Biography:

Allal Boutajangout graduated from Free University of Brussels (ULB-Erasme Hospital), School of Medicine (PhD in Neuropathology). He completed his Postdoctoral training at New York University School of Medicine. He is a Research Associate Professor of Neurology and  Neuroscience & Physiology and Psychiatry. He is also the chief of Neurodegeneration and Drug Discovery Program within Center for Cognitive Neurology  at NYU. He received prestigious award Margaret M Cahn for his outstanding research in the field of Alzheimer’s and other awards from: Alzheimer association, NIH pilot grant, Toyama Company, Revalesio Company and co-investigator in 5 RO1 NIH grants. He has published more than 30 papers in reputed journals and serves as a reviewer for many scientific journals.

Abstract:

Alzheimer’s disease (AD) is an age-related progressive disorder characterized by the extracellular accumulation of amyloid β (Aβ) peptides as plaques and cerebral amyloid angiopathy (CAA), as well as intracellular neurofibrillary tangles (NFTs). AD is the most common cause of dementia globally. Care for patients with dementia accounts for ~1% of current global GDP, with this expected to rise substantially in the near future. No effective treatment is available to prevent or cure AD. Currently available treatments for AD provide largely symptomatic relief, with only minor effects on the course of the disease; hence, there is an urgent need for better therapeutic interventions. Aβ has become a major target for disease modifying treatments of AD. Unfortunately, the ongoing trials targeting amyloid Aβ failed in phase III trials. So far, the clinical benefits to the patients are limited and have no effect on tau related pathology. Previously, we reported for the first time, that active and passive immunotherapy targeting tau pathology reduces tau pathology and improves cognitive decline in two different NFT models. Recently, we developed a new monoclonal antibody against PHF-tau that reduces tau pathology and improves cognitive decline without inflammation. We have also explored the potential effects of hUCB-MSC on AD pathology. Our results suggest that use of these stem cells is associated with a reduction of amyloid burden, which correlates with improvements of cognitive function in a transgenic AD mouse model. These promising approaches using immunotherapy targeting tau or stem cells to reduce Aβ pathology in animal AD models provide critical data prior to potential clinical trials.

Biography:

Giovanni Antioco Putzu is a Medical Doctor since 1992, with specialization in Paediatric Neurology. He achived his PhD in 1996. During PHD studies, He was a Research Fellow in Hammersmith Hospital of London, UK in 1992, then He moved in Marseille to work at INSERM (Genetics) and in Neurophathology. The Author has published more than 15 papers in the field of Neuromuscular Disorders.

Abstract:

GBS is an auto-immune life-threatening inflammatory polineuropathy that may produce severe functional disability. Vaccines, viral, fungine or bacterial infections may trigger the disease. On the basis of neuropathological and neurophysiological findings, GBS is classified in demyelinating and axonal forms. In both features, functional disability is directly correlated to axonal loss. Involvement of amyelinic axons is responsible for autonomic disturbances, which, along with bulbar spread of the disease, represent a potential cause of death in GBS. A consistent number of patients both in the early or recovery phases may complain of neuropathic pain that requires an adequate treatment. Immunological aspect of the disease, i.e auto-antibodies directed against GM1 and recently to contactin-associated protein 1 (Caspr) of the paranodal region of myelinated nerves, have already been investigated. We have demonstrated that TNF-alpha was immunolocalized in both myelinated and unmyelinated axons the sural nerve of GBS patients. We concluded that this substance may be directly responsible for axoal loss( G.A. Putzu et al, J. Neurol Sci, 2000).

Interferon-gamma, which is a stimulator of IL28A was also easily detected in the sural nerve of GBS patients. The role of adhesion molecules like ICAM in the immune process of GBS will be also discussed. The therapeutic approach of GBS is aimed to avoid death in the acute phase (respiratory failure in Landry paralysis, cardiac rhythm anomalies in disautonomia). The efficacy of plasmapheris and intravenous immunoglobulins in the treatment of GBS is nowadays clearly demostrated. The next frontier is the theoretical possibility to use monoclonal antibodies (i.e, anti-INF-gamma) as a therapeutic tool in GBS.

We also rewied the literature on GBS-like conditions that may clinically mimick GBS.

Biography:

Neurologist, Peter Silburn is a Professor of Clinical Neuroscience at The University of Queensland, Director of the Asia-Pacific Centre for Neuromodulation, and a world expert in the treatment and research of Parkinson's disease, related neurodegenerative disorders and Deep Brain Stimulation (DBS). Professor Silburn's work in DBS is changing the lives of patients with a wide range of diseases and conditions for whom standard medical therapies have not been effective, including patients with Parkinson's disease, Dystonia, Tourette's syndrome, Essential Tremor, and Post-stroke disorders.

Professor Silburn graduated from The University of Queensland in 1988 and commenced training in neurology at The Princess Alexandra Hospital, completing his training at Oxford in The United Kingdom at the Radcliffe Infirmary. He was subsequently the Clinical Lecturer in Neurology at the University of Oxford.

He then went to the Karolinska Institute, Stockholm, as a Research Fellow in the Department of Molecular Medicine. He returned to Brisbane in July 1996, commenced private practice and established affiliations with The University of Queensland.

He became full Professor in Neurobiology in 2006 and Foundation Professor of Clinical Neuroscience at the UQ School of Medicine in 2007.

Abstract: