we discuss the role of innate immunity in the pathogenesis of neuroinflammatory diseases, how the JAK/STAT signaling pathway regulates the innate immune response, and finally, the potential for ameliorating neuroinflammation by utilization of JAK/STAT inhibitors.

23 Review The Neuropsychology (Broadly Conceived) of Multiple System Atrophy, Progressive Supranuclear Palsy, and Corticobasal Degeneration. 2017

Gerstenecker, Adam. ·Department of Neurology, University of Alabama at Birmingham, Birmingham, AL, USA. · Alzheimer's Disease Center, University of Alabama at Birmingham, Birmingham, AL, USA. ·Arch Clin Neuropsychol · Pubmed #28961692.

ABSTRACT: Objective: To review the cognitive and behavioral features of the different atypical parkinsonian syndromes in which motor symptoms dominate early clinical symptomology: multiple systems atrophy (MSA), progressive supranuclear palsy (PSP), and corticobasal degeneration (CBD). The impact of cognitive and behavioral deficits on quality of life, associations between neuropsychological and neuropsychiatric findings and brain imaging, and cognitive and behavioral symptom management are also discussed. Method: A review of the available MSA, PSP, and CBD literature was conducted, with emphasis given to studies investigating the cognitive and behavioral features of the syndromes. Results: Although the three reviewed atypical parkinsonian syndromes share many similarities to each other and PD from a neuropsychological perspective, differences in prevalence and severity of cognitive impairment and patterns of performance on neuropsychological and neuropsychiatric measures exist in the research literature. Conclusions: Cognitive and behavioral features are early and pervasive aspects of MSA, PSP, and CBD.

24 Review Past, present, and future of Parkinson's disease: A special essay on the 200th Anniversary of the Shaking Palsy. 2017

Obeso, J A / Stamelou, M / Goetz, C G / Poewe, W / Lang, A E / Weintraub, D / Burn, D / Halliday, G M / Bezard, E / Przedborski, S / Lehericy, S / Brooks, D J / Rothwell, J C / Hallett, M / DeLong, M R / Marras, C / Tanner, C M / Ross, G W / Langston, J W / Klein, C / Bonifati, V / Jankovic, J / Lozano, A M / Deuschl, G / Bergman, H / Tolosa, E / Rodriguez-Violante, M / Fahn, S / Postuma, R B / Berg, D / Marek, K / Standaert, D G / Surmeier, D J / Olanow, C W / Kordower, J H / Calabresi, P / Schapira, A H V / Stoessl, A J. ·HM CINAC, Hospital Universitario HM Puerta del Sur, Mostoles, Madrid, Spain. · Universidad CEU San Pablo, Madrid, Spain. · CIBERNED, Madrid, Spain. · Department of Neurology, Philipps University, Marburg, Germany. · Parkinson's Disease and Movement Disorders Department, HYGEIA Hospital and Attikon Hospital, University of Athens, Athens, Greece. · Department of Neurological Sciences, Rush University Medical Center, Chicago, Illinois, USA. · Department of Neurology, Medical University Innsbruck, Innsbruck, Austria. · Morton and Gloria Shulman Movement Disorders Clinic and the Edmond J Safra Program in Parkinson's Disease, Toronto Western Hospital, Toronto, Canada. · Department of Medicine, University of Toronto, Toronto, Canada. · Department of Psychiatry, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania, USA. · Parkinson's Disease and Mental Illness Research, Education and Clinical Centers (PADRECC and MIRECC), Corporal Michael J. Crescenz Veteran's Affairs Medical Center, Philadelphia, Pennsylvania, USA. · Medical Sciences, Newcastle University, Newcastle, UK. · Brain and Mind Centre, Sydney Medical School, The University of Sydney, Sydney, Australia. · School of Medical Sciences, University of New South Wales and Neuroscience Research Australia, Sydney, Australia. · Université de Bordeaux, Institut des Maladies Neurodégénératives, Centre National de la Recherche Scientifique Unité Mixte de Recherche 5293, Institut des Maladies Neurodégénératives, Bordeaux, France. · China Academy of Medical Sciences, Institute of Lab Animal Sciences, Beijing, China. · Departments of Neurology, Pathology, and Cell Biology, the Center for Motor Neuron Biology and Disease, Columbia University, New York, New York, USA. · Columbia Translational Neuroscience Initiative, Columbia University, New York, New York, USA. · Institut du Cerveau et de la Moelle épinière - ICM, Centre de NeuroImagerie de Recherche - CENIR, Sorbonne Universités, UPMC Univ Paris 06, Inserm U1127, CNRS UMR 7225, Paris, France. · Groupe Hospitalier Pitié-Salpêtrière, Paris, France. · Clinical Sciences Department, Newcastle University, Newcastle, UK. · Department of Nuclear Medicine, Aarhus University, Aarhus, Denmark. · Human Neurophysiology, Sobell Department, UCL Institute of Neurology, London, UK. · Human Motor Control Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland, USA. · Department of Neurology, Emory University School of Medicine, Atlanta, Georgia, USA. · Morton and Gloria Shulman Movement Disorders Centre and the Edmond J Safra Program in Parkinson's disease, Toronto Western Hospital, University of Toronto, Toronto, Canada. · Movement Disorders and Neuromodulation Center, Department of Neurology, University of California-San Francisco, San Francisco, California, USA. · Parkinson's Disease Research, Education and Clinical Center, San Francisco Veterans Affairs Medical Center, San Francisco, California, USA. · Veterans Affairs Pacific Islands Health Care System, Honolulu, Hawaii, USA. · Parkinson's Institute, Sunnyvale, California, USA. · Institute of Neurogenetics, University of Luebeck, Luebeck, Germany. · Department of Clinical Genetics, Erasmus University Medical Center, Rotterdam, The Netherlands. · Parkinson's Disease Center and Movement Disorders Clinic, Department of Neurology, Baylor College of Medicine, Houston, Texas, USA. · Department of Neurosurgery, Toronto Western Hospital, University of Toronto, Toronto, Canada. · Department of Neurology, Universitätsklinikum Schleswig-Holstein, Christian Albrechts University Kiel, Kiel, Germany. · Department of Medical Neurobiology, Institute of Medical Research Israel-Canada, Jerusalem, Israel. · Edmond and Lily Safra Center for Brain Sciences, The Hebrew University, Jerusalem, Israel. · Department of Neurosurgery, Hadassah University Hospital, Jerusalem, Israel. · Parkinson's Disease and Movement Disorders Unit, Neurology Service, Institut Clínic de Neurociències, Hospital Clínic de Barcelona, Barcelona, Spain. · Department of Medicine, Universitat de Barcelona, IDIBAPS, Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED) Barcelona, Spain. · Movement Disorders Clinic, Clinical Neurodegenerative Research Unit, Mexico City, Mexico. · Instituto Nacional de Neurología y Neurocirugía, Mexico City, Mexico. · Department of Neurology, Columbia University Medical Center, New York, New York, USA. · Department of Neurology, McGill University, Montreal General Hospital, Montreal, Quebec, Canada. · Klinik für Neurologie, UKSH, Campus Kiel, Christian-Albrechts-Universität, Kiel, Germany. · Institute for Neurodegenerative Disorders, New Haven, Connecticut, USA. · Department of Neurology, University of Alabama at Birmingham, Birmingham, Alabama, USA. · Department of Physiology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, USA. · Departments of Neurology and Neuroscience, Mount Sinai School of Medicine, New York, New York, USA. · Research Center for Brain Repair, Rush University Medical Center, Chicago, Illinois, USA. · Neuroscience Graduate Program, Rush University Medical Center, Chicago, Illinois, USA. · Neurological Clinic, Department of Medicine, Hospital Santa Maria della Misericordia, University of Perugia, Perugia, Italy. · Laboratory of Neurophysiology, Santa Lucia Foundation, IRCCS, Rome, Italy. · University Department of Clinical Neurosciences, UCL Institute of Neurology, University College London, London, UK. · Pacific Parkinson's Research Centre, Division of Neurology & Djavadf Mowafaghian Centre for Brain Health, University of British Columbia, British Columbia, Canada. · Vancouver Coastal Health, Vancouver, British Columbia, Canada. ·Mov Disord · Pubmed #28887905.

