Speaker & Session Highlights

This page highlights WPC 2010 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 for patients in the meantime.

Speakers of the Week: Deborah Elkis-Abuhoff, Ph.D., ATR-BC, LCAT


We asked each highlighted speaker to tell us about the talk they will be giving and/or why their topic is important and to project where they think the science in this area will be going in the future We also asked them to explain why this topic is important to people living with Parkinson's.

Read about previously highlighted speakers, in the order they were introduced:
Patrik Brundin, MD, PhD
Roger Barker, MD, PhD
Joseph Jankovic, MD
Robert Iansek, B.Med.Sci., MB.BS, PhD., FRACP
Margarita Makoutonina , Senior Clinician, MDP , B. Health Sci. Occ.Th.
Lucille Leader, Dip ION MBANT NTCC
Beate Ritz, MD, PhD
C. Warren Olanow, MD
Patrick Aebischer, MD
Laura Marsh, MD
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: Deborah Elkis-Abuhoff, Ph.D., ATR-BC, LCAT
Asst. Prof in the Department of Counseling, Research, Special Education and Rehabilitation,
Hofstra University, Hempstead, New York, USA
Talk Title: Art Therapy and Parkinson's Disease
Session: Workshop 7
Date: Wednesday, September 29 , 2010 from16:30 – 17:30
* NOTE: Dr. Abuhoff will host two sessions on clay therapy in the Renewal Room. Interested delegates should sign up onsite to ensure a seat in her sessions.


We asked Dr. Abuhoff what is innovative and new in this particular field and why it's important to PD research overall. She explained that the nature of creative arts therapy is that it taps into the psychosocial aspect of Parkinson's disease, which is often neglected to the areas of science such as neurophysiology and neuropsychology. Until there is a cure, people living with Parkinson's disease need to find ways of increasing their quality of life. The engagement in Creative Arts Therapy has been found to be a strong approach serving as a means of support for those challenged by Parkinson's disease.

The theory is that Creative Arts Therapy in all it's forms, music, dance, art, etc. will significantly decrease psychosocial stressors to the point that Parkinson's disease is not seen as the end of a life, but rather a tool in which to continue living.

We asked her to explain why someone living with PD should be interested in this work and/or how she expects it will ultimately help someone living with PD. The engagement in Creative Arts Therapy is exciting, creative, and most of all fun. These are examples that are not within the typical Parkinson's diseased person's life. The manipulation of modeling clay led to research finding significant reduction in areas of compulsions, fears, and depression. It brings back some joy, some pleasure, something interesting, and it is potentially life enhancing.

Read about Dr. Abuhoff's relevant work in the article "Effects of Clay Manipulation on Somatic Dysfunction and Emotional Distress in Patients With Parkinson’s Disease" published in 2008 in Art Therapy: Journal of the American Art Therapy Association, 25(3) pp. 122-128 © AATA, Inc.


Learn about Dr. Elkis-Abuhoff
 Deborah Elkis–Abuhoff, Ph.D., ATR-BC, LCAT is assistant professor in the Department of Counseling, Research, Special Education and Rehabilitation, and teaches courses in the graduate Creative Arts Therapy program at Hofstra University, Hempstead, New York, USA. Dr. Elkis-Abuhoff holds both psychology and creative arts therapy licenses in New York State. Dr. Elkis-Abuhoff's research interests bring together the areas of behavioral medicine and creative arts therapy. Her recent research includes clay manipulation with those diagnosed with Parkinson's disease. She and her research team have published in both peer-reviewed journals, and have presented to a national and international audience.

 


Speaker: Professor Patrik Brundin, MD, PhD
Professor of Neuroscience at Lund University
Talk Title: Future Therapies 
Session: Fundamentals of PD Pre-congress Course
Date: Tuesday, September 28, 2010
Time: 15:00 – 15:25


We invited Professor Brundin to tell us about his talk on Future Therapies and to explain why this is an important area of research and why we should be excited about what is going on is this field. He explained that several future therapies for Parkinson's disease can be envisaged. Two of the most exciting are cell and gene therapy.

In cell therapy , the basic concept is to replace dead nerve cells by new ones. One can foresee that this is achieved either by transplantation to the brain or by activating stem cells in the patient's own body (e.g. by injecting growth factors) and having them differentiate into the right type of nerve cells.

Studies over the past 25 years have demonstrated that it is possible to transplant brain cells and achieve both symptomatic relief and long-term survival of the transplanted cells. Two problems have been that the results have varied greatly from patient to patient and that some have exhibited involuntary movements (dyskinesias) after transplantation surgery. The challenge is now to avoid dyskinesias developing and create a cell therapy that both reliably improves symptoms and is safe. The European Union started funding a large 5-year, multicenter trial with cell transplantation in Parkinson's disease in 2010. In this trial the transplanted cells will be obtained from aborted fetuses. In the more distant future, the idea is to use stem cells as starting material and make these cells differentiate into dopamine-producing nerve cells in the culture dish before injecting them into the brains of patients. This will require a deep understanding of the developmental biology of dopamine (the neurotransmitter that is lost in Parkinson's disease) nerve cells and techniques to apply this knowledge in stem cells. It will be very important to ensure that all the stem cells have stopped dividing in the cell cultures before surgery, and thereby avoid the risk of stem cell tumor growth in the brain.

The gene therapy strategy for Parkinson's disease follows two primary routes. For both approaches, clinical trials have been initiated. One is to genetically engineer viruses to produce growth factors (for example GDNF and Neurturin), and then inject the viruses into the affected brain regions of people with Parkinson's disease. The idea is that the viruses lead to the local production of growth factors in the brain and that these factors either protect the patients nerve cells from dying or promotes the regeneration and function of the cells that remain at the time of surgery. The second gene therapy concept is based on engineering viruses with genes that produce genes for the enzymes that can make the precursor for dopamine, i.e. L-Dopa. By injecting these genes into the brain the aim is to avoid the need for L-Dopa medication, and possibly avoid the development of L-dopa induced dyskinesias by providing a continuous and stable delivery of the molecule.

