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Parkinson Disease: HELP
Articles from University of New South Wales
Based on 118 articles published since 2008
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These are the 118 published articles about Parkinson Disease that originated from University of New South Wales during 2008-2019.
 
+ Citations + Abstracts
Pages: 1 · 2 · 3 · 4 · 5
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 Editorial Managing psychosis in Parkinson's disease without drugs. 2015

Wand, Anne P F / Peisah, Carmelle. ·Older Persons' Mental Health Service, St George Hospital, Rear Demountable, 7 Chapel St, Kogarah, NSW 2217, Australia. · Faculty of Medicine, University of New South Wales, Sydney, Australia. · South Eastern Sydney Local Health District, Sydney, Australia. · Sydney Medical School, University of Sydney, Sydney, Australia. ·Neurodegener Dis Manag · Pubmed #26295719.

ABSTRACT: -- No abstract --

3 Editorial The end of life with PD can be well-lived: the neurologist's role. 2015

Worthington, John M / Ney, John. ·From The University of New South Wales (J.M.W.), South Western Sydney Clinical School, Australia · and University of Washington (J.N.), Seattle. ·Neurology · Pubmed #26138945.

ABSTRACT: -- No abstract --

4 Review Methamphetamine use and future risk for Parkinson's disease: Evidence and clinical implications. 2018

Lappin, Julia M / Darke, Shane / Farrell, Michael. ·National Drug and Alcohol Research Centre, University of New South Wales, Sydney, Australia; School of Psychiatry, University of New South Wales, Sydney, Australia. Electronic address: j.lappin@unsw.edu.au. · National Drug and Alcohol Research Centre, University of New South Wales, Sydney, Australia. ·Drug Alcohol Depend · Pubmed #29665491.

ABSTRACT: BACKGROUND: Methamphetamine use has been posited to be a risk factor for the development of Parkinson's disease (PD) and parkinsonism. The clinical implications of a potential association between methamphetamine use and PD are considered. METHODS: A review of methamphetamine and PD and parkinsonism was conducted, including evidence from animal models, clinical and population studies. RESULTS: There is biological plausibility to a link between methamphetamine use and PD. Though clinical and epidemiological evidence in this area is scant, a number of studies suggest that methamphetamine is associated with a moderately increased risk of PD and parkinsonism, and may also lead to premature onset of PD. The long lag time between exposure to methamphetamine and onset of PD, the potential for recovery from neurotoxic effects, and tobacco smoking each may attenuate the association. Individual and drug use characteristics that may modulate a user's risk remain poorly understood. CONCLUSIONS: The use of methamphetamine may be an initiating event in the development of PD and parkinsonism, in addition to other risk factors that a given individual may hold. Clinicians should be vigilant to signs of prodromal and emerging PD among methamphetamine users. In individuals with premature onset illness, information on current or prior exposure to methamphetamine should be sought.

5 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.

6 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.

7 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

8 Review Neuroprotective Effects of Citrus Fruit-Derived Flavonoids, Nobiletin and Tangeretin in Alzheimer's and Parkinson's Disease. 2017

Braidy, Nady / Behzad, Sahar / Habtemariam, Solomon / Ahmed, Touqeer / Daglia, Maria / Nabavi, Seyed Mohammad / Sobarzo-Sanchez, Eduardo / Nabavi, Seyed Fazel. ·Centre for Healthy Brain Ageing, School of Psychiatry, University of New South Wales, Sydney. Australia. · School of Pharmacy, Shahid Beheshti University of Medical Sciences, Tehran, Iran. · Pharmacognosy Research Laboratories, Medway School of Science, University of Greenwich, Central Avenue, Chatham-Maritime, Kent ME4 4TB, United Kingdom. · Attaur- Rahman School of Applied Biosciences, National University of Sciences and Technology, Islamabad. Pakistan. · Department of Drug Sciences, Medicinal Chemistry and Pharmaceutical Technology Section, University of Pavia, Lombardy, Italy. · Applied Biotechnology Research Center, Baqiyatallah University of Medical Sciences, Tehran, Iran. · Departamento de Farmacia y Tecnología Farmacéutica, Facultad de Farmacia, Universidad de Santiago de Compostela, 15782. Spain. ·CNS Neurol Disord Drug Targets · Pubmed #28474543.

ABSTRACT: Neurodegenerative diseases, namely Alzheimer's disease and Parkinson's disease represent a deleterious impact worldwide. Despite extensive preclinical and clinical research in neurodegenerative disorders, therapeutic strategies aimed at the prevention and chronic treatment of neurodegenerative conditions have not been successfully translated to the clinic. Therefore, the identification of novel pharmacological intervention derived from natural products is warranted. Nobiletin and tangeretin are important citrus flavonoids derived from the peel and other parts of Citrus L. genus, and have been shown to exhibit neuroprotective effects in several in vitro and in vivo studies. Apart from there antioxidant and anti-inflammatory effects, nobiletin and tangeretin have been shown to attenuate cholinergic deficits, reduce the abnormal accumulation of neurotoxic amyloid-beta peptides, reverse N-methyl- D-aspartate (NMDA) receptor hypofunction, ameliorate ischemic injury, inhibit hyperphosphorylation of tau protein, enhance neprilysin levels, modulate several signaling cascades, and protect against 1-methyl-4-phenylpyridinium (MPP(+)) and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) toxicity. Taken together, these naturally occurring phytochemicals may represent beneficial drug candidates for the treatment and prevention of Alzheimer's and Parkinson's disease.

9 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.

10 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.

11 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.

12 Review PPARs in the central nervous system: roles in neurodegeneration and neuroinflammation. 2017

Zolezzi, Juan M / Santos, Manuel J / Bastías-Candia, Sussy / Pinto, Claudio / Godoy, Juan A / Inestrosa, Nibaldo C. ·Centro de Envejecimiento y Regeneración (CARE-UC), P. Catholic University of Chile, PO Box 114-D, 8331150, Santiago, Chile. · Facultad de Ciencias Biológicas, Departamento de Biología Celular y Molecular, Pontificia Universidad Católica de Chile, Alameda 340, 8331150, Santiago, Chile. · Facultad de Ciencias, Departamento de Biología, Universidad de Tarapacá, Gral. Velásquez 1775, 1000007, Arica, Chile. · Faculty of Medicine, Centre for Healthy Brain Ageing, School of Psychiatry, University of New South Wales, Avoca Street Randwick NSW 2031, Sydney, Australia. · Centro de Excelencia en Biomedicina de Magallanes (CEBIMA), Universidad de Magallanes, PO Box 113-D, Avenida Bulnes 01855, 6210427, Punta Arenas, Chile. ·Biol Rev Camb Philos Soc · Pubmed #28220655.

ABSTRACT: Over 25 years have passed since peroxisome proliferators-activated receptors (PPARs), were first described. Like other members of the nuclear receptors superfamily, PPARs have been defined as critical sensors and master regulators of cellular metabolism. Recognized as ligand-activated transcription factors, they are involved in lipid, glucose and amino acid metabolism, taking part in different cellular processes, including cellular differentiation and apoptosis, inflammatory modulation and attenuation of acute and chronic neurological damage in vivo and in vitro. Interestingly, PPAR activation can simultaneously reprogram the immune response, stimulate metabolic and mitochondrial functions, promote axonal growth, induce progenitor cells to differentiate into myelinating oligodendrocytes, and improve brain clearance of toxic molecules such as β-amyloid peptide. Although the molecular mechanisms and cross-talk with different molecular pathways are still the focus of intense research, PPARs are considered potential therapeutic targets for several neuropathological conditions, including degenerative disorders such as Alzheimer's, Parkinson's and Huntington's disease. This review considers recent advances regarding PPARs, as well as new PPAR agonists. We focus on the mechanisms behind the neuroprotective effects exerted by PPARs and summarise the roles of PPARs in different pathologies of the central nervous system, especially those associated with degenerative and inflammatory mechanisms.

13 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.

