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Parkinson Disease: HELP
Articles from Veterans Health System
Based on 515 articles published since 2009
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These are the 515 published articles about Parkinson Disease that originated from Veterans Health System during 2009-2019.
 
+ Citations + Abstracts
Pages: 1 · 2 · 3 · 4 · 5 · 6 · 7 · 8 · 9 · 10 · 11 · 12 · 13 · 14 · 15 · 16 · 17 · 18 · 19 · 20
1 Editorial Mendel and urate: Acid test or random noise? 2018

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

ABSTRACT: -- No abstract --

2 Editorial Don't ask, don't tell: Impulse control disorders in PD. 2018

Boylan, Laura S / Kostić, Vladimir S. ·From Division of Neurology (L.S.B.), Essentia Health, Duluth, MN · Albany-Stratton VA Medical Center (L.S.B.), Albany · Bellevue Hospital/New York University School of Medicine, Department of Neurology (L.S.B.), NY · and Institute of Neurology CCS (V.S.K.), School of Medicine University of Belgrade, Serbia. ·Neurology · Pubmed #29925552.

ABSTRACT: -- No abstract --

3 Editorial Diabetes and Parkinson disease: A sweet spot? 2018

Das, Rohit R / Unger, Marcus M. ·From the Department of Neurology and Neurotherapeutics (R.R.D.), University of Texas Southwestern Medical Center, Dallas · Health Services Research and Development Service (R.R.D.), Roudebush Veterans Affairs Medical Center, Indianapolis, IN · and Department of Neurology (M.M.U.), Saarland University, Homburg/Saar, Germany. ·Neurology · Pubmed #29626175.

ABSTRACT: -- No abstract --

4 Editorial Cholinergic forebrain density loss in Parkinson disease: More than just cognitive changes. 2018

Bohnen, Nicolaas I / Teipel, Stefan J. ·From the Departments of Radiology (N.I.B.) and Neurology (N.I.B.), University of Michigan · VA Ann Arbor Healthcare System (N.I.B.), MI · German Center for Neurodegenerative Diseases (S.J.T.,) Rostock · and Department of Psychosomatic Medicine (S.J.T.), University of Rostock, Germany. ·Neurology · Pubmed #29618621.

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? II. Neuroimaging in Parkinson's disease. 2017

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

ABSTRACT: -- No abstract --

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

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

ABSTRACT: -- No abstract --

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

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

ABSTRACT: -- No abstract --

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

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

ABSTRACT: -- No abstract --

10 Editorial Parkinson Disease Risk in Patients With Rosacea. 2016

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

ABSTRACT: -- No abstract --

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

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

ABSTRACT: -- No abstract --

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

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

ABSTRACT: -- No abstract --

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

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

ABSTRACT: -- No abstract --

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

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

ABSTRACT: -- No abstract --

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

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

ABSTRACT: -- No abstract --

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

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

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

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

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

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

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

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

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

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

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

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

20 Review International Parkinson and movement disorder society evidence-based medicine review: Update on treatments for the motor symptoms of Parkinson's disease. 2018

Fox, Susan H / Katzenschlager, Regina / Lim, Shen-Yang / Barton, Brandon / de Bie, Rob M A / Seppi, Klaus / Coelho, Miguel / Sampaio, Cristina / Anonymous1591441. ·Edmund J. Safra Program, Movement Disorder Clinic, Toronto Western Hospital, Toronto, Ontario, Canada. · University of Toronto Department of Medicine, Toronto, Ontario, Canada. · Department of Neurology and Karl Landsteiner Institute for Neuroimmunological and Neurodegenerative Disorders, Danube Hospital, Vienna, Austria. · Division of Neurology and the Mah Pooi Soo & Tan Chin Nam Centre for Parkinson's & Related Disorders, University of Malaya, Kuala Lumpur, Malaysia. · Rush University Medical Center, Chicago, Illinois, USA. · Jesse Brown VA Medical Center, Chicago, Illinois, USA. · Department of Neurology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands. · Department of Neurology, Medical University Innsbruck, Innsbruck, Austria. · Department of Neurology, Santa Maria Hospital, Instituto de Medicina Molecular, University of Lisbon, Lisbon, Portugal. · Cure Huntington's Disease Initiative (CHDI) Management/CHDI Foundation, Princeton, NJ, USA. · Instituto de Medicina Molecular, University of Lisbon, Lisbon, Portugal. ·Mov Disord · Pubmed #29570866.

ABSTRACT: OBJECTIVE: The objective of this review was to update evidence-based medicine recommendations for treating motor symptoms of Parkinson's disease (PD). BACKGROUND: The Movement Disorder Society Evidence-Based Medicine Committee recommendations for treatments of PD were first published in 2002 and updated in 2011, and we continued the review to December 31, 2016. METHODS: Level I studies of interventions for motor symptoms were reviewed. Criteria for inclusion and quality scoring were as previously reported. Five clinical indications were considered, and conclusions regarding the implications for clinical practice are reported. RESULTS: A total of 143 new studies qualified. There are no clinically useful interventions to prevent/delay disease progression. For monotherapy of early PD, nonergot dopamine agonists, oral levodopa preparations, selegiline, and rasagiline are clinically useful. For adjunct therapy in early/stable PD, nonergot dopamine agonists, rasagiline, and zonisamide are clinically useful. For adjunct therapy in optimized PD for general or specific motor symptoms including gait, rivastigmine is possibly useful and physiotherapy is clinically useful; exercise-based movement strategy training and formalized patterned exercises are possibly useful. There are no new studies and no changes in the conclusions for the prevention/delay of motor complications. For treating motor fluctuations, most nonergot dopamine agonists, pergolide, levodopa ER, levodopa intestinal infusion, entacapone, opicapone, rasagiline, zonisamide, safinamide, and bilateral STN and GPi DBS are clinically useful. For dyskinesia, amantadine, clozapine, and bilateral STN DBS and GPi DBS are clinically useful. CONCLUSIONS: The options for treating PD symptoms continues to expand. These recommendations allow the treating physician to determine which intervention to recommend to an individual patient. © 2018 International Parkinson and Movement Disorder Society.

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

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

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

22 Review Parkinson's disease from the gut. 2018

Liddle, Rodger A. ·Department of Medicine, Duke University Medical Center and Department of Veterans Affairs Health Care System, Durham, NC 27710, United States. Electronic address: rodger.liddle@duke.edu. ·Brain Res · Pubmed #29360467.

ABSTRACT: Parkinson's disease (PD) is a debilitating neurodegenerative condition associated with tremor, rigidity, dementia, and gastrointestinal symptoms such as constipation, nausea and vomiting. The pathological hallmarks of PD are Lewy bodies and neurites in the brain and peripheral nerves. The major constituent of Lewy bodies is the neuronal protein α-synuclein. Misfolding of α-synuclein confers prion-like properties enabling its spread from cell to cell. Misfolded α-synuclein also serves as a template and induces misfolding of endogenous α-synuclein in recipient cells leading to the formation of oligomers that progress to fibrils and eventually Lewy bodies. Accumulating evidence suggests that PD may arise in the gut. Clinically, gastrointestinal symptoms often appear in patients before other neurological signs and aggregates of α-synuclein have been found in enteric nerves of PD patients. Importantly, patients undergoing vagotomy have a reduced risk of developing PD. Experimentally, abnormal forms of α-synuclein appear in enteric nerves before they appear in the brain and injection of abnormal α-synuclein into the wall of the intestine spreads to the vagus nerve. Ingested toxins and alterations in gut microbiota can induce α-synuclein aggregation and PD, however, it is not known how PD starts. Recently, it has been shown that sensory cells of the gut known as enteroendocrine cells (EECs) contain α-synuclein and synapse with enteric nerves, thus providing a connection from the gut to the brain. It is possible that abnormal α-synuclein first develops in EECs and spreads to the nervous system.

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

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

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

24 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.

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

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

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

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