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Parkinson Disease: HELP
Articles from Perth
Based on 163 articles published since 2008
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These are the 163 published articles about Parkinson Disease that originated from Perth during 2008-2019.
 
+ Citations + Abstracts
Pages: 1 · 2 · 3 · 4 · 5 · 6 · 7
1 Editorial Electrophysiological insights into freezing in Parkinson's disease. 2016

Shine, James M. ·Department of Psychology, Stanford University, Stanford, CA, USA; Neuroscience Research Australia, The University of New South Wales, Sydney, NSW, Australia. Electronic address: macshine@stanford.edu. ·Clin Neurophysiol · Pubmed #27178847.

ABSTRACT: -- No abstract --

2 Review Parkinson's Disease Is Not Simply a Prion Disorder. 2017

Surmeier, D James / Obeso, José A / Halliday, Glenda M. ·Department of Physiology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois 60611, j-surmeier@northwestern.edu. · CINAC, HM Puerta del Sur, Hospitales de Madrid, Mostoles and CEU-San Pablo University, 28938 Madrid, Spain. · Network Center for Biomedical Research on Neurodegenerative Diseases, Instituto Carlos III, 28029 Madrid, Spain. · Brain and Mind Centre, Sydney Medical School, University of Sydney, Sydney, 2006 New South Wales, Australia, and. · School of Medical Sciences, University of New South Wales and Neuroscience Research Australia, Sydney, 2052 New South Wales, Australia. ·J Neurosci · Pubmed #29021297.

ABSTRACT: The notion that prion-like spreading of misfolded α-synuclein (α-SYN) causes Parkinson's disease (PD) has received a great deal of attention. Although attractive in its simplicity, the hypothesis is difficult to reconcile with postmortem analysis of human brains and connectome-mapping studies. An alternative hypothesis is that PD pathology is governed by regional or cell-autonomous factors. Although these factors provide an explanation for the pattern of neuronal loss in PD, they do not readily explain the apparently staged distribution of Lewy pathology in many PD brains, the feature of the disease that initially motivated the spreading hypothesis by Braak and colleagues. While each hypothesis alone has its shortcomings, a synthesis of the two can explain much of what we know about the etiopathology of PD.

3 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.

4 Review Calcium, mitochondrial dysfunction and slowing the progression of Parkinson's disease. 2017

Surmeier, D James / Halliday, Glenda M / Simuni, Tanya. ·Department of Physiology, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA; Department of Neurology, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA. Electronic address: j-surmeier@northwestern.edu. · Brain and Mind Centre, Sydney Medical School, University of Sydney, 2006, Australia; School of Medical Sciences, University of New South Wales, Neuroscience Research Australia, Sydney 2052, Australia. · Department of Neurology, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA. ·Exp Neurol · Pubmed #28780195.

ABSTRACT: Parkinson's disease is characterized by progressively distributed Lewy pathology and neurodegeneration. The motor symptoms of clinical Parkinson's disease (cPD) are unequivocally linked to the degeneration of dopaminergic neurons in the substantia nigra pars compacta (SNc). Several features of these neurons appear to make them selectively vulnerable to factors thought to cause cPD, like aging, genetic mutations and environmental toxins. Among these features, Ca

5 Review Cognitive Training and Noninvasive Brain Stimulation for Cognition in Parkinson's Disease: A Meta-analysis. 2017

Lawrence, Blake J / Gasson, Natalie / Bucks, Romola S / Troeung, Lakkhina / Loftus, Andrea M. ·1 Curtin University, Bentley, Western Australia, Australia. · 2 The University of Western Australia, Perth, Western Australia, Australia. · 3 The University of Notre Dame Australia, Fremantle, Western Australia, Australia. ·Neurorehabil Neural Repair · Pubmed #28583011.

ABSTRACT: BACKGROUND: Many people with Parkinson's disease (PD) experience cognitive decline. It is not known whether cognitive training or noninvasive brain stimulation are effective at alleviating cognitive deficits in PD. OBJECTIVE: To examine cognitive training and non-invasive brain stimulation interventions for cognition in PD. METHODS: An extensive search was conducted of published and unpublished studies in online databases. Studies were selected if they were controlled trials examining standard (not individualized) or tailored (individualized) cognitive training, repetitive transcranial magnetic stimulation (rTMS), or transcranial direct current stimulation (tDCS) in PD, with outcomes measured by standardized neuropsychological tests. RESULTS: Fourteen controlled trials met inclusion criteria. For executive function, the pooled effect size (Hedges' g) for cognitive training (standard and tailored combined) was small ( g = 0.42) but statistically significant (95% CI 0.15-0.68). The pooled effect for standard cognitive training (alone) was medium ( g = 0.51) and significant (95% CI 0.16-0.85). For attention/working memory, small pooled effect sizes were found when combining standard and tailored cognitive training ( g = 0.23; 95% CI 0.02-0.44) and for standard cognitive training alone ( g = 0.29; 95% CI 0.04-0.53), both significant. For memory, small but significant pooled effect sizes were also found when combining standard and tailored cognitive training and for standard cognitive training alone. CONCLUSIONS: The results suggest that standard and tailored cognitive training may improve executive function, attention/working memory, and memory in PD. Future studies must adopt randomized controlled trial designs to explore the therapeutic potential of these interventions.

