El Dr. Teodoro Del Ser Quijano se licenció en Psicología (1973), Sociología Política (1976) y Medicina (1976), se doctoró en Medicina (1987) y trabajó como Profesor Asociado de Neuropsicología (1986-1989) en la Universidad Complutensede MadridSe especializó en Neurología en el Hospital 12 de Octubre de Madrid (1977-1981) y ha hecho estudios postdoctorales en Neurología, Neuropatología y Neuropsicología en la "Clinique Psychiatrique Universitaire Bel-Air" (Génève), "Unité de Recherches Neuropsychologiques et Neuroliguistiques" (Paris) y Department of Neurological Sciences, University of Western Ontario.Desde 1987 ha trabajado como Neurólogo Clínico y Jefe de Sección de Neurología en el Hospital Severo Ochoa de Leganés (Madrid).Ha realizado estudios clinicopatológicos sobre demencia vascular y demencia con cuerpos de Lewy, estudios epidemiológicos sobre la demencia, el deterioro cognitivo ligero y la demencia tras el ictus, y estudios clínicos y neuropsicológicos sobre la enfermedad de Alzheimer y otras demencias.Ha participado en el diseño y ejecución de numerosos ensayos clínicos en la enfermedad de Alzheimer, demencia vascular y demencia con cuerpos de Lewy. Desde diciembre de 2004 se ha incorporado a Neuropharma como Director de Desarrollo Clínico.
PD : NeuroPharma posee un equipo de primera linea y no solo a nivel Nacional .
Dementia with Lewy bodies
An interview with Teodoro Del Ser, Hospital Severo Ochoa, Madrid, Spain
Dr Del Ser has been involved in several clinical pathological studies focusing on different aspects of dementia. He has been Associate Professor of Neuropsychology at the University of Madrid, co-ordinator of the Dementia Group of the Spanish Neurological Society and member of several clinical trial advisory boards.
Dementia with Lewy bodies (DLB) is the second most common cause of cognitive impairment in patients over the age of 70. Only Alzheimer’s disease (AD) is more frequent. The disease is characterized by fluctuating cognitive impairment, visual hallucinations and parkinsonism. The clinical symptoms are correlated with an extensive cholinergic deficit, particularly in the cortex. In this issue of Alzheimer Insights we interview Dr Del Ser, who discusses current understanding of DLB, its clinical diagnosis and potential treatment strategies.
What is our current understanding of the cause of DLB? Is there any evidence that the disease could have a genetic origin?
As with most other neurodegenerative diseases, the exact cause of DLB has not been determined. In terms of a genetic origin, there are a few familial cases of DLB, but generally the disease is sporadic and the cause unknown.
What are the clinical features of DLB and how do they differ/overlap with those of AD?
Some of the key symptoms of DLB and their rates in both DLB patients and AD patients are shown in Table1 [1]. In the early stages, DLB has very distinct features from AD. Dementia is characterized by attentional deficits and prominent frontal-subcortical and visuospatial dysfunction. In addition, mild signs of parkinsonism frequently appear at the onset of DLB. Although such symptoms can appear in AD, they are generally only seen in the later stages of the disease. Psychotic symptoms, particularly visual hallucinations, are a very characteristic feature of DLB. More difficult to define but a very useful sign of DLB, are the large fluctuations in cognitive performance observed over relatively short periods of time. Within a day or so there can be a dramatic change in the patient’s cognitive state from near normal to significantly impaired. This is in contrast to the progressive cognitive decline seen in AD patients.