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Speaker & Session Highlights
Leading up to the WPC 2010, we will highlight faculty and their sessions giving attendees a sneak preview of what's to come. We are thrilled and honored that these outstanding members of the Parkinson's community have agreed to participate in the WPC 2010. The speakers we highlight on this page are just a few of our speakers who we believe help move the science and care forward, expediting the discovery of a cure and improving quality of life in the meantime..
Speaker of the Week: Laura Marsh, MD
We asked each highlighted speaker to:
-tell us about the talk they will be giving and/or why their topic is important;
-to project where they think the science in this area will be going in the future; and if appropriate,
-to explain why this topic is important to people living with Parkinson's.
Read about previously highlighted speakers, with the most recently introduced person first:
David J Brooks, MD, DSc, FRCP, FMed, Sci
J. Timothy Greenamyre, MD, PhD
Bastiaan Bloem, MD, PhD
Glenda Halliday, PhD, BScHons
Speaker of the Week
Speaker: Laura Marsh, MD,
Executive Director of the Mental Health Care Line of the Michael E. DeBakey Veterans Affairs Medical Center and a Professor of Psychiatry and Neurology at the Baylor College of Medicine in Houston, TX, USA
Talk Title: Depression and Cognitive Dysfunction in PD: What is the Relationship?
Session: PD and Cognition
Session Time: 13:30 to 15:00
Date: Thursday, September 30, 2010
When asked what is innovative and new in the field and why the talk she is giving on “Depression and Cognitive Dysfunction in PD" is important to PD research overall Dr. Marsh explained: An association between dementia, increased depressive symptoms, and disability in PD has been recognized for many years. More recent work focuses on how depressive symptoms and disorders are related to selective cognitive deficits that develop earlier in the course of PD, before the onset of dementia. Understanding these relationships better and how they relate longitudinally will help to focus treatment approaches. For example, treating selective cognitive deficits could reduce depressive symptoms and improve longitudinal functioning.
We then asked Dr. Marsh to theorize where research in this field may go in the future and what we could expect to see from people studying this topic: Research in this area will seek to understand the etiology, pathophysiology, course, and treatments of cognitive dysfunction and depression in PD. The ultimate goal is to develop pharmacological and nonpharmacological treatments that slow, limit, or halt disease progression, including the cognitive and psychiatric manifestations of the disease. Cognitive and psychiatric features may also facilitate identification of biological markers that predict development of PD or help to target treatments.
Lastly, we asked Dr. Marsh to explain why someone living with PD should be interested in this topic how she expects that it will ultimately help someone living with PD: Depression and cognitive dysfunction are both common problems in individuals with PD that have negative effects on quality of life, disability, and caregiver burden. While there are established treatments for depression and some evidence of treatment approaches for cognitive dysfunction, both disturbances are under-recognized by clinicians and individuals with PD and, thus, under-treated. Since symptoms of depressive and cognitive disturbances overlap and each condition aggravates the other, a better understanding of these relationships over the course of PD and how they manifest will help to define treatment strategies and focus research on underlying causes.
Learn about some of Dr. Marsh's articles and publications
Marsh L, William JR, Gerstenhaber M, Biglan K. Atomoxetine for the treatment of executive dysfunction in Parkinson's disease: A pilot open-label study. Movement Disorders 2009; 24(2): 277-282. PMID: 19025777
Psychiatric Issues in Parkinson's Disease: A Practical Guide. MM Menza, L Marsh (eds), Taylor and Francis, New York: Taylor and Francis, 2005, 156-174.
Learn about Laura Marsh, MD
Laura Marsh, M.D. is the Executive Director of the Mental Health Care Line of the Michael E. DeBakey Veterans Affairs Medical Center and a Professor of Psychiatry and Neurology at the Baylor College of Medicine in Houston, TX. A geriatric psychiatrist who focuses on psychiatric disturbances in patients with neurological disorders, her current clinical and academic research interests focus on improving the characterization, detection, and treatment of Parkinson's disease—related psychiatric disturbances. Dr. Marsh completed her psychiatry residency training at Johns Hopkins University School of Medicine in Baltimore, MD and completed research fellowships in brain neuroimaging and neuropsychiatric disorders at the National Institute of Mental Health and at Stanford University School of Medicine. She was a member of the Stanford faculty from 1994 until 1998, when she returned to Johns Hopkins. There, Dr. Marsh was director and principal investigator of the Clinical Research Program of the NIH-funded Morris K. Udall Parkinson's Disease Research Center and developed independent clinical and research programs focused on improving the recognition and treatment of neuropsychiatric disturbances in Parkinson's disease. To that end, she was the recipient of an NIH-funded RO1 entitled “Methods of Optimal Depression Detection in PD (MOOD-PD)”. She relocated to Houston in 2009 where she continues her research on Parkinson's disease and focuses on strategies to integrate psychiatric and mental health care with other medical specialties. Dr. Marsh serves on the scientific or clinical advisory boards for the American Parkinson Disease Association, the National Parkinson Foundation, and the Parkinson's Study Group and has published widely on psychiatric disorders in PD and related conditions, including as co-editor of the book, Psychiatric Issues in Parkinson's Disease: A Practical Guide.