6 Review Interaction of LRRK2 and α-Synuclein in Parkinson's Disease. 2017

Daher, João Paulo Lima. ·Faculty of Medicine, School of Medical Sciences, University of New South Wales, Sydney, NSW, 2052, Australia. jpldaher@gmail.com. · Neuroscience Research Australia, Barker St, Randwick, NSW, 2031, Australia. jpldaher@gmail.com. ·Adv Neurobiol · Pubmed #28353286.

ABSTRACT: Parkinson's disease (PD) is a progressively debilitating neurodegenerative syndrome. It is best described as a movement disorder characterized by motor dysfunctions, progressive degeneration of dopaminergic neurons of the substantia nigra pars compacta, and abnormal intraneuronal protein aggregates, named Lewy bodies and Lewy neurites. Nevertheless, knowledge of the molecular events leading to this pathophysiology is incomplete. To date, only mutations in the α-synuclein and LRRK2-encoding genes have been associated with typical findings of clinical and pathologic PD. LRRK2 appears to have a central role in the pathogenesis of PD as it is associated with α-synuclein pathology and other proteins implicated in neurodegeneration. Thus, LRRK2 dysfunction may influence the accumulation of α-synuclein and its pathology through diverse pathomechanisms altering cellular functions and signaling pathways, including immune system, autophagy, vesicle trafficking, and retromer complex modulation. Consequently, development of novel LRRK2 inhibitors can be justified to treat the neurodegeneration associated with abnormal α-synuclein accumulation.

7 Review LRRK2 and the Immune System. 2017

Dzamko, Nicolas L. ·School of Medical Sciences, University of NSW, Kensington, NSW, 2052, Australia. n.dzamko@neura.edu.au. · Neuroscience Research Australia, Randwick, NSW, 2031, Australia. n.dzamko@neura.edu.au. ·Adv Neurobiol · Pubmed #28353282.

ABSTRACT: Polymorphisms in leucine-rich repeat kinase 2 (LRRK2) have been linked to familial Parkinson's disease, increased risk of sporadic Parkinson's disease, increased risk of Crohn's inflammatory bowel disease, and increased susceptibility to leprosy. As well as LRRK2 mutations, these diseases share in common immune dysfunction and inflammation. LRRK2 is highly expressed in particular immune cells and has been biochemically linked to the intertwined pathways regulating inflammation, mitochondrial function, and autophagy/lysosomal function. This review outlines what is currently understood about LRRK2 function in the immune system and the potential implications of LRRK2 dysfunction for diseases genetically linked to this enigmatic enzyme.

8 Review Parkinson disease. 2017

Poewe, Werner / Seppi, Klaus / Tanner, Caroline M / Halliday, Glenda M / Brundin, Patrik / Volkmann, Jens / Schrag, Anette-Eleonore / Lang, Anthony E. ·Department of Neurology, Medical University Innsbruck, Anichstrasse 35, A-6020 Innsbruck, Austria. · Parkinson's Disease Research Education and Clinical Center, San Francisco Veteran's Affairs Medical Center, San Francisco, California, USA. · Department of Neurology, University of California - San Francisco, San Francisco, California, USA. · Brain and Mind Centre, Sydney Medical School, University of Sydney, Sydney, New South Wales, Australia. · Faculty of Medicine, University of New South Wales &Neuroscience Research Australia, Sydney, New South Wales, Australia. · Van Andel Research Institute, Center for Neurodegenerative Science, Grand Rapids, Michigan, USA. · Department of Neurology, University Hospital of Würzburg, Würzburg, Germany. · Department of Clinical Neuroscience, UCL Institute of Neurology, London, UK. · Division of Neurology, Department of Medicine, University of Toronto, Toronto, Ontario, Canada. ·Nat Rev Dis Primers · Pubmed #28332488.

ABSTRACT: Parkinson disease is the second-most common neurodegenerative disorder that affects 2-3% of the population ≥65 years of age. Neuronal loss in the substantia nigra, which causes striatal dopamine deficiency, and intracellular inclusions containing aggregates of α-synuclein are the neuropathological hallmarks of Parkinson disease. Multiple other cell types throughout the central and peripheral autonomic nervous system are also involved, probably from early disease onwards. Although clinical diagnosis relies on the presence of bradykinesia and other cardinal motor features, Parkinson disease is associated with many non-motor symptoms that add to overall disability. The underlying molecular pathogenesis involves multiple pathways and mechanisms: α-synuclein proteostasis, mitochondrial function, oxidative stress, calcium homeostasis, axonal transport and neuroinflammation. Recent research into diagnostic biomarkers has taken advantage of neuroimaging in which several modalities, including PET, single-photon emission CT (SPECT) and novel MRI techniques, have been shown to aid early and differential diagnosis. Treatment of Parkinson disease is anchored on pharmacological substitution of striatal dopamine, in addition to non-dopaminergic approaches to address both motor and non-motor symptoms and deep brain stimulation for those developing intractable L-DOPA-related motor complications. Experimental therapies have tried to restore striatal dopamine by gene-based and cell-based approaches, and most recently, aggregation and cellular transport of α-synuclein have become therapeutic targets. One of the greatest current challenges is to identify markers for prodromal disease stages, which would allow novel disease-modifying therapies to be started earlier.

9 Review Selective neuronal vulnerability in Parkinson disease. 2017

Surmeier, D James / Obeso, José A / Halliday, Glenda M. ·Department of Physiology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois 60611, USA. · Centro Integral de Neurociencias A.C. (CINAC), HM Puerta del Sur, Hospitales de Madrid, Mostoles and CEU San Pablo University, 28938 Madrid, Spain. · Network Center for Biomedical Research on Neurodegenerative Diseases (CIBERNED), Instituto Carlos III, 28031 Madrid, Spain. · Brain and Mind Centre, Sydney Medical School, The University of Sydney, Sydney 2006, Australia. · School of Medical Sciences, University of New South Wales and Neuroscience Research Australia, Sydney 2052, Australia. ·Nat Rev Neurosci · Pubmed #28104909.

