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Symposium 2007

Symposium 2007 - Agendas and Abstracts



Agenda & Abstracts
Friday, March 16, 2007
Babcock Auditorium 9:30 am – 5:00 pm

9:30 am – 9:45 am     Complimentary coffee and muffins
Babcock Auditorium foyer
9:50 am– 10:00 am    

Introduction and Welcome

Morning Session    


10:00 am - 11:00 am    

Functional MRI Studies of Typical Reading, Hyperlexia and Dyslexia

Guinevere Eden, DPhil
Associate Professor of Pediatrics
Georgetown University Medical Center

Moderator: Frank B. Wood, Ph.D., Dept. Neurology

Abstract: Developmental dyslexia is a common developmental disorder (observed in 5-10% of the population) in which individuals fail to acquire normal reading skills. Developmental dyslexia is thought to results form neural injury before birth resulting in changes in neuronal migration and abnormalities in the visual and auditory pathways. Dr. Eden's research is focused on the pathophysiology of developmental dyslexia utilizing post-mortem studies and, more recently, in-vivo observations by means of magnetic resonance imaging (MRI), functional MRI (fMRI) and positron emission tomography (PET). The results indicate that dyslexia is accompanied by fundamental changes in the anatomy and physiology of the brain, which can be attributed to an anomalous brain development.

11:00 am - 12:00 pm

Apoptosis in the Cortical Neuropathology of Schizophrenia

L. Fredrik Jarskog, MD
Associate Professor of Psychiatry
University of North Carolina at Chapel Hill

Moderator: Christopher P. Turner, PhD
Department of Neurobiology and Anatomy

Abstract: Schizophrenia is widely thought to be a neurodevelopmental disorder that is characterized by altered synaptic connectivity. However, the disorder is also recognized for progressive clinical and structural brain changes that are not readily explained in a neurodevelopmental framework alone. Apoptosis is a mechanism that could contribute to subtle neuroprogressive pathology without producing classic neurodegeneration. Somewhat paradoxically, accumulating evidence suggests that apoptotic activity may actually be downregulated in postmortem cortical tissue in schizophrenia. Furthermore, antipsychotics produce complex effects on apoptotic regulation in the central nervous system, activating both pro- and anti-apoptotic signaling pathways. Evidence of altered apoptotic regulation in schizophrenia in postmortem brain tissue and preclinical animal models from our lab and others will be reviewed and placed in context of current etiopathogenic hypotheses of schizophrenia.

12:00 pm- 1:30 pm

Lunch (pre-registration required)
Commons Rooms 1-3

1:30 pm - 2:30 pmProgress and Prospects in Motoneuron Disease

Jeffrey D. Rothstein, MD, PhD
Professor of Neurology and Neuroscience
Johns Hopkins University School of Medicine

Moderator: Carol Milligan, PhD
Department of Neurobiology and Anatomy

Abstract: ALS is a progressive, invariably fatal neuromuscular disease, characterized by wasting and weakness of muscles.  The clinical phenotype is the result of degeneration of both upper and lower motor neurons, along with dysfunction glial elements such as astrocytes and microglia. The disease can initiate clinically with either upper or lower motor neurons. It is largely sporadic disease, but approximately 5% is inherited.  Multiple genes have been identified in the familial form- including mutations of superoxide dismutase, senataxin, p150, and ALSin.  Animal models (mouse fly, fish) for most of these mutation have been generated- and most, although not all, recapitulate the human disease to some extent. Over the last 10 years these models, predominately the mutant SOD1 mouse, have been used to identify therapeutic candidates.  Riluzole, the only effective drug in humans, is marginally effective in the mouse.  Since the FDA approval of riluzole in 1995, more than 100 drug candidates have been examined in the G93A SOD1 mouse. Several drug candidates- including IGF1 and talampanel, have had some of borderline efficacy in phase 2 or 3 clinical trials, and are efficacious in the ALS mouse. The vast majority of drugs studied to date in the mouse model, unfortunately, are not efficacious in humans.  We will examine various therapeutic pathways that have been examined in human and mouse models and explore new approaches to ALS therapeutics including- potent anti-excitotoxic, inflammatory, protein aggregation, as well as mutation specific gene inactivation approaches. In addition, the use of protein biomarker and surrogate markers (e.g. PET ligands) to improve the chances of capturing effective therapeutics in ALS subpopulations will be discussed. The use of phenotypic screening assays for small molecules alone and in combination will be discussed.  Stem cells as drug delivery and therapeutic replacement strategies will be reviewed and new approaches to motor neuron and astroglial engraftment will be presented. 

Support: NIH, Robert Packard Center for ALS Research, MDA, ALSA.

2:30 pm - 3:30 pmAlzheimer’s Disease: From Pathology and Pathogenesis to Future Therapeutics

Juan C. Troncoso, MD
Associate Professor, Departments of Pathology and Neurology,
Alzheimer’s Disease Research Center
Johns Hopkins University School of Medicine

Moderator: Michelle M. Nicolle, PhD
Department of Physiology and Pharmacology

Abstract: On this 100 year anniversary of the report of Alzheimer's disease (AD), it is fitting to make a retrospective voyage through its fifty years of solitude and almost fifty years of hard work and breakthroughs, that augur the future prevention and treatment of this disease. In this review, we will succinctly cover the clinical features of AD, with emphasis on the concepts of mild cognitive impairment and asymptomatic AD; the major pathological features of the disorder, i.e. plaques, tangles, and loss of neurons and synapses, from the perspective of a longitudinal study of aging; and the pathogenesis of the disease. Then, following a brief review of the genetics of the disease, i.e. mutations in the APP and presenilin genes and ApoE polymorphisms, we will examine some of the transgenic animal models that have been helpful to understand the pathogenesis of AD and to design and test therapies. Finally, we will discuss what is new in the field of early detection of AD, i.e. imaging of brain Aβ amyloid, and the emerging mechanism-based therapeutics options for AD, including secretase inhibitors, amyloid “busters”, anti-inflammatory, and immunotherapy.

3:30 pm - 3:50 pmCoffee break
3:50 pm - 4:50 pmCombining Stem Cell and Growth Factor Therapy for Diseases of the Brain

Clive N. Svendsen, PhD
Professor of Anatomy and Neurology
University of Wisconsin at Madison

Moderator: Cesar C. Santos, MD
Department of Neurology

Abstract: Human stem cells can now be used as a source of tissue for generating neurons and glia in the culture dish. As they can be genetically modified they represent powerful cellular tools for understanding human neural development and a potential source of tissue for brain repair. Dr. Svendsen’s laboratory has modified human neural stem cells to release the powerful growth factor GDNF which is normally very difficult to deliver directly to neurons of the brain. Following transplantation into models of Parkinson's disease and ALS, human neural stem cells can migrate, differentiate and secrete GDNF for long periods. This in turn leads to the protection and stimulation of both dopamine and motor neurons.

4:50 pm - 5:00 pmWrap-up / Thank You



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