Speaker: David J Brooks, MD, DSc, FRCP, FMed, Sci
Hartnett Professor of Neurology and Head of Neuroscience in the
Department of Medicine, Imperial College, London
Talk Title: DAT and Spect Imaging
Session: Early Diagnosis and PD (Modalities to Monitor Disease Progression)
Date: Wednesday, September 29, 2010
Time: 14:30 to 16:00
When asked to explain what is innovative and new in the field, Professor Brooks explained that
DAT SPECT imaging is able to provide a rationale for the use of dopaminergic agents in patients suspected of having a dopamine deficient parkinsonian syndrome. It can also identify inappropriate usage of dopaminergic drugs in apparently drug resistant PD cases. More innovatively it is being used to identify the presence of subclinical dopamine deficiency in at-risk subjects for PD such as those with a family history, a late-onset sleep disorder or loss of sense of smell.
He went on to explain that it's important to PD research overall because in order to trial new symptomatic and neuroprotective drugs in PD it is essential to know that only appropriate patients with striatal dopamine deficiency are being enrolled into studies. Additionally, DAT SPECT provides an objective biomarker for following disease progression.
We asked to theorize where research in this field may go in the future and what we could expect to see from people studying this topic he said that to date DAT imaging has been confined to striatal areas but non-motor problems may well come from dopamine disruption in other brain regions. Higher sensitivity SPECT cameras will allow examination of limbic and cortical areas. Additionally, studies to determine the utility of DAT SPECT will be performed, designed to demonstrate improved quality of life following early knowledge of dopaminergic status in patients with suspected PD.
Lastly, we asked him to tell us why someone living with PD should be interested in this work and/or how he expects that it will ultimately help someone living with PD. He said that
DAT SPECT is most likely to help confirm diagnosis and rationalise treatment in early suspected PD than help someone living with established PD. If neuroprotective drugs become available DAT SPECT could help identify subclinical disease in at-risk subjects and so prevent onset of symptoms.
Read Professor Brooks' work which is at press now for The Journal of Nuclear Medicine on "Imaging approaches to Parkinson's disease".
Learn about David J. Brooks, MD, DSc, FRCP, FMed, Sci
Professor Brooks is Hartnett Professor of Neurology and Head of Neuroscience in the Department of Medicine, Imperial College, London. He is also Head of the Neurology Group at the Medical Research Council Clinical Sciences Centre, Hammersmith Hospital, London. Additionally, he is Head of Neurology, Medical Diagnostics, GE Healthcare PLC.
He has been a member of the Research Advisory Panels of the UK Parkinson's Disease Society, the German Dementia and Parkinson Networks, and Inserm. He has been a member of the Scientific Advisory Board of the Michael J. Fox Foundation for Parkinson's Disease Research (2002-2006), UK Medical Research Council Neuroscience and Mental Health Board (2004-2007), UK Huntington's Disease Association, and was Chairman of the Scientific Issues Committee of the Movement Disorder Society (1998-2002) and a Director of the International Society of Cerebral Blood Flow and Metabolism (1993-1997). He was Chairman of the Council of Management of the UK Parkinson's Disease Society 1997-8.
He is on the Editorial Boards of Brain, Journal of Neural Transmission, Synapse, Molecular Imaging and Biology, Neurotherapeutics and Current Trends in Neurology, and was on the editorial boards of the Journal of Neurology, Neurosurgery, and Psychiatry 1998-2004 and Movement Disorders 1994-1998.
In 2001 he was elected a Fellow of the Academy of Medical Science, UK. In 2002 he was invited to give the Stan Fahn Lecture at the International Congress of Movement Disorders, Miami, in 2003 the George Cotzias Lecture in Madrid, in 2004 the Charles E Wilson Lecture, the Psychobiology Institute, Jerusalem March 2004, in 2005 the Kuhl-Lassen lecture at the Society of Nuclear Medicine, Toronto, and in 2006 the Sprague lecture at UC Irvine .
