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[Advances in molecular pathology of Alzheimer's disease].

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.