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The physiopathological basis for treatment in Multiple Sclerosis

Life and Matter Sciences International Symposium March 15 - 16, 2001 Madrid

Multiple sclerosis (MS) is the most common chronic demyelinating disease of the central nervous system (CNS).

Organized by:

Fundación Ramón Areces

Coordinator/s:

José Carlos Álvarez-CermeñoServicio de Neurología. Hospital Universitario Ramón y Cajal. Madrid.

It affects young adults in the most active period of life, leading to major perturbations in their daily and professional activities. Therefore, the full economic and emotional costs of the disease are substantial. An overwhelming deal of information on MS pathogenesis has appeared during the last decade. It is currently believed that autoreactive CD4 cells play a paramount role at the initial steps of CNS inflammation, although other cells such as glia and macrophages are implicated as well. Complement and autoantibodies against different myelin antigens may also play a role, taking into account that heterogeneity in MS pathogenesis is currently accepted.

Magnetic resonance imaging (MRI) has provided new and important data on MS pathogenesis being the most accurate method to assess disease activity. Likewise, MR spectroscopy (MRS) has showed that demyelination, the hallmark of the disease, is not able to completely explain the permanent deficits of patients. Axonal damage seems to be the major cause of patients' impairment and this finding has been confirmed pathologically. It has been also shown that axonal loss may contribute to the brain atrophy that MS patients may show in MRI studies.

The evidence that MS has an autoimmune pathogenesis has led to the successful use of interferon beta in its treatment, positively affecting the natural history of the disease. Such medication diminishes the relapse rate, disease progression and brain atrophy. Likewise, immunosupressors and stem cell transplantation may be useful in selected cases.

We are living a historical age in the research of MS. The investigation of last recent years has provided new insights in the mechanisms of the disease as well as treatments that, although not curative, greatly improve the quality of live of our patients. Some of the invited speakers are responsible for those advances. We all gratefully acknowledge their effort.

Thursday, 15 - Friday, 16

 

Participants

José María Segovia
Consejo Científico.
Fundación Ramón Areces.

José Carlos Álvarez-Cermeño
Coordinador del Simposio.

Óscar Fernández
Servicio de Neurología.
Complejo Hospitalario Universitario Carlos Haya.
Málaga.

Rafael Fernández Muñoz
Unidad de Virología.
Hospital Universitario Ramón y Cajal.
Madrid.

Carmen Guaza
Unidad de Plasticidad Neural.
Instituto Cajal.
CSIC.
Madrid.

Melchor Álvarez de Mon
Departamento de Medicina.
Universidad de Alcalá de Henares.

Peter Werner
Department of Neurology and Neuropathology.

Albert Einstein
College of Medicine.
Nueva York. EE.UU.

Bruce D. Trapp
Cleveland Clinic Foundation.
Cleveland. EE.UU.

Guillermo Izquierdo
Servicio de Neurología.
Hospital Universitario Virgen Macarena.
Sevilla.

Alberto Alcázar
Servicio de Bioquímica de Investigación.
Hospital Universitario Ramón y Cajal.
Madrid.

Luisa María Villar
Servicio de Inmunología.
Hospital Universitario Ramón y Cajal.
Madrid.

Edward J. Thompson
Dept. of Neuroimmunology.
National Hospital for Neurology & Neurosurgery.
The Institute of Neurology.
Queen Square.
Londres. Reino Unido.

Xavier Montalbán
Unidad de Neuroinmunología Clínica.
Hospital Valle de Hebrón.
Barcelona.

Txomin Arbizu
Unidad de Esclerosis Múltiple.
Ciudad Sanitaria y Universitaria de Bellvitge.
L'Hospitalet de LLobregat. Barcelona.

Donald W. Paty
Professor, Neurology.
UBC Hospital.
Vancouver. Canadá.

Lawrence Jacobs
State University of New York at Buffalo.
Buffalo General Hospital.
Buffalo. EE.UU.

Antonio García Merino
Servicio de Neurología.
Hospital Universitario Clínica Puerta de Hierro.
Madrid.

Fransesc Graus
Servicio de Neurología.
Hospital Clínic i Provincial.
Barcelona.

see all

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