ABSTRACT
INTRODUCTION: Alzheimer's disease (AD) results from the progressive accumulation of a specific protein (beta peptide) in the brain parenchyma in the form of amyloid deposits. DEVELOPMENT: Amyloid deposition in AD may be the result of multiple genetic and environmental factors which may alter the metabolism and degradation of the beta amyloid precursor protein. Amyloid deposits are toxic to the nervous tissue and lead to synaptic loss, neurofibrillary tangle formation and progressive neuronal loss. CONCLUSIONS: Synaptic loss is related to memory decline in the early stages of the disease and neurofibrillary tangle formation and neuronal loss to dementia in later stages of the disease. This series of events, known as the amyloid cascade, is supported by many genetic and experimental studies.
Subject(s)
Alzheimer Disease/pathology , Amyloid beta-Peptides/metabolism , Alzheimer Disease/physiopathology , Amyloid beta-Peptides/genetics , Amyloid beta-Protein Precursor/genetics , Amyloid beta-Protein Precursor/metabolism , Animals , Neurofibrils/pathology , Synapses/physiologyABSTRACT
Introducción. La enfermedad de Alzheimer (EA) es el resultado de la acumulación progresiva de una proteína específica(proteína beta) en el parénquima cerebral, en forma de depósitos amiloides. Desarrollo. Los depósitos amiloides en la EA son el resultado de factores genéticos y ambientales que alteran el metabolismo de la proteína precursora del amiloide beta. La acumulación de amiloide en el tejido cerebral desencadena fenómenos tóxicos que se traducen en pérdida sináptica y, más tarde, en la formación de ovillos neurofibrilares y muerte neuronal. Conclusiones. La pérdida sináptica se correlaciona con los trastornos de memoria característicos de las primeras fases de la enfermedad, y la pérdida neuronal, con la demencia en fases más avanzadas. Esta sucesión de hechos, conocida como 'cascada amiloide', se apoya en múltiples estudios genéticos y experimentales (AU)
Introduction. Alzheimer's disease (AD) results from the progressive accumulation of a specific protein (beta peptide) in the brain parenchyma in the form of amyloid deposits. Development. Amyloid deposition in AD may be the result of multiplegenetic and environmental factors which may alter the metabolism and degradation of the beta amyloid precursor protein. Amyloid deposits are toxic to the nervous tissue and lead to synaptic loss, neurofibrillary tangle formation and progressive neuronal loss. Conclusions. Synaptic loss is related to memory decline in the early stages of the disease and neurofibrillary tangle formation and neuronal loss to dementia in later stages of the disease. This series of events, known as the amyloid cascade, is supported by many genetic and experimental studies (AU)
