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 PROGRAMA
Chairman:
Juan José López-Ibor
Francisco Mora
Pabellón San Carlos, Hospital Clínico - Madrid, April 23 & 24, 2004
 
Viernes / Friday 23
08:30 – 08:50 Recogida de Acreditaciones / Registration
08:50 Opening and welcome addresses:

Why this symposium.
09:00 Keynote Address
Moderador/Chairperson: Juan José López-Ibor
Servicio de Psiquiatría. Hospital Clínico San Carlos, Madrid, Es.
  Arvid Carlsson
Department of Pharmacology. University of Göteborg, Sw.



The Dopamine System: Still an important target for Drug Discovery / El Sistema Dopamínico: aun una diana importante para el descubrimiento de fármacos.
Following the proposal by Carlsson and Lindqvist in 1963 that major neuroleptics act by blocking dopamine (and noradrenaline) receptors, the dopamine system has been a target in attempts to discover novel antipsychotics with improved balance between efficacy and side effects. The present paper will deal with the most recent group of agents acting on this target, i.e. the dopamine system stabilizers; they seem to offer significant advantages compared to current antipsychotics.
SESION 1 Parkinson's disease
Moderador/Chairperson: Juan Carlos Gómez
Director Médico. Lilly S.A., Madrid, Es.
09:40 Peter Jenner
Neurodegenerative Diseases Research Centre. GKT School of Biomedical Sciences, King’s College, London, UK.



Molecular mechanisms in Parkinson’s disease / Mecanismos moleculares de la enfermedad de Parkinson.
Neuronal cell death in Parkinson’s disease may be associated with a failure of proteaolysis linked to alterations in the function of the ubiquitin-proteasome system. Inhibition of proteasomal function leads to dopaminergic cell death both in vitro and in vivo. Inflammatory changes also occur in the substantia nigra in PD as a result of reactive gliosis. Glial cell activation using LPS leads to destruction of dopaminergic neurones suggesting that inflammation may contribute to disease progression.
10:10 José López Barneo
Departamento de Fisiología. Hospital Universitario Virgen del Rocío, Sevilla, Es.



Dopamine and GDNF-producing cells in the carotid body: their use for autotransplantation in Parkinson’s disease / Células productoras de dopamina y GDNF en el cuerpo carotídeo: su utilización para autotransplante en la enfermedad de Parkinson.
Several dopamine-producing cells have been used for the last few years in transplantation studies designed to treat Parkinson's disease, both in human and in animal models of Parkinson's disease. We have developed a technique based in the intrastriatal autotransplantation of cells of the carotid body that secrete dopamine and glial cell line-derived neurotrophic factor (GDNF). We will present the status of our current research. We will also discuss the advantages, limitations and future perspectives of this new methodology for treatment of Parkinson's disease.
10:40 Café/Coffee
11:10

José Obeso
Unidad de Trastornos del Movimiento y Ganglios Basales. Univ. de Navarra, Pamplona, Es.




Pathophysiology of the basal ganglia: therapeutic consequences for Parkinson’s disease / Patofisiología de los ganglios basales: consecuencias terapéuticas para la enfermedad de Parkinson.
The severity of dopamine depletion and the associated pathophysiologic abnormalities in the basal ganglia circuits determine the severity of parkinsonian signs. Cell replacement therapy has spurred considerable enthusiasm, most recently for the use of embryonic stem cells. However, Parkinson’s disease is a multi-systems degeneration; many symptoms fail to respond to current treatment and will likely be resistant even to the most "successful" dopamine cellular replacement therapy.
11:40 Eduardo Tolosa
Servicio de Neurología. Hospital Clínic, Barcelona, Es.