When asked what makes both cell and gene therapy exciting for people with Parkinson's disease, Professor Brundin said that they aim at improving brain function through a reparative approach. Ultimately they could lead to patients having few problems with movements and requiring little drug therapy. If these restorative therapies are applied early in the disease, it is possible to imagine that they can prevent development of significant symptoms.


Read about Professor Brundin and his colleagues' relevant work in the article “Emerging restorative treatments for Parkinson's disease” published in May 2008 in Progress in Neurobiology.


Learn about Professor Brundin
Patrik Brundin, MD, PhD is a Professor of Neuroscience at Lund University in Sweden. His field of expertise is neural transplantation, in particular in Parkinson's disease. He also focused on stem cells for brain repair, Huntington's disease pathogenesis, in particular transgenic mouse disease models and Parkinson's disease pathogenesis.

Professor Brundin is a renowned researcher in the field of Parkinson's disease and has published over three hundred papers on this and closely related topics. In 1988 he obtained his PhD thesis at Lund University, Sweden, on the topic of intracerebral transplantation in Parkinson's disease. He was part of the research team that first developed a clinical procedure for intracerebral transplantation in this disease. In 1992, he obtained an MD at the same University and in 1994 his license to practice clinical medicine. He presently holds a professorship in Neuroscience at Lund University, and leads a research group that is active in several areas of investigation related to experimental models of neurodegenerative diseases. In 1995-2000 he was president of the Network for European CNS Transplantation and Repair (NECTAR). In 2001, he was identified as one of the 0.5% most cited scientists in his area and he has received numerous awards for his work. He presently coordinates numerous national and international research programs and scientific projects that focus on neurological disorders of the basal ganglia. He has edited a book on restorative therapies in Parkinson's disease, is a member of the editorial board of several renowned journals and a consultant for biotechnological and pharmaceutical companies.



Speaker: Roger Barker, MD, PhD
University Reader in Clinical Neuroscience at the University of Cambridge
 Plenary title: Experimental Therapeutics: How to Treat PD in the Future
Talk title: Gene and Cell Based Therapies
Date: Friday, October 1 from 9:10 -10:45

 

 

 

We asked Dr. Barker to tell us what is innovative and new in the field of gene and cell based therapies and why it is important to Parkinson's research overall. He explained... There has been a long interest in trying to repair the brain in Parkinson's disease (PD) by replacing, or encouraging the growth of, the dopaminergic nerve cells that are lost as part of the core pathology in the condition. This has been undertaken in two major ways: (a) replacing the lost cells with transplants derived from the developing fetal human brain and (b) directly putting in growth factors for the dopamine cells into the PD brain. These approaches have met with mixed success, and the reasons for this are now being better defined which will lead to a new round of trials in which there is more stringent patient selection and better preparation of the restorative agent.

 

When asked to explain where he thinks research may go in the future in this field, he went on to explain that the major new developments that will happen in this area are likely to be:

  • The development of dopaminergic cell replacement therapies derived from stem cells sources;
  • The use of stem cells derived from the patient themselves to better understand disease. This will involve making stem cells (iPS cells) from the skin cells of patients to study disease processes in different types of PD which can then be used for drug screening and the development of new disease modifying approaches;
  • The use of better gene therapy delivery systems not only for growth factors enabling more robust regeneration within the degenerating dopamine systems of the brain, but also for delivering disease modifying therapies.


On answering the question about why patients should be interested and excited about this field of research, he wrote that the excitement in this field is in the development of therapies that actually repair the brain in PD such that cell losses can be reversed and/or slowed down. As such this approach has the potential to help some patients with PD, although at the moment none of these therapies are truly curative as they only target one area of the disease process, the dopamine cell loss, albeit an area that has been shown to mediate many of the features of PD. However as we get to better understand how to do repair this area of pathology more effectively, we will also start to develop therapies that have effects on other cell populations lost in PD, not just the dopaminergic nerve cells.

Learn more about Roger Barker, MD, PhD
Dr Roger A Barker is currently the University Reader in Clinical Neuroscience at the University of Cambridge and an Honorary Consultant in Neurology at Addenbrooke's Hospital in Cambridge . He qualified from Oxford University and St Thomas ' Hospital in London and undertook a PhD on cell therapies for Parkinson's disease in Cambridge . He subsequently has gone on to set up clinical and basic research programmes around two related basal ganglia disorders- Parkinson's and Huntington' disease. His primary aim is toe better define the extent of problems in these disorders, their basis and how they can best be treated including with stem cell therapies.

 

Speaker: Joseph Jankovic, MD
Professor of Neurology, Distinguished Chair in Movement Disorders, Director, Parkinson's Disease Center and Movement Disorders Clinic, Department of Neurology, Baylor College of Medicine, Houston, Texas
Chair of Session: Management of Orthostatic Hypotension in Parkinson's Disease (PD): Scientific Insights and Therapeutic Opportunities
Date: Tuesday, September 28, 2010
and
Speaker: Treatment of blepharospasm and cervical dystonia
Session title: Treatment of Hyperkinesias Associated with PD
Date: Wednesday, September 29 from 16:30-18:00


We asked Dr. Jankovic to tell us what is innovative and new in the field of hyperkinesia and botulinum toxin and why it's important to PD research overall: The use of botulinum toxin (BoNT) in the treatment of different clinical indications has been expanding over the last three decades since its initial introduction as a powerful therapeutic tool, making it the most versatile drug on the market. In addition to its use in the treatment of a variety of neurological and non-neurological disorders, BoNT has been used in the treatment of primary dystonias and dystonias associated with a variety of neurodegenerative disorders, including Parkinson's disease (PD). Besides blepharospasm, camptocormia, and cervical and limb dystonia, highlighted in this review, BoNT has been also used effectively in the treatment of other troublesome symptoms associated with PD, such as hand, jaw, tongue and lip tremor, lid apraxia, jaw clenching and tooth grinding (bruxism), painful rigidity, freezing of gait, drooling (sialorrhea), swalloing problems (dysphagia associated with achalasia), oily skin (seborrhea), excessive sweating (hyperhidrosis), frequent urination (overactive bladder and enlarges prostate), and constipation. Future studies should address which unique properties of the various BoNT preparations make them particularly suitable for the various indications. For example, while BoNT type A is used for most of the indications, BoNT type may be more appropriate for the treatment of sialorrhea. The use of various types and new formulations of BoNT in the treatment of symptoms associated with neurodegenerative disorders will be explored in future clinical trials. Finally, other medical and surgical treatments, including deep brain stimulation (DBS), play an important role in the management of the various motor and non-motor symptoms associated with PD.


We asked Dr. Jankovic 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 explained that it is increasingly recognized that PD is not merely a motor disorder, but non-motor symptoms such as cognitive and behavioral problems, sensory symptoms, and sleep and autonomic disorders also adversely impact on the quality of life of a patient with PD, particularly in advanced stages of the disease. Furthermore, patients with PD manifest not only paucity of movement, but also abnormal involuntary movements such as tremor, levodopa-induced dyskinesia, and various forms of dystonia, treated effectively with BoNT. In addition to BoNT, highlighted in the Hyperkinesia symposium, other non-dopaminergic drugs play a critical role in the treatment of the whole patient. For example, droxidopa, which acts on the noradrenerdgic system, has been found to effectively stabilize blood pressure in PD patients whose dysautonomia is complicated by orthostatic hypotension. This latter drug is highlighted in another session, chaired by Dr. Jankovic, “Management of Orthostatic Hypotension in PD”, Tuesday, 9/28/10.


We asked Dr. Jankovic to explain why someone living with PD should be interested in this work and/or how he expects additional research in this area will ultimately help someone living with PD.
People with PD are interested in being viewed by their physicians as not only patients who have dopamine deficiency, but individuals with a variety of concerns, often beyond the classic symptoms typically attributed to PD. Thus, physicians involved in the care of patients with PD must look at the whole person and try to address and manage all troublesome symptoms that may or may not be directly related to dopamine deficiency. We are physicians must use our experience and fund of knowledge to tailor the treatment to each individual patients. This requires persistence, innovation, discovery, creativity, and even serendipity observations.

Read some of Dr. Jankovic's publications on this topic

•  “Treatment of Hyperkinetic Movement Disorders” in Lancet Neurology 2009; 8:844-56.

•  “Disease Oriented Approach to Botulinum-toxin use” in Toxicon 54 (2009) 614-623.

•  “Camptocormia, head drop and other bent spine syndromes: heterogeneous etiology and pathogenesis of parkinsonian deformities”. Mov Disord 25 (2010);25:527-8.

 

Learn about Dr. Joseph Jankovic
After completing his chief residency in Neurology at the Neurological Institute, Columbia University , New York City, Dr. Jankovic joined the faculty of Baylor College of Medicine in 1977. He found the Parkinson's Disease Center and Movement Disorders Clinic, which has since been recognized as a " Center of Excellence " by the National Parkinson Foundation and the Huntington Disease Society of America. Dr. Jankovic is past president of the Movement Disorder Society and an Honorary Member of the American Neurological Association, Australian Association of Neurologists, and French Neurological Society. Selected in 2009 as a “Great Teacher” by the National Institute of Health, Dr. Jankovic is the recipient of many other honors including the 2007 American Academy of Neurology (AAN) Movement Disorders Research Award, sponsored by the Parkinson's Disease Foundation, the 2008 Guthrie Family Humanitarian Award, presented by the Huntington's Disease Society of America, the 2009 Lifetime Achievement Award from the national Tourette Syndrome Association, the 2010 Baylor College of Medicine Alumni Association Distinguished Faculty Award and the 2010 Fulbright & Jaworski Faculty Excellence Award for Teaching and Evaluation. Dr. Jankovic currently holds the endowed Baylor College of Medicine Distinguished Chair in Movement Disorders.

Dr. Jankovic has published over 800 original articles and chapters and has edited or co-edited 40 books and volumes Since 2004 Dr. Jankovic has been listed as Highly Cited Researcher (ISIHighlyCited.com). Dr. Jankovic is current or past member of numerous scientific and medical advisory boards of national foundations including the Dystonia Medical Research Foundation, International Tremor Foundation, Tourette Syndrome Association, and World Federation of Neurology Research Committee on Parkinson's Disease and Related Disorders. Dr. Jankovic also serves on the executive scientific advisory board of the Michael J. Fox Foundation for Parkinson's Research and on the National Parkinson Foundation Clinical and Scientific Advisory Board. He has served on editorial boards of Neurology, Movement Disorders, Journal of Neurology Neurosurgery and Psychiatry, Acta Neurologica Scandinavica, Journal of Neurological Sciences, Neurology Medlink, and other journals. Dr. Jankovic has mentored numerous fellows and other trainees many of whom have become leaders in the field of movement disorders. (www.jankovic.org)



Speaker: Robert Iansek, B.Med.Sci., MB.BS, PhD., FRACP
Professor of Geriatric Neurology at Monash University in Melbourne, Director of the Victorian Comprehensive Parkinson Program and Director of Clinical Research Centre for Movement Disorders & Gait at the Kingston Centre, Southern Health in Melbourne.
Talk title: Health Systems Coordination and Evaluation of Outcomes
Session: Comprehensive Care: The Role of the Nurse in the Management of PD
Date: Thursday, September 30 from 13:00 to 15:00

When explaining about innovation in the field of comprehensive care and why it's important to PD research overall Professor Iansek explains that the concept of provision of comprehensive care for people with Parkinson's and their family is not new and our program has been providing care of this nature for nearly 17 years in both the government as well as in private hospitals. This comprehensive nature of care includes medical management, rehabilitative strategies as well as supportive services provided on a continuous basis for people with Parkinson's and their family. The program has numerous contact points where this comprehensive service is delivered and these include inpatient, outpatient, outreach, telemedicine, and telephone support.

