EVALUAN EL EFECTO DE LAS ESTATINAS SOBRE LA PRODUCCION DE
β-AMILOIDE
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A pesar de su notable efecto sobre el metabolismo del
colesterol, el tratamiento con estatinas, dentro de su intervalo
terapéutico, no parece asociarse con modificación significativa de la
concentración de β-amiloide en personas con hipercolesterolemia o enfermedad
de Alzheimer. En consecuencia, en dosis clínicamente útiles, las estatinas
podrían carecer de repercusión sobre la producción o segregación de
β-amiloide, según propone la estrategia actualmente debatida para detener la
progresión de la enfermedad de Alzheimer. Otros efectos de las estatinas
pueden ser responsables de su acción protectora contra la demencia. |
participó en la investigación
Kaj Blennow*
MD, PhD, Göteborg University, Mölndal, Suecia*
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Recepción del artículo: 5 de Septiembre, 2006
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Aprobación: 13 de Septiembre, 2006
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Resumen
Hasta la fecha, se formularon numerosas
hipótesis en un intento por establecer la causa de la enfermedad de
Alzheimer (EA), la forma más frecuente de demencia. Aquella que considera el
papel del colesterol, basada principalmente en estudios en cultivos
celulares y en animales, afirma que los niveles aumentados de colesterol
inducen la vía amiloidogénica durante el metabolismo de la proteína
precursora de amiloide (PPA) y, en consecuencia, promueven la producción del
péptido beta amiloide (βA), principal constituyente de las placas seniles.
Representa una teoría ampliamente aceptada que la adición de βA en las
placas es un evento inicial en la EA, el cual resulta en neurodegeneración.
La presente revisión se centra en la hipótesis del colesterol y su
aplicación a los seres humanos. Se revisa y discute el papel del tratamiento
para reducir los niveles de colesterol con estatinas.
Palabras clave
enfermedad de Alzheimer, colesterol,
estatinas, ß-amiloide, líquido cefalorraquídeo
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Especialidades
Principal: Bioquímica
Relacionadas: Anatomía
Patológica, Farmacología, Medicina
Farmacéutica, Medicina
Interna, Cardiología, Toxicología
Enviar
correspondencia a: Kina Höglund, Department of Neuroscience and
Physiology, Section of Psychiatry and Neurochemistry, Neurochemistrylab,
Göteborg University, S-431080, Mölndal, Suecia
Artículo
completo
(castellano)
Extensión:
+/- 13.2 páginas impresas en papel A4
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STATIN-INDUCED REDUCTION OF ß-AMYLOID PRODUCTION IN
ALZHEIMER'S DISEASE
Abstract
To date a number of
hypotheses have been postulated trying to state the cause of Alzheimer's
disease (AD), the most common form of dementia. The cholesterol hypothesis,
based primarily on cell- and animal studies, states that increased levels of
cholesterol induces the amyloidogenic pathway of the processing of the
amyloid precursor protein (APP), thereby promoting production of the
ß-amyloid peptide(Aß). The Aß peptide is the major constituent of senile
plaques, which together with atrophy and neurofibrillary tangles is the main
neuropathological finding in AD. It is a widely accepted theory that
aggregation of Aß into plaques is a initial event in AD, driving
neurodegeneration. This review focuses on the cholesterol hypothesis and its
implementation on human beings. The role of cholesterol lowering treatment
using statins is reviewed and discussed.
Key words
Alzheimer's disease, cholesterol, statins, B-amyloid, CSF
Full
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