Emerging strategies in the treatment of Parkinson disease / Nuevas estrategias en el tratamiento de la Enfermedad de Parkinson.
In recent years new treatments have become available that have greatly improved both motor and non-motor complication of Parkinson disease. These include new atypical antipsychotics and the anticholinesterase inhibitors and stimulants such as modafinil. Newer treatments are furthermore emerging which are likely to be effective in both the symptomatic and neuroprotective treatment of Parkinson disease, such as some trophic factors, anti-adenosine A2 receptor drugs or those with antiglutamatergic properties. These new available treatments and the new, emerging, strategies will be reviewed.
12:10

Discusión 1: Parkinson's disease

12:45
SEMINARIO 1 SEMINARIO 2
13:45 Almuerzo
SESION 2

Schizophrenia: a neurodegenerative disorder?
Moderador/Chairperson: Enrique Baca
Servicio de Psiquiatría. Clínica Puerta de Hierro, Madrid, Es.

15:15

Robin M Murray
Department of Psychiatry. Institute of Psychiatry, King’s College, London, UK.




Schizophrenia: Between development and degeneration / Esquizofrenia: entre el desarrollo y la degeneración.
Although the neurodevelopmental model was the predominant model of schizophrenia throughout the 1990s’s, it is clear that it cannot explain all characteristics of schizophrenia. The question is whether the decline that occurs in a proportion of patients is simply a consequence of the psychological and social disruption caused by psychosis or whether this is the result of progression of brain structural and neuropsychological abnormalities.
15:45 Tim Crow
Prince of Wales International Centre for Research into Schizophrenia and Depression. Oxford, UK.



An evolutionary perspective on schizophrenia / Una perspectiva evolutiva sobre la esquizofrenia.
Schizophrenic illnesses occur in all populations whit similar features. Some balancing advantage to the biological disadvantage associated with the generic predisposition is required. This, it is suggested, is the human capacity for language, and that the relevant genetic variation goes back to the origin of the species at some point in E. Africa 100-150.000 years ago.
16:15 Maria Carlsson
Sahlgrenska Academy (Medical School), Institute of Clinical Neuroscience. Univ. of Göteborg, Sw.



The role of glutamate in schizophrenia / Papel del glutamato en la esquizofrenia.
Cognitive and negative symptoms of schizophrenia constitute the major therapeutic challenges in this disorder. This presentation will discuss recent findings from our rodent hypoglutamatergic models for cognitive and negative symptoms of schizophrenia. The effects of traditional neuroleptics, a newer generation antipsychotics, as well as those of so called dopamine stabilizers will be presented.
16:45 Gary D Tollefson
Lilly Research Laboratories. Indianapolis, USA.



Neuroprotection and cognitive enhancement. The future of the treatment of schizophrenia / Neuroprotección y mejora cognitiva. Futuro del tratamiento de la esquizofrenia.
While undoubtedly schizophrenia has a neurodevelopmental aspect, both studies of associated clinical and structural brain pathomorphology suggest a progressive course. The loss of cortical gray volume and ventricular enlargement represents a new treatment target. Data suggesting a neuroplasticity benefit with the atypical olanzapine will be shared.
17:15 Discusión 2: Schizophrenia: a neurodegenerative disorder?
17:45 Café / Coffee
18:15
SEMINARIO 1 SEMINARIO 3
Sábado / Saturday 24
SESSION 3 Alzheimer's disease
Moderador/Chairperson: Justo García de Yébenes
Servicio de Neurología. Fundación Jiménez Díaz, Madrid, Es.
09:00 Ezio Giacobini
University Hospitals of Geneva, Department of Geriatrics. University of Geneva, Ch.