His research involves the use of positron emission tomography and magnetic resonance imaging to diagnose and study the progression of Alzheimer's and Parkinson's disease and their validation of biomarkers therapeutic trials. To date, he has published over 300 reports in peer reviewed journals, including Nature. His research is supported by grants from the UK Medical Research Council, the Alzheimer's Research Trust, UK Parkinson's Disease Society, the Michael J Fox foundation, and industry.
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Speaker: J. Timothy Greenamyre, MD, PhD
Professor & Vice-Chair of Neurology
Director, Pittsburgh Institute for Neurodegenerative Diseases
Talk Title: Pesticides and PD
Session:
Environment, Epidemiology and PD
Date: Wednesday, September 29, 2010
Time: 14:30 to 16:00
What is innovative and new in this particular field and why it's important to PD research overall?
Most cases of PD are believed to result from an interaction between an individual's genetic make-up and a lifetime of toxic exposures. In addition, there is increasing evidence that PD is associated with impaired function of mitochondria – the cell's power plants. In this context, we developed a model of PD based on chronic systemic administration of rotenone, which is both a pesticide and mitochondrial toxin. For the first time, this model was able to recapitulate the Lewy bodies that characterize the PD brain. In addition, the rotenone model provided the first proof-of-concept that mitochondrial impairment throughout the body could be associated with selective degeneration of the substantia nigra dopamine neurons that die in PD. The rotenone model also recapitulates many other features of PD including sleep disturbances and gastrointestinal problems. Based on this work in rodents, rotenone has been the subject of human epidemiological studies, and it has been shown that exposure to rotenone – a common household pesticide – increases the risk of developing PD.
Theorize where research in this field may go in the future and what we could expect to see from people studying this topic
We believe the rotenone model of PD provides critical information about how an environmental exposure can cause PD. One of the next steps we are exploring is how an individual's genetic make-up alters their risk of PD after an environmental exposure. By defining the interactions between genetic and environmental risk factors for PD, we believe that it will be possible to prevent or delay many cases of PD. For example, we may be able to determine that individuals with a certain genetic background (e.g., alpha-synuclein promoter polymorphisms that increase expression, or certain LRRK2 mutations) should absolutely avoid certain types of chemicals. Since the greatest costs associated with PD are (i) loss of productivity and (ii) long-term inpatient care, delaying disease onset will have a major impact on both quality of life and health care costs. Moreover, this line of investigation should point the way to further mechanistic studies that identify new targets for pharmacological or genetic therapeutic approaches to PD.
So, why should someone affected by PD care about this line of research?
First, development of accurate models of PD is essential for developing and testing new treatment strategies. That is, the more accurately a PD “model” recapitulates the human disease, the more likely it is that a treatment that works in the model will ultimately be translated into an effective therapy for individuals with PD. In this regard, we feel that the rotenone model is quite accurate in reproducing many aspects of PD. Second, as we begin to delineate the earliest cellular events that lead to neurodegeneration in an accurate model of PD, it should be possible to devise therapies that prevent (or at least slow) the progression of the disease. Third, we hope to be able to define some of the “gene-environment interactions” that make some people particularly susceptible or resistant to developing PD. By doing so, it should be possible to devise strategies to reduce an individual's risk of developing the disease.
Read about Professor Greenamyre and his colleagues' published work on the “Chronic rotenone exposure reproduces Parkinson's disease gastrointestinal neuropathology” published in July 2009 in the journal Neurobiology of Disease.
Learn more about J. Timothy Greenamyre, M.D., Ph.D.
Professor Greenamyre is Vice-Chair of Neurology at the University of Pittsburgh School of Medicine, UPMC Endowed Chair & Chief of the Movement Disorders Division, and Director of the Pittsburgh Institute for Neurodegenerative Diseases (PIND) and the American Parkinson Disease Association Advanced Center for Parkinson's Disease Research at the University of Pittsburgh. He is a member of the Scientific Advisory Boards of the Michael J. Fox Foundation and the Parkinson's Disease Foundation. He is the Editor of Neurobiology of Disease .
His lab is interested in mechanisms that cause nerve cell death in disorders such as Parkinson's, Huntington's and Alzheimer's diseases. With respect to Parkinson's disease, he is interested in interactions between environmental toxins (natural or man-made) and genes that increase or decrease an individual's susceptibility to developing the disease. The work focuses on mitochondrial impairment, oxidative damage and protein aggregation. In Huntington's disease, the lab focuses on mitochondrial calcium handling and proteomics. The general strategy is to define mechanisms that cause nerve cell death, and then use them as potential ''targets'' for therapeutic intervention. The lab employs in vivo models of neurodegeneration and in vitro culture of cells and brain slices to study mechanisms of degeneration with a variety of biochemical, anatomical and physiological techniques.