14 Review A Mini Review on the Chemistry and Neuroprotective Effects of Silymarin. 2017

Devi, Kasi Pandima / Malar, Dicson Sheeja / Braidy, Nady / Nabavi, Seyed Mohammad / Nabavi, Seyed Fazel. ·Department of Biotechnology, Alagappa University, Karaikudi-630 004, Tamil Nadu. India. · Centre for Healthy Brain Ageing, School of Psychiatry, University of New South Wales, Australia. · Applied Biotechnology Research Center, Baqiyatallah University of Medical Sciences, Tehran, Iran. ·Curr Drug Targets · Pubmed #28025940.

ABSTRACT: BACKGROUND: The plant milk thistle and silymarin has been traditionally used as a natural remedy for the treatment of various ailments including neurological disorders such as Alzheimer's and Parkinson's disease and cerebral ischemia for over 2000 years. OBJECTIVE: In this article we review the neuroprotective effects of silymarin against various neurological dysfunctions. RESULTS: The neuroprotective effects conferred by silymarin include modulation of various antioxidant mechanisms, and several kinases involved in cell signaling pathways, inhibition of the inflammatory response generated during neurodegeneration, neurotropic effects, regulation of neurotransmitters and inhibition of apoptosis. The ease of availability, comparative low cost and safety profile provide additional advantages for the use of this compound as a potent drug with immense clinical benefit. However, there is a growing need for improvements in the bioavailability of silymarin and related products, and more consistent and reliable human trials are required to accurately validate the neuroprotective efficacy of this natural compound. CONCLUSION: The promising outcomes of the studies mentioned in this review provide renewed insight into the clinical relevance of silymarin in a variety of neurodegenerative disorders where neuroinflammation and oxidative stress are pathologically relevant to disease progression.

15 Review Mild parkinsonian features in dystonia: Literature review, mechanisms and clinical perspectives. 2017

Haggstrom, Lucy / Darveniza, Paul / Tisch, Stephen. ·School of Medicine, University of New South Wales, Sydney, Australia. Electronic address: lucyhaggstrom@icloud.com. · School of Medicine, University of New South Wales, Sydney, Australia; Department of Neurology, St Vincent's Hospital, Sydney, Australia. Electronic address: pdarveniza@stvincents.com.au. · School of Medicine, University of New South Wales, Sydney, Australia; Department of Neurology, St Vincent's Hospital, Sydney, Australia. Electronic address: stisch@stvincents.com.au. ·Parkinsonism Relat Disord · Pubmed #27825543.

ABSTRACT: Dystonia is a hyperkinetic movement disorder that can be highly stigmatizing and disabling. Substantial evidence from animal models, neuropathological, neurophysiological, neuroimaging and clinical studies emphasizes the role of dopaminergic dysfunction in the pathophysiology of dystonia, illustrating possible pathophysiological overlap with parkinsonism. Furthermore, basal ganglia dysfunction has been implicated in the pathogenesis of dystonia, and is well established to underlie the manifestations of Parkinson's disease. Clinically, parkinsonian features are a key characteristic of some combined dystonias, including dopa-responsive dystonia, and Parkinson's disease often presents with dystonia. Moreover, many treatments effective in Parkinson's disease, both medical and surgical, also offer some benefit in dystonia. Therefore, mild parkinsonian features might logically accompany idiopathic and inherited isolated dystonias. However, as the current literature is particularly scant, the present review aimed to investigate mild parkinsonism in idiopathic and inherited dystonia. We found limited evidence alluding to the presence of mildly reduced arm-swing, increased tone, and non-decremental bradykinesia in adult-onset focal dystonia. Tremor, with postures, action and rest, also occurs commonly in idiopathic isolated dystonia, and can simulate Parkinson's disease tremor and be a cause of 'scans without evidence of dopaminergic deficit'. Parkinsonian features in monogenic isolated dystonias have been less well investigated, despite the potential benefit of correlating pathophysiological and clinical findings. The recognition and improved clinical characterization of parkinsonian features in idiopathic and inherited isolated dystonia extends the clinical spectrum of motor features in dystonia, which may help avoid incorrect diagnosis and inform therapeutic research.