ABSTRACT: Intracellular α-synuclein (α-syn)-rich protein aggregates called Lewy pathology (LP) and neuronal death are commonly found in the brains of patients with clinical Parkinson disease (cPD). It is widely believed that LP appears early in the disease and spreads in synaptically coupled brain networks, driving neuronal dysfunction and death. However, post-mortem analysis of human brains and connectome-mapping studies show that the pattern of LP in cPD is not consistent with this simple model, arguing that, if LP propagates in cPD, it must be gated by cell- or region-autonomous mechanisms. Moreover, the correlation between LP and neuronal death is weak. In this Review, we briefly discuss the evidence for and against the spreading LP model, as well as evidence that cell-autonomous factors govern both α-syn pathology and neuronal death.

10 Review Exercise to prevent falls in older adults: an updated systematic review and meta-analysis. 2017

Sherrington, Catherine / Michaleff, Zoe A / Fairhall, Nicola / Paul, Serene S / Tiedemann, Anne / Whitney, Julie / Cumming, Robert G / Herbert, Robert D / Close, Jacqueline C T / Lord, Stephen R. ·The George Institute for Global Health, Sydney Medical School, The University of Sydney, Sydney, New South Wales, Australia. · Arthritis Research UK Primary Care Centre, Research Institute for Primary Care and Health Sciences, Keele University, UK. · Clinical Age Research Unit, King's College Hospital, London, UK. · School of Public Health, Sydney Medical School, The University of Sydney, Sydney, New South Wales, Australia. · Neuroscience Research Australia, University of New South Wales, Sydney, New South Wales, Australia. · Prince of Wales Clinical School, University of New South Wales, Sydney, New South Wales, Australia. ·Br J Sports Med · Pubmed #27707740.

ABSTRACT: OBJECTIVE: Previous meta-analyses have found that exercise prevents falls in older people. This study aimed to test whether this effect is still present when new trials are added, and it explores whether characteristics of the trial design, sample or intervention are associated with greater fall prevention effects. DESIGN: Update of a systematic review with random effects meta-analysis and meta-regression. DATA SOURCES: Cochrane Library, CINAHL, MEDLINE, EMBASE, PubMed, PEDro and SafetyLit were searched from January 2010 to January 2016. STUDY ELIGIBILITY CRITERIA: We included randomised controlled trials that compared fall rates in older people randomised to receive exercise as a single intervention with fall rates in those randomised to a control group. RESULTS: 99 comparisons from 88 trials with 19 478 participants were available for meta-analysis. Overall, exercise reduced the rate of falls in community-dwelling older people by 21% (pooled rate ratio 0.79, 95% CI 0.73 to 0.85, p<0.001, I SUMMARY/CONCLUSIONS: Exercise as a single intervention can prevent falls in community-dwelling older people. Exercise programmes that challenge balance and are of a higher dose have larger effects. The impact of exercise as a single intervention in clinical groups and aged care facility residents requires further investigation, but promising results are evident for people with Parkinson's disease and cognitive impairment.

11 Review What Is the Link Between Hallucinations, Dreams, and Hypnagogic-Hypnopompic Experiences? 2016

Waters, Flavie / Blom, Jan Dirk / Dang-Vu, Thien Thanh / Cheyne, Allan J / Alderson-Day, Ben / Woodruff, Peter / Collerton, Daniel. ·Clinical Research Centre, Graylands Hospital, North Metro Health Service Mental Health, Perth, Australia; School of Psychiatry and Clinical Neurosciences, The University of Western Australia, Perth, Australia; flavie.waters@health.wa.gov.au. · Center for Studies in Behavioral Neurobiology, PERFORM Center and Department of Exercise Science, Concordia University; and Centre de Recherches de l'Institut Universitaire de Gériatrie de Montréal and Department of Neurosciences, University of Montreal, Montreal, QC, Canada; · Department of Psychology, University of Waterloo, Waterloo, ON, Canada; · Department of Psychology, Durham University, Durham, UK; · University of Sheffield, UK, Hamad Medical Corporation, Doha, Qatar; · Clinical Psychology, Northumberland, Tyne and Wear NHS Foundation Trust, and Institute of Neuroscience, Newcastle University, Newcastle upon Tyne, UK. ·Schizophr Bull · Pubmed #27358492.

ABSTRACT: By definition, hallucinations occur only in the full waking state. Yet similarities to sleep-related experiences such as hypnagogic and hypnopompic hallucinations, dreams and parasomnias, have been noted since antiquity. These observations have prompted researchers to suggest a common aetiology for these phenomena based on the neurobiology of rapid eye movement (REM) sleep. With our recent understanding of hallucinations in different population groups and at the neurobiological, cognitive and interpersonal levels, it is now possible to draw comparisons between the 2 sets of experiences as never before. In the current article, we make detailed comparisons between sleep-related experiences and hallucinations in Parkinson's disease, schizophrenia and eye disease, at the levels of phenomenology (content, sensory modalities involved, perceptual attributes) and of brain function (brain activations, resting-state networks, neurotransmitter action). Findings show that sleep-related experiences share considerable overlap with hallucinations at the level of subjective descriptions and underlying brain mechanisms. Key differences remain however: (1) Sleep-related perceptions are immersive and largely cut off from reality, whereas hallucinations are discrete and overlaid on veridical perceptions; and (2) Sleep-related perceptions involve only a subset of neural networks implicated in hallucinations, reflecting perceptual signals processed in a functionally and cognitively closed-loop circuit. In summary, both phenomena are non-veridical perceptions that share some phenomenological and neural similarities, but insufficient evidence exists to fully support the notion that the majority of hallucinations depend on REM processes or REM intrusions into waking consciousness.