ABSTRACT: This article reviews and summarizes 200 years of Parkinson's disease. It comprises a relevant history of Dr. James Parkinson's himself and what he described accurately and what he missed from today's perspective. Parkinson's disease today is understood as a multietiological condition with uncertain etiopathogenesis. Many advances have occurred regarding pathophysiology and symptomatic treatments, but critically important issues are still pending resolution. Among the latter, the need to modify disease progression is undoubtedly a priority. In sum, this multiple-author article, prepared to commemorate the bicentenary of the shaking palsy, provides a historical state-of-the-art account of what has been achieved, the current situation, and how to progress toward resolving Parkinson's disease. © 2017 International Parkinson and Movement Disorder Society.

25 Review Achieving neuroprotection with LRRK2 kinase inhibitors in Parkinson disease. 2017

West, Andrew B. ·Center for Neurodegeneration and Experimental Therapeutics, 1719 6th Ave. South, University of Alabama at Birmingham, Birmingham, AL 35294, United States of America. Electronic address: abwest@uab.edu. ·Exp Neurol · Pubmed #28764903.

ABSTRACT: In the translation of discoveries from the laboratory to the clinic, the track record in developing disease-modifying therapies in neurodegenerative disease is poor. A carefully designed development pipeline built from discoveries in both pre-clinical models and patient populations is necessary to optimize the chances for success. Genetic variation in the leucine-rich repeat kinase two gene (LRRK2) is linked to Parkinson disease (PD) susceptibility. Pathogenic mutations, particularly those in the LRRK2 GTPase (Roc) and COR domains, increase LRRK2 kinase activities in cells and tissues. In some PD models, small molecule LRRK2 kinase inhibitors that block these activities also provide neuroprotection. Herein, the genetic and biochemical evidence that supports the involvement of LRRK2 kinase activity in PD susceptibility is reviewed. Issues related to the definition of a therapeutic window for LRRK2 inhibition and the safety of chronic dosing are discussed. Finally, recommendations are given for a biomarker-guided initial entry of LRRK2 kinase inhibitors in PD patients. Four key areas must be considered for achieving neuroprotection with LRRK2 kinase inhibitors in PD: 1) identification of patient populations most likely to benefit from LRRK2 kinase inhibitors, 2) prioritization of superior LRRK2 small molecule inhibitors based on open disclosures of drug performance, 3) incorporation of biomarkers and empirical measures of LRRK2 kinase inhibition in clinical trials, and 4) utilization of appropriate efficacy measures guided in part by rigorous pre-clinical modeling. Meticulous and rational development decisions can potentially prevent incredibly costly errors and provide the best chances for LRRK2 inhibitors to slow the progression of PD.

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