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


METHODS
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.
Coria-Balanzat
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Clínica contra las Enfermedades Nerviosas, Servicio de Neurología, Hospital Son Dureta, Palma de Mallorca, Baleares, Spain. fcoriab@meditex.es
D000544:Alzheimer Disease / Q000473:pathology* / Q000503:physiopathology; D016229:Amyloid beta-Peptides / Q000235:genetics / Q000378:metabolism*; D016564:Amyloid beta-Protein Precursor / Q000235:genetics / Q000378:metabolism; D000818:Animals; D009454:Neurofibrils / Q000473:pathology; D013569:Synapses / Q000502:physiology
D016229:Amyloid beta-Peptides; D016564:Amyloid beta-Protein Precursor