12 Review Copper dyshomoeostasis in Parkinson's disease: implications for pathogenesis and indications for novel therapeutics. 2016

Davies, Katherine M / Mercer, Julian F B / Chen, Nicholas / Double, Kay L. ·Neuroscience Research Australia, Sydney, NSW 2031, Australia School of Medical Sciences, Faculty of Medicine, University of New South Wales, Sydney, NSW 2052, Australia. · Centre for Cellular and Molecular Biology, School of Life and Environmental Sciences, Deakin University, Melbourne, VIC 3125, Australia. · Neuroscience Research Australia, Sydney, NSW 2031, Australia. · Brain and Mind Centre and Discipline of Biomedical Sciences, School of Medical Sciences, Sydney Medical School, The University of Sydney, Sydney, NSW 2050, Australia kay.double@sydney.edu.au. ·Clin Sci (Lond) · Pubmed #26957644.

ABSTRACT: Copper is a biometal essential for normal brain development and function, thus copper deficiency or excess results in central nervous system disease. Well-characterized disorders of disrupted copper homoeostasis with neuronal degeneration include Menkes disease and Wilson's disease but a large body of evidence also implicates disrupted copper pathways in other neurodegenerative disorders, including Parkinson's disease, Alzheimer's disease, Amyotrophic lateral sclerosis, Huntington's disease and prion diseases. In this short review we critically evaluate the data regarding changes in systemic and brain copper levels in Parkinson's disease, where alterations in brain copper are associated with regional neuronal cell death and disease pathology. We review copper regulating mechanisms in the human brain and the effects of dysfunction within these systems. We then examine the evidence for a role for copper in pathogenic processes in Parkinson's disease and consider reports of diverse copper-modulating strategies in in vitro and in vivo models of this disorder. Copper-modulating therapies are currently advancing through clinical trials for Alzheimer's and Huntington's disease and may also hold promise as disease modifying agents in Parkinson's disease.

13 Review The relationship between sleep and cognition in Parkinson's disease: A meta-analysis. 2016

Pushpanathan, Maria E / Loftus, Andrea M / Thomas, Meghan G / Gasson, Natalie / Bucks, Romola S. ·School of Psychology, University of Western Australia, Australia; ParkC Collaborative, Western Australia, Australia. · School of Psychology and Speech Pathology, Curtin University, Australia; ParkC Collaborative, Western Australia, Australia. · Experimental and Regenerative Neuroscience, School of Animal Biology, University of Western Australia, Australia; ParkC Collaborative, Western Australia, Australia; Parkinson's Centre, Vario Health Institute, Edith Cowan University, Australia. · School of Psychology, University of Western Australia, Australia; ParkC Collaborative, Western Australia, Australia. Electronic address: romola.bucks@uwa.edu.au. ·Sleep Med Rev · Pubmed #26365136.

ABSTRACT: It is well established that sleep disorders have neuropsychological consequences in otherwise healthy people. Studies of night-time sleep problems and cognition in Parkinson's disease (PD), however, paint a mixed picture, with many reporting no relationship between sleep problems and neuropsychological performance. This review aimed to meta-analyse this research and to examine the factors underlying these mixed results. A literature search was conducted of published and unpublished studies, resulting in 16 papers that met inclusion criteria. Data were analysed in the domains of: global cognitive function; memory (general, long-term verbal recognition, long-term verbal recall); and executive function (general, shifting, updating, inhibition, generativity, fluid reasoning). There was a significant effect of sleep on global cognitive function, long-term verbal recall, long-term verbal recognition, shifting, updating, generativity, and fluid reasoning. Although there are effects on memory and executive function associated with poor sleep in PD, the effects were driven by a small number of studies. Numerous methodological issues were identified. Further studies are needed reliably to determine whether disturbed sleep impacts on cognition via mechanisms of hypoxia, hypercapnia, sleep fragmentation, chronic sleep debt or decreased REM and/or slow wave sleep in PD, as this may have important clinical implications.

14 Review Neuropathology of α-synuclein propagation and braak hypothesis. 2016

McCann, Heather / Cartwright, Heidi / Halliday, Glenda M. ·Neuroscience Research Australia, Sydney, Australia. · University of New South Wales, Sydney, Australia. ·Mov Disord · Pubmed #26340605.