The process of coordination of care through these multiple contact points and ensuring that the standard of care is maintained by the staff involved at different contact points has been the main challenge in running such a broad program.

The issue of evaluation of outcomes is also quite complex when dealing with a multidisciplinary approach and the use of multiple contact points. The innovative component has been the ability to assess outcomes for People with Parkinson's and their families who have been referred to our service. We have over the last 3 years prospectively looked at the comprehensiveness of care delivered by our program as well as the costs of that care to determine whether it addresses the needs of People with Parkinson's and their families, as well as keeping the costs of that care to the bare minimum.


On talking about the future directions in this field of research Professor Iansek explained that research in service delivery is very much dependent on the capacity to assess the complexity of Parkinson's disease, the ability to monitor its progression over time and the ability to measure effectiveness of mitigating against this progression and the cumulative effects of problems that occur with chronic illness and age. We have recently received funding from the National Parkinson's Foundation to look at service delivery models prospectively over a 3-5 year period, and we are in the process of establishing that comparison currently. I believe that the comparison of service delivery models is of extreme importance and that the aspects that are examined relate to the capacity of the model to deal with the complexity of Parkinson's disease, as well as the costs involved. We need to ascertain which service delivery model is most appropriate for People with Parkinson, depending on their particular aspects in regard to geographical location, service availability and expertise of service delivery staff. I believe that in the future this will be defined, and the funding capacity to deal with these issues will be better known. Hopefully then more comprehensive care will be readily available for People with Parkinson worldwide.


We asked Professor Iansek why this research should interest people with Parkinson and he replied people living with Parkinson's would be interested in this approach because it deals directly with their own care needs and addresses all their care needs as well as providing continuity of care throughout the life of the individual. This is exactly what has been enunciated in the Parkinson's charter since its inception in 1997


Read about Professor Iansek's and Ms. Makoutonina's recent publications:
Morris M.E, Iansek R., Kirkwood B., “A Randomized Controlled Trial of Movement Strategies Compared with Exercise for People with Parkinson's disease” Movement Disorders Vol.24 (1) 2009 pp 64-71

Morris M.E., Watts J.J., Iansek R., Jolley D., Campbell D., Murphy A.T., Martin C.L, "Quantifying the profile and progression of impairments, activity, participation, and quality of life in people with Parkinson disease: protocol for a prospective cohort study." BMC Geriatrics 2009, 9:2 doi: 10.1186/1471-2318-9-2

Makoutonina M, Iansek R., Simpson P, "Optimising care of residents with Parkinsonism in supervised facilities." in Parkinsonism & Related Disorders 2010


Learn about Professor Robert Iansek
Professor Iansek is a Professor of Geriatric Neurology at Monash University in Melbourne, and Director of the Victorian Comprehensive Parkinson Program (VCPP) as well as Director of Clinical Research Centre for Movement Disorders & Gait at the Kingston Centre, Southern Health in Melbourne.

He is a Neurologist by training and has over 25 years neurophysiological research experience, having published over 150 articles, books, and videos. His main research interests' concern basal ganglia function and malfunction in Parkinson's disease, cortical gait control mechanisms and rehabilitation in Parkinson's disease.

Professor Iansek was instrumental in the development and use of multi disciplinary rehabilitation for people with Parkinson's disease and its implementation in both the public and private health systems in Australia.

 



Speaker: Margarita Makoutonina , Senior Clinician, MDP , B. Health Sci. Occ.Th.
Talk Title: Symptom Management to Prevent Onset of Disability
Session: Care Delivery from a Family Perspective
Date: Thursday, September 30 from 15:30 - 17:00


When asked what is innovative and new in the field of symptom management and why it's important to PD research overall Ms. Makoutonina explained that despite the benefits of medical and surgical interventions for people with Parkinson's disease (PwP), patients still develop progressive disability in both the motor and non-motor domains.

Pharmacological management is the core of medical practice, however there is growing evidence of pathological involvement outside the basal ganglia which contributes to a number of additional symptoms over time. These non motor symptoms concern mood, cognition, dementia, blood pressure, bladder and bowel function, sleep, and neurophychiatric complications to medication. The non motor symptoms are generally not responsive to dopamine replacement therapy. Due to the progressive nature of the disease, the symptomatic response to treatment also wanes over time. These progressive and additive symptoms puts stress on the care-giver and family, leading to family disruption, deterioration of quality of life and loss of independence.

Inpatient rehabilitation (Iansek et. al.1995), medical management and provision of supportive services have been extensively used by our Movement Disorder Program ( MDP ) for longer than decade and quite unique on an international basis. It provides the comprehensive approach and continuity of the care/therapy provision. It centres on education for the person with PD and their care-giver, intensive assessment, evidence based interventions, movement rehabilitation and drug manipulation, under intense monitoring, to tailor medication and rehabilitation to each individual's needs.

The Occupational Therapist plays a vital role within MDP . The OT conducts the comprehensive assessments of the patient with PD at different times to reflect these changes in functional ability during ON and OFF phenomenon. During assessment key problem areas are indentified and specific follow-up interventions are planned to manage those symptoms, to support the patient and to help them maintain their usual level of self-care, work and leisure activities and therefore to prevent disability.

In addition, there is increasing evidence that implementation of Parkinson's disease specific assessments by the OT assists in the design of targeted rehabilitation and provision of the best practice in occupational therapy for PwP. This rehabilitation provides the most effective and comprehensive care for PwP and consequently delays the onset of disability.


We asked Ms. Makoutonina 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 she explained that it is important to recognise that the Occupational Therapist does not work in isolation, but as part of the Movement Disorders Program team. All members of the team share the theoretical knowledge, as the foundation of the comprehensive care model. This model proves to be the cost effective and efficient as it provides specialist knowledge in one facility.

The Victorian Comprehensive Parkinson Program (VCPP), under the direction of Professor Robert Iansek, is currently participating in a comparison of service delivery models, sponsored by the NPF. This comparison will be a prospective study performed over 3 – 5 years and it is hoped it will highlight the most cost effective model, which also provides the comprehensive care required by all PwP.


Ms. Makoutonina explained why someone living with PD should be interested in this work and how she expects that it will ultimately help someone living with PD because treatment of PwPs is symptomatic and typically it commences when problems impede on activities of daily living, work commitments or enjoyment of life. The implementation of the comprehensive care model she is working on with Professor Iansek has the capacity to delay the disability caused by PD, improve quality of life and maintain independence. It is able to do so for the following reasons and these reasons are precisely what PwP require and need.

•  It provides the research based rehabilitation that is designed specifically for PwP.
•  It combined medical management and rehabilitation and addresses all motor and non motor symptoms
•  It provides comprehensive and continuous care.
•  It is proactive and preventative, rather than reactive to care needs.
•  It empowers the patients and the care givers through an extensive education program.
•  Most importantly, it complies with the Parkinson's Charter.



Learn more about Margarita Makoutonina
Margarita Makoutonina is the Senior Clinician in the Victorian Comprehensive Parkinson Program (VCPP), National Centre of Excellence, Melbourne, Australia. Margarita is an Occupational Therapist by training, has over 12 years neuro physiological research experience, having been co-author of several posters and research papers. Ms Makoutonina has been lecturer at the RMIT University and Mayfield Education Institute for nine years.

Ms. Makoutonina holds a Bachelor of Applied Science in Occupational Therapy, a Master's Degree in Education with Honours, a Bachelor of Education with Honours, and a Certificate IV in Assessment and Workplace Training. She is a member of the Health Professionals Working Group of the Movement Disorders Society and is actively involved in the development of the MDS website section for Health Professionals.

Ms. Makoutonina has used her Senior Clinician/Occupational Therapist, research and lecturer knowledge and experience to assist with the development and utilization of a specific rehabilitation program for people with Parkinson's.

Ms Makoutonina attended and presented her research papers at the: Parkinson's Congress of Neurologists (Italy, 2009), Movement Disorders Society Congress (Paris, 2009), 12 th International Congress of PD and MDP (USA, 2008), Cabrini Institute Research Conference (Melbourne, 2008), Centre of Clinical Excellence in Clinical Gait Analysis and Gait Rehabilitation (Melbourne, 2008), Asian Pacific Conference Singapore, (Singapore, 2006), First World Parkinson Congress (USA, 2006), Research papers at International Parkinson's Conferences (Melbourne, 2005; New Zealand, 2002)

She has conducted the following specialist training seminars: Multidisciplinary team (Italy, 2009), Occupational Therapy Association Australia, Parkinson's Disease Practical Management for General Practitioners and Health Professionals, Australia Victoria (2009, 2004-2008), Residential Care Facilities (2006-2008) locally and interstate



Speaker: Lucille Leader, Dip ION MBANT NTCC
Dip ION Graduate of the Institute for Optimum Nutrition (ION)
MBANT Member of the British Association of Applied Nutrition and Nutritional Therapy
NTCC Nutritional Therapy Council Certificate
Talk Title:  Nutrition and Dopamine Metabolism in Parkinson's Disease
Session: Nutrition and PD
Date: Friday October 1, 2010 from 14:45-15:45


On what is innovative and new in the field of nutrition and why it's important to Parkinson's disease research overall, Lucille Leader explained that metabolic compromises are manifested in Parkinson's disease and that contemporary biochemical evidence, which forms the basis for Nutritional Therapy, points to the implication of nutritional aspects in these metabolic cellular functions.

Establishing the biochemical individuality at cellular level of each person with Parkinson's disease can enhance therapeutic management and potentially be of invaluable assistance in personalized, general cellular support within the constraints of a degenerative illness.

Some cellular problems manifested include:
•  inadequacies in the production of the neurotransmitter dopamine (metabolised from dietary protein), dependent at metabolic outset on digestive enzymes with nutritional co-enzymes).
•  inadequate prostaglandin protection from inflammatory responses (prostaglandins are metabolised from dietary essential fatty acids with their enzymes and nutritional coenzymes).
•  the formation of excess free radicals from oxidative stress are quenched by individual anti-oxidants (which include specific vitamins and minerals) and anti-oxidant enzymes (dependent on nutritional coenzymes).
•  compromised mitochondrial function for cell energy production (dependent upon glucose and specific nutrients).
•  disturbed catecholamine response to stress resulting in inhibition of the rate-limiting enzyme tyrosine hydroxylase (with its nutritional co-enzymes).

Therefore, it is important for clinicians to assess, at cellular level, how to optimally support the metabolic and biochemical processes implicated in endogenous dopamine production, as well as those other cellular needs of the Parkinson's patient.  It is essential that clinicians identify the cellular biochemical aberrations (excesses and deficiencies) by innovative contemporary laboratory tests (nutritional, other specialised biochemistry and routine medical). This enables the therapeutic spectrum to be broadened so that concomitant with dopaminergic pharmaceuticals, the appropriate adjuvant care based on “individualized” patient protocols which are supportive of metabolism, can be offered to patients.

Nutritional Therapy utilizes such biochemically-based analyses as part of its specialist approach. Patients, both “on” and “not yet” on dopaminergic drug therapy, may benefit from nutritional support based on their individual biochemistry. This is an innovative approach as to date monotherapy (dopaminergic drugs) has been the most popular form of management in Parkinson's disease. Although this is helpful in the control of Parkinson's disease symptoms, it has not taken into account the biochemical individuality of patients which could be contributory to their compromised cellular functions.


Also important in the field of Nutritional Therapy is the monitoring of Drug-Nutrient interactions. These special “trials” for the individual patient are aimed at reducing potential drug-induced side effects such as dyskinesia by ascertaining the most appropriate dose and timing of drugs for optimum efficacy. They are innovative and very helpful to patients, caregivers, neurologists, general practitioners, nutritional therapists and dieticians and will be presented at Ms. Leader's workshop.

Going one step further, we asked Ms. Leader where research in this field may go in the future and what we could expect to see from people studying this topic to which she responded: The gold standard, therapeutic approach to the management of Parkinson's disease has been the administration of pharmaceuticals: L-dopa, which the brain metabolizes to dopamine, as well as other dopaminergic drugs.

What has been relatively neglected has been interest into which biochemical factors could possibly be compromising the metabolic pathways of dietary protein ingestion to the endogenous production of dopamine in the brain, dopamine's further metabolism to noradrenaline and adrenaline as well as other associated biochemical disturbances.

My analytical work since 1996 has pointed the way to the analysis of the biochemical needs of metabolism in order for appropriate dietary protein to proceed metabolically. I have noted compromise in the production of digestive and other enzymes, which are dependent on nutritional co-enzymes. Enzymes initiate the breakdown of protein for its metabolism through to dopamine, digest carbohydrates and fats which are implicated in the mitochondrial cellular energy cycle and also assist in the production of anti-inflammatory prostaglandins.

Other tests I have authorized have also demonstrated anti-oxidant deficiencies and other nutritionally-based aspects of cellular metabolism. As such, the way forward for research could be for every clinician to establish the “biochemical individuality” and cellular needs of each individual with Parkinson's disease. This would ensure that both dopamine metabolism from dietary protein, as well as other vital, associated cellular requirements, can be either up- or down-regulated by appropriate nutritional supplementation, dietary manipulation and enzymes.

In this way, extensive data about cellular deficiencies or excesses pertinent to Parkinson's disease could be collected for analysis by an appointed national or international data bank. The knowledge gleaned from this could provide information about necessary cellular support as adjuvant care alongside dopaminergic drug administration.


Lastly, we asked Ms. Leader to explain why someone living with PD should be interested in this work and/or how it will ultimately help someone living with PD to which she replied contemporary Nutritional Therapy offers people living with Parkinson's disease the opportunity to improve their functional health by using a two-fold approach encompassing both nutritional and pharmaceutical drug therapy. Clinical experience demonstrates that this may be helpful in reducing symptoms as well as promoting wellbeing and functional health, whether people have commenced drug therapy or not.

It is important for people with Parkinson's to realize that not only are they deficient in the neurotransmitter dopamine which controls their movement and is implicated in mood and stress control (dopamine metabolizes to adrenalin which the body releases in response to stress), but that there are additional cellular deficiencies and excesses which contribute to the inability of the body to metabolize an adequate supply of dopamine, as well as other cellular necessities which energize and protect cells.

Nutritional intervention can modulate many functional health aspects in Parkinson's, including the degree of chronic inflammation as well as up-regulating the production of cellular energy. Antioxidant enzymes can be supported in their role of quenching free radical cascade and may therefore contribute to neuro-protection from excess oxidative stress.

During the Workshop “Nutrition and Dopamine Metabolism in Parkinson's Disease” on October 1, 2010, I shall present the following subjects which will demonstrate how Nutritional Therapy can help people living with PD to improve their general functional health. These subjects are also of great importance to caregivers, enabling them, as well as people living with Parkinson's, to make informed choices about supportive therapy, with more confidence. Nutritional Therapy within the Functional Medicine context, will demonstrate a more personalized and effective “integrated” medical approach for people with PD.

Workshop Subjects include:

•  Knowing when to take dopaminergic drugs in relation to different food groups for optimum effect and reduction of potential drug side effects

  • How to monitor the correct dosage and optimum timing of taking dopaminergic drugs for optimum absorption and reduced side effects
  • Reducing dyskinesia
  • Optimising bowel function without harsh laxatives
  • Understanding the Gut-Brain Axis
  • Laboratory tests to establish biochemical individuality on which to base therapy (nutritional and drug)
  • Nutritional supplements based on biochemical test results
  • Improving energy
  • Knowing which foods are helpful and which are contraindicated
  • Improving sexuality and sleep
  • How to prepare for surgery and optimize recovery
  • Nutritional factors in stress management and stress management techniques
  • Understanding how the body makes its dopamine, adrenaline, energy, sleep and hormones and protects itself against oxidative stress and excess free radicals
  • Weight control
  • Swallowing problems (dysphagia), Speech problems and solutions
  • Specialised feeding (tube/duodenal/intravenous)


Read about Ms. Leader's most recent published work
Amongst other publications including the EPNN and EPDA journals, Lucille is the author and co-author of five successful books on Parkinson's Disease and an innovative publication about medical collaboration for Nutritional Therapists. She works in collaboration with her husband Dr Geoffrey Leader MB ChB FRCA who is an early pioneer in the concept of multidisciplinary management in Parkinson's Disease. He is the Medical Director of their multidisciplinary Parkinson's Disease Management Clinic at The Highgate Hospital, London UK.


Recent book publications: Parkinson's Disease Reducing Symptoms with Nutrition and Drugs, Parkinson's Disease Dopamine Metabolism Applied Biochemistry and Nutrition, Parkinson's Disease The Way Forward!, and Medical Collaboration for Nutritional Therapists.


Learn more about Lucille Leader
Ms. Leader is a Member of the British Association of Applied Nutrition and Nutritional Therapy (MBANT), holds a Nutritional Therapy Council Certificate (NTCC), is a DipION Graduate of the Institute for Optimum Nutrition (ION) and a Council Member, Food and Health Forum, Royal Society of Medicine, UK.

Ms. Leader has lectured in Europe for the European Parkinson's Disease Association (EPDA) presenting Specialized Biochemically-based Nutritional Management in Parkinson's Disease, in Vienna at the First Congress for Sexuality and Nutrition in Parkinson's Disease, in South Africa for the Johannesburg Parkinson's Disease Society, and at UK Parkinson's Disease Support Groups. She was invited by The BBC in the UK and SABC in South Africa to broadcast on the subject of specialised nutritional management in Parkison's Disease.