Early diagnosis and treatment of Alzheimer’s disease: present and future / Diagnóstico temprano de la enfermedad de Alzheimer: presente y futuro.
Various forms of pharmacological treatment are being tested clinically in an effort to slow down or block the conversion of Mild Cognitive Impairment to Alzheimer’s Disease. Experimental and clinical data suggest that cholinesterase inhibitors (ChEI), in addition to symptomatic benefit, might have a delaying effect on Alzheimer’s Disease progress (Giacobini, 2000). Other approaches being investigated include anti-inflammatories (rofecoxib), 1200 pats, 3yrs; anti-oxidants (vit E) + ChEI (donepezil), 769 pats, 3 yrs; nootropics (piracetam), 675 pats, 1yr; AMPA receptor agonists (ampakine), 160 pats, 4 wk. Besides, data from the recent vaccination study (Nitsch et al, 2003; Hock et al, 2003), with pre-aggregated A-beta-42, show that patients who generated amyloid plaque immunoreactivity over one year period, had significantly slower rate of decline of cognitive functions and improvement in activities of daily living. These preliminary results suggest that targeting A-beta with immunization could be of benefit to early cases of Alzheimer’s Disease.
09:30

Jesús Ávila
Centro de Biología Molecular "Severo Ochoa". CSIC, Es.




Tau proteins and tauopathies / Proteínas Tau y taupatías.
The role of tau protein in pathological disorders like Alzheimer’s disease, and other pathologies, has two main characteristics: the phosphorylation of the protein, and its aberrant polymerization.
The mechanisms for these two features will be indicated.
10:00 Café / Coffee
10:30
Peter Davies
Department of Pathology. Albert Einstein College of Medicine, New York, USA.



Tau pathology and tangles in Alzheimer's disease as a target for pharmacotherapy / Patología de Tau y redes como diana farmacoterapéutica en la enfermedad de Alzheimer.
Abnormalities in tau in Alzheimer’s disease include conformational changes as well as hyperphosphorylation. These alterations are exquistively sensitive indicators of neuronal damage in this disease. There is now also evidence that tau abnormalities are responsible for the death of neurons, and the mechanisms involved are very obvious targets for new therapeutics.
11:00

Steven Paul
Executive Vice President, Science and Technology. Lilly Research Laboratories. Indianapolis, USA.




Alzheimer's disease: Genetic and pharmacological evidence supporting the amyloid cascade hypothesis / Evidencia genética y farmacológica en soporte de la hipótesis de cascada de amiloide.
Revolutionary advances in our understanding of the genetic and consequent cellular/biochemical etiologies of a group of phenotypically similar neurodegenerative disorders, referred to as Alzheimer’s Disease (AD), have heralded a new era in potential therapeutic intervention. I will review these findings, including recent data from our laboratory delineating an important role for apoE in the process of amyloidogenesis in vivo, and present several ongoing approaches to drug discovery made possible by this new information. Similar approaches to other neuropsychiatric disorders will undoubtedly prove feasible once the genetic underpinnings of their etiologies are delineated.
11:30 Discusión 3: Alzheimer's disease
12:00
SEMINARIO 2 SEMINARIO 3
13:00 Conferencia Clausura
Moderador / Chairperson: Francisco Mora
Catedrático de Fisiología. Facultad de Medicina, UCM. Madrid, Es.



Francesc Artigas
Profesor Investigación CSIC, IIBB. Presidente, Sociedad Española de Neurociencias.



The role of prefrontal cortex in mental health and disease / Papel del cortex prefrontal en la salud y la enfermedad mentalesl.
The prefrontal cortex (PFC) is involved in many higher brain functions which are altered in severe psychiatric disorders. PFC pyramidal neurons express the receptors for which antipsychotic drugs show high affinity. The current evidence supporting a major role of these neurons in the pathophysiology and treatment of schizophrenia, and possibly major depression, will be reviewed.
13:40 Despedida
Juan José López-Ibor
Francisco Mora Teruel
José Antonio Gutiérrez Fuentes
Juan Carlos Gómez Pérez
 
(*)SEMINARIOS
  SEMINARIO 1
  Ponente: Gurutz Linazasoro
Centro de Neurología y Neurocirugía Funcional, Clínica Quirón, San Sebastián, Guipúzcoa.