ABSTRACT: Parkinson's disease is a progressive neurodegenerative disorder with multiple factors contributing to increasing severity of pathology in specific brain regions. The Braak hypothesis of Lewy pathology progression in Parkinson's disease proposes a systematic spread of α-synuclein that can be staged, with the later stages correlating with clinical aspects of the disease. The spread of pathology through the different stages suggests progression, a theory that has proven correct from evidence of pathology in healthy neurons grafted into the brains of patients with Parkinson's disease. Progression of pathology occurs on a number of levels, within a cell, between nearby cells, and then over longer distances throughout the brain, and evidence using prion proteins suggests two dissociable mechanisms-intracellular toxicity versus a nontoxic infectious mechanism for propagation. In Parkinson's disease, intracellular changes associated with mitochondria and lysosome dysfunction appear important for α-synuclein propagation, with high stress conditions favoring mitochondrial cell death mechanisms. Functional neurons appear necessary for propagation. Unconventional exocytosis releases α-synuclein under stress conditions, and endocytic uptake occurs in nearby cells. This cell-to-cell transmission of α-synuclein has been recapitulated in both cell culture and animal models, but the timeframe of transmission is considerably shorter than that observed in transplanted neurons. The time course of Lewy pathology formation in patients is consistent with the long time course observed in grafted neurons, and the restricted neuronal loss in Parkinson's disease is potentially important for the propagation of α-synuclein through relatively intact circuits.

15 Review MDS research criteria for prodromal Parkinson's disease. 2015

Berg, Daniela / Postuma, Ronald B / Adler, Charles H / Bloem, Bastiaan R / Chan, Piu / Dubois, Bruno / Gasser, Thomas / Goetz, Christopher G / Halliday, Glenda / Joseph, Lawrence / Lang, Anthony E / Liepelt-Scarfone, Inga / Litvan, Irene / Marek, Kenneth / Obeso, José / Oertel, Wolfgang / Olanow, C Warren / Poewe, Werner / Stern, Matthew / Deuschl, Günther. ·Department of Neurodegeneration, Hertie-Institute for Clinical Brain Research and German Center for Neurodegenerative Diseases, Tuebingen, Germany. · Department of Neurology, Montreal General Hospital, Montreal, Quebec, Canada. · The Parkinson's Disease and Movement Disorders Center, Department of Neurology, Mayo Clinic, Scottsdale, Arizona, USA. · Department of Neurology, Radboud University Medical Center, Donders Institute for Brain, Cognition and Behavior, Nijmegen, The Netherlands. · Xuanwu Hospital of Capitol of Medical University, Beijing, China. · Hopital De La Salpetriere, Paris, France. · Rush University Medical Center, Chicago, Illinois, USA. · Neuroscience Research Australia & University of NSW, Randwick, Australia. · Department of Epidemiology and Biostatistics, McGill University, Montreal, Quebec, Canada. · Division of Neurology, Toronto Western Hospital, Toronto, Ontario, Canada. · Department of Neurosciences, University of California San Diego, La Jolla, California, USA. · Institute for Neurodegenerative Disorders, New Haven, Connecticut, USA. · University of Navarra-FIMA, Pamplona, Spain. · Department of Neurology, Philipps University of Marburg, Marburg, Germany. · Department of Neurology, The Mount Sinai Hospital, New York, New York, USA. · Department of Neurology, Innsbruck Medical University, Innsbruck, Austria. · Penn Neurological Institute, Philadelphia, Pennsylvania, USA. · Department of Neurology, Christian-Albrechts University, Kiel, Germany. ·Mov Disord · Pubmed #26474317.

ABSTRACT: This article describes research criteria and probability methodology for the diagnosis of prodromal PD. Prodromal disease refers to the stage wherein early symptoms or signs of PD neurodegeneration are present, but classic clinical diagnosis based on fully evolved motor parkinsonism is not yet possible. Given the lack of clear neuroprotective/disease-modifying therapy for prodromal PD, these criteria were developed for research purposes only. The criteria are based upon the likelihood of prodromal disease being present with probable prodromal PD defined as ≥80% certainty. Certainty estimates rely upon calculation of an individual's risk of having prodromal PD, using a Bayesian naïve classifier. In this methodology, a previous probability of prodromal disease is delineated based upon age. Then, the probability of prodromal PD is calculated by adding diagnostic information, expressed as likelihood ratios. This diagnostic information combines estimates of background risk (from environmental risk factors and genetic findings) and results of diagnostic marker testing. In order to be included, diagnostic markers had to have prospective evidence documenting ability to predict clinical PD. They include motor and nonmotor clinical symptoms, clinical signs, and ancillary diagnostic tests. These criteria represent a first step in the formal delineation of early stages of PD and will require constant updating as more information becomes available.

16 Review MDS clinical diagnostic criteria for Parkinson's disease. 2015

Postuma, Ronald B / Berg, Daniela / Stern, Matthew / Poewe, Werner / Olanow, C Warren / Oertel, Wolfgang / Obeso, José / Marek, Kenneth / Litvan, Irene / Lang, Anthony E / Halliday, Glenda / Goetz, Christopher G / Gasser, Thomas / Dubois, Bruno / Chan, Piu / Bloem, Bastiaan R / Adler, Charles H / Deuschl, Günther. ·Department of Neurology, Montreal General Hospital, Montreal, Quebec, Canada. · Department of Neurodegeneration, Hertie-Institute for Clinical Brain Research and German Center for Neurodegenerative Diseases, Tuebingen, Germany. · Penn Neurological Institute, Philadelphia, Pennsylvania, USA. · Department of Neurology, Innsbruck Medical University, Innsbruck, Austria. · Department of Neurology, The Mount Sinai Hospital, New York, New York, USA. · Department of Neurology, Philipps University of Marburg, Marburg, Germany. · University of Navarra-FIMA, Pamplona, Spain. · Institute for Neurodegenerative Disorders, New Haven, Connecticut, USA. · Department of Neurosciences, UC San Diego, La Jolla, California, USA. · Division of Neurology, Toronto Western Hospital, Toronto, Ontario, Canada. · Neuroscience Research Australia & University of NSW, Randwick, Australia. · Rush University Medical Center, Chicago, Illinois, USA. · Hopital De La Salpetriere, Paris, France. · Xuanwu Hospital of Capitol of Medical University, Beijing, Peoples Republic of China. · Department of Neurology, Radboud University Medical Center, Donders Institute for Brain, Cognition and Behaviour, Nijmegen, Netherlands. · The Parkinson's Disease and Movement Disorders Center, Department of Neurology, Mayo Clinic, Scottsdale, Arizona, USA. · Department of Neurology, Christian-Albrechts University, Kiel, Germany. ·Mov Disord · Pubmed #26474316.

ABSTRACT: This document presents the Movement Disorder Society Clinical Diagnostic Criteria for Parkinson's disease (PD). The Movement Disorder Society PD Criteria are intended for use in clinical research but also may be used to guide clinical diagnosis. The benchmark for these criteria is expert clinical diagnosis; the criteria aim to systematize the diagnostic process, to make it reproducible across centers and applicable by clinicians with less expertise in PD diagnosis. Although motor abnormalities remain central, increasing recognition has been given to nonmotor manifestations; these are incorporated into both the current criteria and particularly into separate criteria for prodromal PD. Similar to previous criteria, the Movement Disorder Society PD Criteria retain motor parkinsonism as the core feature of the disease, defined as bradykinesia plus rest tremor or rigidity. Explicit instructions for defining these cardinal features are included. After documentation of parkinsonism, determination of PD as the cause of parkinsonism relies on three categories of diagnostic features: absolute exclusion criteria (which rule out PD), red flags (which must be counterbalanced by additional supportive criteria to allow diagnosis of PD), and supportive criteria (positive features that increase confidence of the PD diagnosis). Two levels of certainty are delineated: clinically established PD (maximizing specificity at the expense of reduced sensitivity) and probable PD (which balances sensitivity and specificity). The Movement Disorder Society criteria retain elements proven valuable in previous criteria and omit aspects that are no longer justified, thereby encapsulating diagnosis according to current knowledge. As understanding of PD expands, the Movement Disorder Society criteria will need continuous revision to accommodate these advances.

17 Review Cognitive Behaviour Therapy for Depression and Anxiety in Parkinson's Disease. 2015

Egan, Sarah J / Laidlaw, Ken / Starkstein, Sergio. ·School of Psychology and Speech Pathology, Curtin University, WA, Australia. · Department of Clinical Psychology, The University of East Anglia, Norfolk, UK. · School of Psychiatry, University of Western Australia, Crawley WA, Australia. ·J Parkinsons Dis · Pubmed #26406124.

ABSTRACT: Evidence is reviewed demonstrating that cognitive behavior therapy (CBT) is effective in the treatment of depression and anxiety in Parkinson's disease. The aims were to review the extant literature, specify a model of cognitive and behavioral maintenance factors in depression and anxiety in Parkinson's disease and provide a guide to treatment. It is argued that treatment should take into account specific cognitive and behavioral maintaining factors. Symptoms of depression and anxiety are highly prevalent in Parkinson's disease and therapists should consider how to augment the efficacy of CBT for patients with Parkinson's disease. Cognitive and behavioral interventions can help people overcome some of the challenges in living with PD by maximizing wellbeing and overall quality of life.

18 Review A systematic review and meta-analysis of strength training in individuals with multiple sclerosis or Parkinson disease. 2015

Cruickshank, Travis M / Reyes, Alvaro R / Ziman, Melanie R. ·From the School of Medical Sciences (TMC, ARR, MRZ), Edith Cowan University · and School of Pathology and Laboratory Medicine (MRZ), University of Western Australia, Perth, Australia. ·Medicine (Baltimore) · Pubmed #25634170.

ABSTRACT: Strength training has, in recent years, been shown to be beneficial for people with Parkinson disease and multiple sclerosis. Consensus regarding its utility for these disorders nevertheless remains contentious among healthcare professionals. Greater clarity is required, especially in regards to the type and magnitude of effects as well as the response differences to strength training between individuals with Parkinson disease or multiple sclerosis. This study examines the effects, magnitude of those effects, and response differences to strength training between patients with Parkinson disease or multiple sclerosis. A comprehensive search of electronic databases including Physiotherapy Evidence Database scale, PubMed, EMBASE, Cochrane Central Register of Controlled Trials, and CINAHL was conducted from inception to July 2014. English articles investigating the effect of strength training for individuals with neurodegenerative disorders were selected. Strength training trials that met the inclusion criteria were found for individuals with Parkinson disease or multiple sclerosis. Individuals with Parkinson disease or multiple sclerosis were included in the study. Strength training interventions included traditional (free weights/machine exercises) and nontraditional programs (eccentric cycling). Included articles were critically appraised using the Physiotherapy Evidence Database scale. Of the 507 articles retrieved, only 20 articles met the inclusion criteria. Of these, 14 were randomized and 6 were nonrandomized controlled articles in Parkinson disease or multiple sclerosis. Six randomized and 2 nonrandomized controlled articles originated from 3 trials and were subsequently pooled for systematic analysis. Strength training was found to significantly improve muscle strength in people with Parkinson disease (15%-83.2%) and multiple sclerosis (4.5%-36%). Significant improvements in mobility (11.4%) and disease progression were also reported in people with Parkinson disease after strength training. Furthermore, significant improvements in fatigue (8.2%), functional capacity (21.5%), quality of life (8.3%), power (17.6%), and electromyography activity (24.4%) were found in individuals with multiple sclerosis after strength training. The limitations of the study were the heterogeneity of interventions and study outcomes in Parkinson disease and multiple sclerosis trials. Strength training is useful for increasing muscle strength in Parkinson disease and to a lesser extent multiple sclerosis.