As Chief of the Movement Disorders Division, Dr. Greenamyre maintains an active clinical practice that is focused on Parkinson's disease, Huntington's disease and related disorders. He is currently listed as one of “The Best Doctors in America” and as one of “America's Top Physicians”. In addition to his laboratory research, Dr. Greenamyre participates in a variety of clinical studies and drug trials.
Speaker: Professor Bastiaan R. Bloem, MD, PhD
Medical director, Parkinson Center Nijmegen (ParC)
Radboud University Nijmegen Medical Center
Talk Title: Comprehensive Care in 2020
Session: Multidisciplinary and Comprehensive Care in PD
Date: Wednesday, September 29, 2010
Time: 14:00 to 16:00
We asked Professor Bloem to tell us what is innovative and new in the field of comprehensive care and why it's important to PD research overall:
Parkinson's disease (PD) is an unusually complex disorder, with both motor symptoms (e.g. slowness, or tremor) and a wide variety of non-motor symptoms (e.g. depression, sleep problems, or fatigue). Until now, medical management is focused mainly on drug treatment. Despite this, most patients become progressively disabled, and those symptoms that are resistant to drug therapy become the major determinants of quality of life. Allied health care may provide complementary benefits to PD patients, even for symptoms that are resistant to pharmacotherapy. This notion is increasingly supported by scientific evidence, and is embedded within recent clinical practice guidelines that are available for physiotherapy, occupational therapy and speech-language therapy. Unfortunately, adequate delivery of allied health care is threatened by the insufficient expertise among therapists, and the generally low patient volumes for each individual therapist. To improve the quality of allied health care, we developed a community-based professional network (ParkinsonNet) with the following active components: training a selected number of expert physiotherapists, to work according to evidence-based guidelines; and structured referrals to these trained therapists, to increase their patient volumes. In a recent paper in the prestigious journal Lancet Neurology, we describe the results of a large trial in 700 patients with PD where we have evaluated the effectiveness of this ParkinsonNet approach. The results showed that implementation of ParkinsonNet networks led to an improved quality of care improved (better adherence to guidelines, and higher patients volumes per therapist), while health care costs were substantially reduced, allowing cost savings that would amount to as much as 70 million Euros in The Netherlands alone.
We asked him to take it one step further and to theorize where research in this field may go in the future and what we could expect to see from people studying this topic and he wrote:
The ParkinsonNet system of care lends itself for further dissemination and extension. Since completion of our trial, we have implemented more than 64 regional ParkinsonNet networks in the Netherlands. This rapid national dissemination underscores how broadly the ParkinsonNet is accepted in the field. It is quite possible that ParkinsonNet can be extended to other countries where the organization of health care is different and where other funding models are in place. Another potential source of extension is the inclusion of additional healthcare disciplines. All ParkinsonNet networks in the Netherlands now feature a selection of trained occupational therapists and speech-language therapists. Furthermore, ParkinsonNet may serve as a model for other chronic disorders, such as diabetes, stroke, dementia or rheumatoid arthritis. As such, the ParkinsonNet system is good for patients (better quality of care; improved transparency within the health care system), for health professionals (greater expertise; larger patient volumes; easier communication with colleagues) and for the society at large (substantial cost savings).
Lastly, we asked Professor Bloem to explain why someone living with PD should be interested in this work and how he expected that it would ultimately help someone living with PD:
He explained that ParkinsonNet gives patients what they want most: they are back in charge of their own disease, e.g. because they can specifically select a well-trained expert of their own choice. Patients are desperate to receive the best possible care, and the Parkinsonnet approach ascertains the presence of high-level expertise that is visible to both patients and the referring physicians. The improved quality of care should ultimately serve to maintain a good quality of life and preserve independence.
Read Professor Bloem and his colleagues' most recent published work on the Efficacy of community-based physiotherapy networks for patients with Parkinson's disease: a cluster-randomised trial published in December 2009 in The Lancet.