16 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.

17 Review Involvement of the kynurenine pathway in the pathogenesis of Parkinson's disease. 2017

Lim, Chai K / Fernández-Gomez, Francisco J / Braidy, Nady / Estrada, Cristina / Costa, Cristina / Costa, Silvia / Bessede, Alban / Fernandez-Villalba, Emiliano / Zinger, Anna / Herrero, Maria Trinidad / Guillemin, Gilles J. ·Neuroinflammation Group, Faculty of Medicine and Health Sciences, Macquarie University, Sydney, Australia. · Clinical & Experimental Neuroscience, Institute of Biomedical Research of Murcia (IMIB), Institute of Aging Research, School of Medicine, University of Murcia, 30100 Murcia, Spain. · Centre for Healthy Brain Ageing, School of Psychiatry, University of New South Wales, Sydney, Australia. · Clinical & Experimental Neuroscience, Institute of Biomedical Research of Murcia (IMIB), Institute of Aging Research, School of Medicine, University of Murcia, 30100 Murcia, Spain; Laboratório de Neuroquímica e Biologia Celular, Instituto de Ciências da Saúde, Universidade Federal da Bahia, Salvador, Brazil. · Laboratório de Neuroquímica e Biologia Celular, Instituto de Ciências da Saúde, Universidade Federal da Bahia, Salvador, Brazil. · ImmuSmol, Pessac, France. · Vascular Immunology Unit, Dept of Pathology, Sydney Medical School, The University of Sydney, Australia. · Clinical & Experimental Neuroscience, Institute of Biomedical Research of Murcia (IMIB), Institute of Aging Research, School of Medicine, University of Murcia, 30100 Murcia, Spain. Electronic address: mtherrer@um.es. · Neuroinflammation Group, Faculty of Medicine and Health Sciences, Macquarie University, Sydney, Australia; Applied Neurosciences Program, Peter Duncan Neurosciences Research Unit, St Vincent's Centre for Applied Medical Research, Sydney, Australia. Electronic address: gilles.guillemin@mq.edu.au. ·Prog Neurobiol · Pubmed #27072742.

ABSTRACT: Parkinson's disease (PD) is a common neurodegenerative disorder characterized by loss of dopaminergic neurons and localized neuroinflammation occurring in the midbrain several years before the actual onset of symptoms. Neuroinflammation leads to microglia activation and release of a large number of proinflammatory mediators. The kynurenine pathway (KP) of tryptophan catabolism is one of the major regulators of the immune response and is also likely to be implicated in the inflammatory and neurotoxic events in Parkinsonism. Several neuroactive compounds are produced through the KP that can be either a neurotoxic, neuroprotective or immunomodulator. Among these metabolites kynurenic acid (KYNA), produced by astrocytes, is considered as neuroprotective whereas quinolinic acid (QUIN), released by activated microglia, can activate the N-methyl-d-aspartate (NMDA) receptor-signalling pathway, leading to excitotoxicity and amplify the inflammatory response. Previous studies have shown that NMDA antagonists can ease symptoms and exert a neuroprotective effect in PD both in vivo and in vitro. There are to date several lines of evidence linking some of the KP intermediates and the neuropathogenesis of PD. Moreover, it is likely that some of the KP metabolites could be used as prognostic biomarkers and that pharmacological modulators of the KP enzymes could represent a new therapeutic strategy for PD.

18 Review Exercise for Individuals with Lewy Body Dementia: A Systematic Review. 2016

Inskip, Michael / Mavros, Yorgi / Sachdev, Perminder S / Fiatarone Singh, Maria A. ·Exercise, Health and Performance Faculty Research Group, Faculty of Health Sciences, University of Sydney, Lidcombe, New South Wales, 2141, Australia. · CHeBA (Centre for Healthy Brain Ageing), School of Psychiatry, University of New South Wales, Randwick, New South Wales, 2031, Australia. · Neuropsychiatric Institute, Prince of Wales Hospital, Randwick, New South Wales, 2031, Australia. · Sydney Medical School, University of Sydney, Sydney, New South Wales, 2006, Australia. · Hebrew SeniorLife, Roslindale, Massachusetts, 02131, United States of America. · Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University, Boston, Massachusetts, 02155, United States of America. ·PLoS One · Pubmed #27258533.