She has lectured in the USA for the Parkinson's Resource Organization, from whom she received a "Quality of Life in Parkinson's" Award in 2004. In the UK she has received the CAM "Highly Commended Outstanding Practice Certificate Award" in 2008 and the CAM “Outstanding Practice Award” in 2010.

She is particularly interested in the biochemical and pathophysiological aspects of Parkinson's Disease and in the Functional Medicine approach to the application of biochemically-based, individualised nutritional recommendations as adjuvant care in the multi-disciplinary management of Parkinson's Disease. Her work includes (amongst other aspects) modulation of inflammation, the citric acid cycle, intestinal function and analysis of status (permeability, enzymes, gut flora, microbiology, parasites), adrenal function, addressing cellular deficiencies/excesses, weight control, specialised feeding (tube, IV), monitoring of drug-nutrient interactions, diet and neuro-protection.


Speaker: Beate Ritz, MD, Ph.D.
Vice Chair of the Department of Epidemiology at the UCLA School of Public Health
Talk: Gene and Environmental Interactions in PD 
Session title: Environment, Epidemiology and PD
Date: Wednesday, September 29 from 14:30 - 16:00

We asked Professor Ritz to tell us what is innovative and new in the field of genetics and environmental research and why it's important to PD research overall. She explained that the vast majority of human PD cases are unlikely to result from a single cause or event. Rather, it is likely that a set of genetic variations cause certain individuals to be more vulnerable to specific environmental exposures even at low doses. In fact, there are likely multiple “sets” of genetic variations that produce susceptibilities to a number of toxins. Therefore, it is paramount to assess genetic susceptibilities in populations for whom we have an array of well-measured environmental exposures available, such as smoking or pesticides, since genetic risk factors may not be identifiable unless environmental toxins unmask their contributions to PD risk. We have recently demonstrated that individuals with specific genetic variations were at increased risk of developing Parkinson's disease when exposed to specific pesticides known or hypothesized to be transported or metabolized by the protein products of those genes. Gene-environment interaction studies such as these not only provide insight into possible etiologic mechanisms of PD but also have the potential to illuminate preventive, therapeutic, and public health and policy issues previously unrecognized.

When asked to theorize where research in genetics may go in the future and what we could expect to see from people studying this topic she went on to explain that studying genetics alone or environment alone is like looking through only one eye — you have limited depth perception. What you observe is simpler because there are only two dimensions, but it is not an accurate representation of the world. Future work in this area requires increased collaboration across fields – by combining the expertise of geneticists with those of epidemiologists, neurologists, toxicologists, exposure assessment specialists, and others we can tease apart the complexity that is PD etiology.

We asked Professor Ritz to explain why someone living with PD should be interested in genetic and environmental reactions and how she expects that research in this area will ultimately help someone living with PD. She explained that improving our understanding of environmental toxins, genetic variation, and their combined impact on idiopathic PD will inform public policy on pesticide regulation, improve prevention efforts aimed at eliminating detrimental environmental exposures, and advance therapeutic developments through improved knowledge about agents that impact the viability of neurons in humans and through the identification of subgroups of susceptible subjects.


Read some of Professor Ritz's and her colleagues' recent articles on Dopamine Transporter Genetic Variants and Pesticides in Parkinson’s Disease published in Environmental Health Perspectives, Volume 117, Number 6 in June 2009 and Paraoxonase 1, Agricultural Organophosphate Exposure, and Parkinson Disease published in Epidemiology, Volume 21, Number 1 in January 2010.

Learn more about Professor Beate Ritz, MD, Ph.D.
Professor Ritz is the Vice Chair of the Department of Epidemiology at the UCLA School of Public Health with appointments in Environmental Health Sciences and Neurology at UCLA. She is the co-director of the NIEHS-funded UCLA Center for Gene-Environment Studies of Parkinson's disease and also participates in the NINDS funded UCLA UDALL center to study non-motor manifestations and progression in Parkinson's disease. Her primary research interests are the effects of occupational and environmental toxins including pesticides. She investigates the long-term effects of pesticide exposures in combination with genetic susceptibility on Parkinson's disease in Central California. She also is the principle investigator of the Parkinson's disease Registry Linkage and Case Control Study (PASIDA) in Denmark studying gene-environment interactions and occupational and pharmaceutical risk and protective factors in more than 17,000 PD patients. Finally, she is conducting a feasibility study to establish a Parkinson's disease registry in California.





Speaker: C. Warren Olanow, MD
Henry P. and Georgette Goldschmidt Professor and Chairman Emeritus of the Department of Neurology, and Professor in the Department of Neuroscience at the Mount Sinai School of Medicine in New York City
Talk: Neuroprotection
Session title: Morning Plenary on “Experimental Therapeutics: How to Treat PD in the Future”
Date: Friday, October 1 from 9:10–10:45


We asked Dr. Olanow to tell us what is innovative and new in the field of neuroprotection and why it's important to PD research overall. He explained that a disease modifying therapy that slows disease progression is one of the major needs in the management of Parkinson's disease. While there are many candidate neuroprotective agents in the laboratory, and some clinical trials have been positive, it has not been possible to delineate and differentiate a disease-modifying effect from a symptomatic or pharmacologic effect of the study drug. New study designs offer a way to overcome this problem. The ability to determine that a drug has a disease-modifying effect in a clinical trial will greatly increase the likelihood that we will be able to develop a neuroprotective therapy in the near future.

We then asked him 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 explained that advances in understanding the cause of PD will lead to the identification of new targets and new candidate neuroprotective agents. These will be tested in better animal models that more closely reflect the cause of PD and then will be evaluated in clinical trials that can delineate a neuroprotective effect of the drug. Finally, long term studies will be used to determine the effect of the agent on the long term course of the disease. It is likely we will see advances in each of these areas in forthcoming years.

Lastly, Dr. Olanow explained why someone living with PD should be interested in this work and/or how it may ultimately help someone living with PD.
Currently, PD is a progressive disease that ultimately leads to disability despite the best of available medical and surgical therapies. A treatment that slows disease progression may prevent the development of disability. Eventually, the ability to identify patients before the onset of the classic motor features of the disease may permit the introduction of a treatment at a very early stage and the prevention of clinical features of the disease as we currently know it. Nothing could be of greater importance to patients with PD than the development of an effective treatment that slows or even stops disease progression.


Read one of Dr. Olanow's and his colleagues' most recent articles A Double-Blind Delayed-Start Trial of Rasagiline in Parkinson's Disease published in the New England Journal of Medicine in 2009.


Learn about C. Warren Olanow, MD, FRCPC
C. Warren Olanow, M.D., FRCPC is the Henry P. and Georgette Goldschmidt Professor and Chairman Emeritus of the Department of Neurology, and Professor in the Department of Neuroscience at the Mount Sinai School of Medicine in New York City. He received his medical degree from the University of Toronto, performed his neurology training at the New York Neurological Institute at Columbia Presbyterian Medical Center, and did post-graduate studies in neuroanatomy at Columbia University. He served on the faculties of McGill University, Duke University, and the University of South Florida prior to assuming his present position. He is Past President of the Movement Disorder Society, Past Treasurer of the American Neurological Association, and Past President of the International Society of Motor Disturbances. He has been named an Honorary Professor at the University of London (Royal Free Hospital) and an Honorary Member of the French Neurological Society. He was appointed to the Board of Directors of the National Space Biomedical Research Institute (NASA) and received the Presidential Award from the Movement Disorder Society. He has served on numerous editorial and scientific advisory boards and has recently been named as Editor in Chief of the journal Movement Disorders.

His research is directed toward defining a neuroprotective therapy for Parkinson's disease. Laboratory efforts focus on understanding the cause of the disease, and specifically the role of proteins in the etiopathogenesis of the disorder. Recent studies test the hypothesis that Parkinson's disease is a prion disorder. Clinically, his interests are in experimental therapeutics and he has run major trials in transplantation, gene therapy, and novel approaches to defining disease modifying therapies. Dr. Olanow has authored more than 300 publications primarily related to Parkinson's disease and neurodegeneration and was ranked #1 in the United States in research citations for Parkinson's disease during the past decade. He has lectured on Parkinson's disease and related disorders at Universities and Conferences throughout the world.

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Speaker: Patrick Aebischer, MD
Talk: Effective Delivery of the Neuroprotectant to the Brain*
Session Title: Neuroprotection
Date: Friday, October 1, 2010 from 11:15 - 12:45

*Professor Aebischer is giving more than one talk. This highlight is only for his talk on neuroprotection.

On what is innovative and new in this particular field and why it is important to PD research overall? Available transgenic mouse models for PD are limited by the absence of specific neurodegeneration in the nigral dopaminergic system and associated motor behaviors. Our lab has been extensively working on the development and characterization of an acute genetic model for PD based on the over-expression of pathogenic forms of alpha-synuclein in the rat substantia nigra using adeno-associated viral vectors. Animals develop mild lesions of the nigrostriatal system, with consistent impairments in motor behavior due both to the loss of nigrostriatal innervation and to the reduction of dopamine release. We are currently in the process of developing similar virus-based model systems for LRRK2-induced pathology. We believe that the development of fully characterized genetic models of nigral neurodegeneration in mammalian species will help define early biomarkers of the pathology and greatly improve the validation of neuroprotective treatments for PD.

Why should someone living with PD should be interested in this work and/or how do you expect that it will ultimately help someone living with PD?
The treatment of PD is severely hampered by the lack of means to halt the progression of this devastating disorder. The efficacy of treatments correcting motor symptoms declines with the loss of nigrostriatal neuronal connections. In addition, degeneration occurs in other parts of the brain and the resulting non-motor symptoms deteriorate the life quality of the patients. Therefore, it appears essential to devise therapeutic strategies targeting the cause of the disease. Genetic studies and recent discoveries in basic research point to the pathogenic accumulation of alpha-synuclein as a major contributor in PD. We are convinced that reliable genetic animal models based on alpha-synuclein accumulation will constitute a powerful system to establish more effective strategies to provide the needed neuroprotection. These efforts may ultimately produce a new generation of treatments to durably improve affected brain functions.

Learn more about Professor Patrick Aebischer, MD
 Patrick Aebischer was trained as an MD (1980) and a Neuroscientist (1983) at the University of Geneva and Fribourg in Switzerland. From 1984 to 1992, he worked at Brown University in Providence (Rhode Island, USA), as an Assistant and then Associate Professor of Medical Sciences. In the fall of 1992, he returned to Switzerland as a Professor and Director of the Surgical Research Division and Gene Therapy Center at the Centre Hospitalier Universitaire Vaudois (CHUV) in Lausanne. In 1999, Patrick Aebischer was nominated President of the Swiss Federal Institute of Technology in Lausanne (EPFL) by the Swiss Federal Council. He took office on March 17th, 2000. His current research focuses on the development of cell and gene transfer approaches for the treatment of neurodegenerative diseases.

 

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: Depression and Cognitive Dysfunction in PD: What is the Relationship?
Session title: PD and Cognition
Date: Thursday, September 30, 2010 from 13:30 to 15:00


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 more 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.

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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: DAT and Spect Imaging
Session title: Early Diagnosis and PD (Modalities to Monitor Disease Progression)
Date: Wednesday, September 29 from 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 more 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: Pesticides and PD
Session title: Environment, Epidemiology and PD
Date: Wednesday, September 29 from 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 from 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.

 


Glenda Halliday, PhD, BScHons

Speaker: Glenda Halliday, PhD, BScHons
Professor of Neuroscience at University of New South Wales
Talk: Nature and Spread of Parkinson's Disease
Session title: Morning Plenary Session on Parkinson's Disease: How does it unravel?
Date: Thursday, September 30, 2010 from 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.

Learn more about Professor Glenda Halliday, PhD, BScHons
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."

 

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