Learn more about Professor Bastiaan R. Bloem, MD, PhD
Professor Bloem is a consultant neurologist at the Department of Neurology, Radboud University Nijmegen Medical Centre, in Nijmegen, the Netherlands. He received his M.D. degree (with honour) at Leiden University Medical Centre in 1993. In 1994, he obtained his PhD degree in Leiden, based on a thesis entitled “Postural reflexes in Parkinson's disease”. He was trained as a neurologist between 1994 and 2000, also at Leiden University Medical Centre. He received additional training as a movement disorders specialist during fellowships at "The Parkinson's Institute", Sunneyvale, California (with Dr. J.W. Langston), and more recently at the Institute of Neurology, Queen Square, London (with Prof. N.P. Quinn and Prof. J.C. Rothwell). In 2002, he founded and became Medical Director of the Parkinson Centre Nijmegen (ParC), which was recognised from 2005 onwards as centre of excellence for Parkinson's disease. He is a board member of the Nijmegen Motor Unit (head: Prof. S. Geurts), a fully equipped gait and balance laboratory. In September 2008, he was appointed as Professor in Neurology, with movement disorders as special area of interest. He is currently President of the International Society for Gait and Postural Research, and is on the editorial board for several national and international journals, including the Movement Disorders journal. Since 2009, he is a member of the European Section Executive Committee of the Movement Disorder Society. In 2009, he also joined the board of ZonMw (The Netherlands Organisation for Health Research and Development). His current main interest is in health care innovation, aiming to develop and scientifically evaluate patient-centred collaborative care. Prof. Bloem has published over 250 publications, including more than 200 peer-reviewed papers.
Speaker: Glenda Halliday, PhD, BScHons
Talk Title: Nature and Spread of Parkinson's Disease
Session: Morning Plenary Session on Parkinson's Disease: How does it unravel?
Date: Thursday, September 30, 2010
Time: 09:10 - 11:10
We asked Professor Halliday why the topic of 'Nature and Spread of Parkinson's Disease' is important and she explained that it is necessary to understand the bases of the pathological progression of disease for effective treatment based therapies.
We then asked her to pinpoint what she feels is innovative and new in the field and why it's important to PD research overall. She identified the following points:
1) protein deposition does spread through the brain from one region to another - potential mechanisms include a prion-like process and/or cellular immune function immaturity;
2) there are different rates of progression for the selective cell loss versus protein accumulation - suggesting different effector mechanisms; and
3) the pathological progression is unlikely to be homogeneous for either cell death or protein accumulation processes, as previously suggested in the breakthrough pathological studies of Heiko Braak and colleagues (who defined progressive stages in Parkinson's disease in 2003) - evidence for different rates of pathological progression for different clinical phenotype/s
She explained that a review of the literature shows that the two major pathologies (accumulation of alpha-synuclein versus neuron loss) have different rates of progression in different clinical subtypes of Parkinson's disease.
We asked her how research in this area will help someone with Parkinson's and why a person living with this condition should care and she explained that for some of the clinical phenotypes of Parkinson's disease, knowledge of the slowly progressive pathology will be a comfort. However, the research will have more immediate benefit for drug companies trying to assess effective treatments for Parkinson's disease. Drugs relatively effective against one rather than both major pathologies may have been discarded if they were tested in large clinical samples without stratifying for clinical subtype. Re-evaluation of drug trial data against clinical subtype may identify effective drugs for certain subtypes of patients with Parkinson's disease.
About Professor Halliday
Glenda Halliday, PhD, BScHons, fills three roles as Professor of Neuroscience at University of New South Wales; Senior Principal Research Fellow at the National Health & Medical Research Council of Australia; and Senior Principal Research Fellow at Prince of Wales Medical Research Institute
About herself she says, "I am an Australian neuroscientist currently working on the pathogenesis of Parkinson's disease and other neurodegenerative disorders. I received my degrees at the University of New South Wales and postdoctoral training at the Centre for Neuroscience, Flinders University of South Australia prior to returning to Sydney as an Australian Research Council Queen Elizabeth II Fellow. I have been a research fellow of the National Health and Medical Research Council of Australia since then and am one of the senior scientists at the Prince of Wales Medical Research Institute (joined in 1993). I head the Ageing and Neurodegeneration Research Programme which investigates neurodegenerative disorders at the Prince of Wales Medical Research Institute, and have published over 250 research articles. I was president of the Australian Neuroscience Society from 2006-2007.
My research has highlighted broader pathological involvement in Parkinson's disease and in dementia associated with Lewy bodies. In particular, my PhD and subsequent postdoctoral work on the anatomy and pathology of dopaminergic systems and other brainstem monoaminergic systems in controls and patients with Parkinson's disease is highly cited, having revealed that more than the dopamine system was damaged in this disorder. My subsequent research has focussed on understanding how this occurs with the suggestion that humoral immunity is involved. My pathological work on dementia with Lewy bodies has been incorporated into highly cited research criteria for the diagnosis of this disorder, highlighting the association between Lewy body deposition and visual hallucinations rather than a loss of function. My current work is focussing on how proteins identified through genetic studies are involved in the disease process."