ABSTRACT: BACKGROUND: Individuals with Lewy body Dementia (LBD), which encompasses both Parkinson disease dementia (PDD) and Dementia with Lewy Bodies (DLB) experience functional decline through Parkinsonism and sedentariness exacerbated by motor, psychiatric and cognitive symptoms. Exercise may improve functional outcomes in Parkinson's disease (PD), and Alzheimer's disease (AD). However, the multi-domain nature of the LBD cluster of symptoms (physical, cognitive, psychiatric, autonomic) results in vulnerable individuals often being excluded from exercise studies evaluating physical function in PD or cognitive function in dementia to avoid confounding results. This review evaluated existing literature reporting the effects of exercise interventions or physical activity (PA) exposure on cluster symptoms in LBD. METHODS: A high-sensitivity search was executed across 19 databases. Full-length articles of any language and quality, published or unpublished, that analysed effects of isolated exercise/physical activity on indicative Dementia with Lewy Bodies or PD-dementia cohorts were evaluated for outcomes inclusive of physical, cognitive, psychiatric, physiological and quality of life measures. The protocol for this review (Reg. #: CRD42015019002) is accessible at http://www.crd.york.ac.uk/PROSPERO/. RESULTS: 111,485 articles were initially retrieved; 288 full articles were reviewed and 89.6% subsequently deemed ineligible due to exclusion of participants with co-existence of dementia and Parkinsonism. Five studies (1 uncontrolled trial, 1 randomized controlled trial and 3 case reports) evaluating 16 participants were included. Interventions were diverse and outcome homogeneity was low. Habitual gait speed outcomes were measured in 13 participants and increased (0.18m/s, 95% CI -0.02, 0.38m/s), exceeding moderate important change (0.14m/s) for PD cohorts. Other outcomes appeared to improve modestly in most participants. DISCUSSION: Scarce research investigating exercise in LBD exists. This review confirms exercise studies in PD and dementia consistently exclude LBD participants. Results in this cohort must be treated with caution until robustly designed, larger studies are commissioned to explore exercise efficacy, feasibility and clinical relevance.

19 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.

20 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.

21 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.

22 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.

23 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.

24 Review Depression and the older medical patient--when and how to intervene. 2014

Mitchell, Philip B / Harvey, Samuel B. ·School of Psychiatry, University of New South Wales, Australia; Black Dog Institute, Sydney, NSW, Australia. Electronic address: phil.mitchell@unsw.edu.au. · School of Psychiatry, University of New South Wales, Australia; Black Dog Institute, Sydney, NSW, Australia; St George Hospital, Sydney, Australia. ·Maturitas · Pubmed #24939806.

ABSTRACT: Depression in the elderly, particularly those with chronic physical health problems, is a common, but complex problem. In this paper we review the research literature on both the epidemiology and management of depression in the older medical patient. After a general overview of depression in the elderly, we discuss some of the particular issues relevant to depression and co-morbid physical illness amongst elderly patients. Depression can be difficult to diagnose in medically unwell older adults, particularly when there is substantial overlap in symptomatology. The epidemiology and evidence base for the treatment of depression in a number of chronic health problems common in an older adults population are then discussed, specifically cardiac disease, cerebrovascular disease, cancer, chronic kidney disease, chronic obstructive pulmonary disease, and Parkinson's disease. For many of these conditions there is emerging evidence that treatments can be effective in reducing depressive symptoms. However, these potential benefits need to be balanced against the often-increased risk of adverse events or interactions with medical treatments. Although co-morbid depression is consistently associated with poorer medical outcomes, there is limited evidence that standard anti-depressive therapy has additional benefits in terms of physical health outcomes. Collaborative care models appear particularly well suited to medically unwell older adult patients, and may provide more generalised benefits across both mental and physical health measures.

25 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.

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