19 Review Inflammation is genetically implicated in Parkinson's disease. 2015

Dzamko, N / Geczy, C L / Halliday, G M. ·School of Medical Sciences, University of NSW, Sydney, NSW 2052, Australia; Neuroscience Research Australia, Randwick, NSW 2031, Australia. Electronic address: n.dzamko@neura.edu.au. · School of Medical Sciences, University of NSW, Sydney, NSW 2052, Australia. · School of Medical Sciences, University of NSW, Sydney, NSW 2052, Australia; Neuroscience Research Australia, Randwick, NSW 2031, Australia. Electronic address: g.halliday@neura.edu.au. ·Neuroscience · Pubmed #25450953.

ABSTRACT: Inflammation has long been associated with the pathogenesis of Parkinson's disease (PD) but the extent to which it is a cause or consequence is sill debated. Over the past decade a number of genes have been implicated in PD. Relatively rare missense mutations in genes such as LRRK2, Parkin, SNCA and PINK1 are causative for familial PD whereas more common variation in genes, including LRRK2, SNCA and GBA, comprise risk factors for sporadic PD. Determining how the function of these genes and the proteins they encode are altered in PD has become a priority, as results will likely provide much needed insights into contributing causes. Accumulating evidence indicates that many of these genes function in pathways that regulate aspects of immunity, particularly inflammation, suggesting close associations between PD and immune homeostasis.

20 Review The impact of dementia development concurrent with Parkinson's disease: a new perspective. 2014

Russell, Alyce / Drozdova, Alesya / Wang, Wei / Thomas, Meghan. ·Parkinson's Centre, School of Medical Sciences, Edith Cowan University, 270 Joondalup Dr, Joondalup, WA 6027, Australia. mgthomas54@gmail.com. ·CNS Neurol Disord Drug Targets · Pubmed #25230219.

ABSTRACT: Dementia is the leading cause of disability worldwide among chronic diseases in the elderly and is a major contributor to mortality. Importantly, dementia that develops as a comorbid condition significantly compounds the burden of disease on the person, their caregivers and the health care system. Dementia is a frequent comorbidity of Parkinson's disease (PD) and about 80% of people with PD will develop dementia during the course of the disease. Incidence of dementia in PD ranges from 54.7 to 107.14 per 1000 person-years while point prevalence estimates range from 19.7 to 35.3%. The range in incidence and point prevalence can be attributed to varying diagnostic criteria, sample biases, and sample size. Nosologically, there is still disagreement on the origins of dementia in PD. Dementia development may be most often caused by the progression of PD-type pathology; however, the occurrence of Alzheimer's disease (AD)-type pathology suggests that an interplay exists between the genes and proteins associated with PD and AD. Furthermore, these genes and proteins may increase the risk and severity of dementia development in people with PD. Understanding the mechanisms of neurodegeneration in PD and AD may, therefore, improve efforts to manage and treat PD dementia. Given this, it is important to adequately define the frequency of PD dementia for informed decision making, particularly in the areas of aged-care and government health policy.

21 Review Glucocerebrosidase deficits in sporadic Parkinson disease. 2014

Murphy, Karen E / Halliday, Glenda M. ·Neuroscience Research Australia; School of Medical Sciences; Faculty of Medicine; University of New South Wales; Sydney, Australia. ·Autophagy · Pubmed #24915553.

ABSTRACT: Parkinson disease (PD) is a progressive neurodegenerative movement disorder characterized pathologically by abnormal SNCA/α-synuclein protein inclusions in neurons. Impaired lysosomal autophagic degradation of cellular proteins is implicated in PD pathogenesis and progression. Heterozygous GBA mutations, encoding lysosomal GBA/glucocerebrosidase (glucosidase, β, acid), are the greatest genetic risk factor for PD, and reduced GBA and SNCA accumulation are related in PD models. Here we review our recent human brain tissue study demonstrating that GBA deficits in sporadic PD are related to the early accumulation of SNCA, and dysregulation of chaperone-mediated autophagy (CMA) pathways and lipid metabolism.

22 Review Neuropsychiatric aspects of dementia. 2014

Ford, Andrew H. ·Western Australian Centre for Health & Ageing (M573), Centre for Medical Research, University of Western Australia, 35 Stirling Highway, Crawley, Perth, WA 6009, Australia. Electronic address: andrew.ford@uwa.edu.au. ·Maturitas · Pubmed #24794580.

ABSTRACT: Dementia affects approximately 6.5% of people over the age of 65. Whilst cognitive impairment is central to the dementia concept, neuropsychiatric symptoms are invariably present at some stage of the illness. Neuropsychiatric symptoms result in a number of negative outcomes for the individual and their caregivers and are associated with higher rates of institutionalization and mortality. A number of factors have been associated with neuropsychiatric symptoms including neurobiological changes, dementia type, and illness severity and duration. Specific patient, caregiver and environmental factors are also important. Neuropsychiatric symptoms can be broadly divided into four clusters: psychotic symptoms, mood/affective symptoms, apathy, and agitation/aggression. Neuropsychiatric symptoms tend to persist over time although differing symptom profiles exist at various stages of the illness. Assessment should take into account the presenting symptoms together with an appreciation of the myriad of likely underlying causes for the symptoms. A structured assessment/rating tool can be helpful. Management should focus on non-pharmacological measures initially with pharmacological approaches reserved for more troubling symptoms. Pharmacological approaches should target specific symptoms although the evidence-base for pharmacological management is quite modest. Any medication trial should include an adequate appreciation of the risk-benefit profile in individual patients and discussion of these with both the individual and their caregiver.