Diagnosis and treatment of Parkinson’s disease / Diagnóstico y tratamiento de la enfermedad de Parkinson.
Since no biological markers of the disease are available, the diagnosis of PD is still based on clinical grounds. Clues to establish a diagnosis will be explained as well as recent advances in complementary tests. Current management of early and late PD will be reviewed emphasizing the role of recent therapies and the potential of emerging therapies.
SEMINARIO 2



Ponente: Enrique Álvarez
Jefe del Servicio de Psiquiatría del Hospital de Sant Pau de Barcelona.




Diagnosis and treatment of Schizophrenia / Diagnóstico y tratamiento de la Esquizofrenia.
La era de la Medicina Científica debe estar presente también en la Psiquiatría. Los clínicos apoyaran sus decisiones en pruebas científicas de su utilidad. Por otra parte la era de la terapéutica de caja negra ha terminado y los Psiquiatras emplearan fármacos de los que conocerán su intimo mecanismo de acción.
SEMINARIO 3
  Ponente: Manuel Martínez Lage
Profesor y Consultor de Neurología, U Trastornos de Memoria, Clínica Universitaria de Navarra, Pamplona.



Diagnosis and treatment of Alzheimer’s disease / Diagnóstico y tratamiento de la enfermedad de Alzheimer.
Early detection of Alzheimer’s disease.
Clinical, biological, and imaging markers.
AchE inhibitors: donepezil and rivastigmine.
Nicotinic AchER modulators: galantamine.
Memantine.
Treatment of behavioral and psychological symptoms.
Antiamyloid therapies. Facts and hopes.
Cognitive psychostimulation.
Viernes 23 Sábado 24
12:45 18:15 12:00
SEM- 1 SEMI-2 SEM- 1 SEM- 3 SEM- 2 SEM- 3
Seminarios: dirigidos a la discusión y orientación de los aspectos prácticos relacionados con la prevención, el diagnóstico y el tratamiento.
PROMOTORES PATROCINIO
Fundación Lilly
Fundación Lilly
COMITÉ CIENTÍFICO (ORGANIZADOR) LUGAR DE CELEBRACIÓN DEL SIMPOSIO
Juan José López-Ibor
Francisco Mora Teruel
José Antonio Gutiérrez Fuentes
Juan Carlos Gómez Pérez
MADRID
CONFERENCIANTES – SPEAKERS
Juan José López-Ibor (Es)
Arvid Carlsson (Sw)
Eduardo Tolosa (Es)
Peter Jenner (UK)
José López Barneo (Es)
José Obeso (Es)
Juan Carlos Gómez (Es)
Enrique Baca (Es)
Robin M Murray (UK)
Tim Crow (UK)
Maria Carlsson (Sw)
Gary D Tollefson (USA)
Justo García de Yébenes (Es)
Ezio Giacobini (Ch)
Jesús Ávila (Es)
Peter Davies (USA)
Steven Paul (USA)
Francisco Mora (Es)
Francesc Artigas (Es)
Gurutz Linazasoro (Es)
Enrique Alvarez (Es)
José Manuel Martínez-Lage (Es)
INFORMACIÓN GENERAL
La acreditación supondrá la asistencia a todas las sesiones plenarias y, como mínimo, a dos seminarios.
Las conferencias tendrán una duración de 30 minutos y se verán seguidas por un coloquio de 10 minutos, estando abiertas al público en general.
Los seminarios se impartirán dos veces cada uno.
Al acreditarse, los asistentes harán una opción previa sobre los seminarios a los que desean asistir, limitándose el número de participantes en cada uno de ellos un máximo de 70 (se respetará rigurosamente el orden de inscripción).
SECRETARIA
Fundación Lilly: Calle Velázquez 94, 6º Izq. 28006 Madrid
Tel: 91 781 50 70-71 / 629 86 14 16
Fax: 917815079
E-mail: fundacionlilly@lilly.com / www.fundacionlilly.com

 

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