23 Review The neurobiological basis of cognitive impairment in Parkinson's disease. 2014

Halliday, Glenda M / Leverenz, James B / Schneider, Jay S / Adler, Charles H. ·Neuroscience Research Australia and the University of New South Wales, Sydney, Australia. ·Mov Disord · Pubmed #24757112.

ABSTRACT: The recent formalization of clinical criteria for Parkinson's disease with dementia (PDD) codifies many studies on this topic, including those assessing biological correlates. These studies show that the emergence of PDD occurs on the background of severe dopamine deficits with, the main pathological drivers of cognitive decline being a synergistic effect between alpha-synuclein and Alzheimer's disease pathology. The presence of these pathologies correlates with a marked loss of limbic and cortically projecting dopamine, noradrenaline, serotonin, and acetylcholine neurons, although the exact timing of these relationships remains to be determined. Genetic factors, such as triplications in the α-synuclein gene, lead to a clear increased risk of PDD, whereas others, such as parkin mutations, are associated with a reduced risk of PDD. The very recent formalization of clinical criteria for PD with mild cognitive impairment (PD-MCI) allows only speculation on its biological and genetic bases. Critical assessment of animal models shows that chronic low-dose MPTP treatment in primates recapitulates PD-MCI over time, enhancing the current biological concept of PD-MCI as having enhanced dopamine deficiency in frontostriatal pathways as well as involvement of other neurotransmitter systems. Data from other animal models support multiple transmitter involvement in cognitive impairment in PD. Whereas dopamine dysfunction has been highlighted because of its obvious role in PD, the role of the other neurotransmitter systems, neurodegenerative pathologies, and genetic factors in PD-MCI remains to be fully elucidated.

24 Review α-Synucleinopathy phenotypes. 2014

McCann, Heather / Stevens, Claire H / Cartwright, Heidi / Halliday, Glenda M. ·Neuroscience Research Australia, Sydney, Australia. ·Parkinsonism Relat Disord · Pubmed #24262191.

ABSTRACT: α-Synucleinopathies are neurodegenerative diseases characterised by the abnormal accumulation of α-synuclein aggregates in neurons, nerve fibres or glial cells. While small amounts of these α-synuclein pathologies can occur in some neurologically normal individuals who do not have associated neurodegeneration, the absence of neurodegeneration in such individuals precludes them from having a degenerative α-synucleinopathy, and it has yet to be established whether such individuals have a form of preclinical disease. There are three main types of α-synucleinopathy, Parkinson's disease (PD), dementia with Lewy bodies (DLB), and multiple system atrophy (MSA), with other rare disorders also having α-synuclein pathologies, such as various neuroaxonal dystrophies. Multiple clinical phenotypes exist for each of the three main α-synucleinopathies, with these phenotypes differing in the dynamic distribution of their underlying neuropathologies. Identifying the factors involved in causing different α-synuclein phenotypes may ultimately lead to more targeted therapeutics as well as more accurate clinical prognosis.

25 Review Respiratory muscle training for respiratory deficits in neurodegenerative disorders: a systematic review. 2013

Reyes, Alvaro / Ziman, Mel / Nosaka, Ken. ·School of Medical Sciences, Edith Cowan University, Joondalup, WA, Australia. Electronic address: a.reyes@ecu.edu.au. · School of Medical Sciences, Edith Cowan University, Joondalup, WA, Australia. · School of Exercise and Health Sciences, Edith Cowan University, Joondalup, WA, Australia. ·Chest · Pubmed #23714850.

ABSTRACT: BACKGROUND: Studies of the impact of respiratory muscle training (RMT) on central neurodegenerative pathologies have been aimed at improving pulmonary function. However, there is no certainty about the effectiveness of RMT in patients affected by these groups of disorders. The purpose of this review was to assess the evidence regarding the efficacy of inspiratory muscle training (IMT) and expiratory muscle training (EMT) on respiratory function in patients with neurodegenerative disorders of the CNS. METHODS: A comprehensive search from 1990 to September 2012 on MEDLINE, Physiotherapy Evidence Database (PEDro), PubMed, Cochrane Library, and Cumulative Index to Nursing and Allied Health Literature (CINAHL) databases was made. Studies reporting on IMT and EMT in patients with neurodegenerative diseases were included. The selected studies were abstracted using a standardized data collection instrument and were assessed by a quality checklist created and adapted from CONSORT (Consolidated Standards for Reporting Trials) and TREND (Transparent Reporting of Evaluation with Nonrandomized Designs). RESULTS: Twenty-four studies were identified by the search strategy. Only 19 studies met the criteria for full review. Ten studies met all the inclusion criteria and were included in the final analysis. Of the 16 parameters present in the quality assessment checklist, only six were achieved for the studies analyzed. CONCLUSIONS: There is some evidence that RMT improves a number of respiratory function parameters in patients with Parkinson disease and multiple sclerosis; however, the number of studies and their quality are not sufficient to conclude whether IMT or EMT is effective in improving respiratory function in patients with neurodegenerative disorders of the CNS.

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