Resumen

GRA MENENDEZ, Silvia; PADRON PEREZ, Noel  y  LLIBRE RODRIGUEZ, Juan de Jesús. Péptido beta amiloide, proteína Tau y enfermedad de Alzheimer. Rev Cubana Invest Bioméd [online]. 2002, vol.21, n.4, pp.253-261. ISSN 0864-0300.

Alzheimer’s disease, the most common cause of dementia, is updated in this paper. Aspects related to chromosomes 21 and 17 are established. The mutations in the gene of amyloid precursor protein, located in chromosome 21, are the responsible for 5 to 20 % of the cases of early-onset family Alzheimer’s disease. The amyloid precursor protein on beign processed by an amyloidogenic route originates the amyloid-beta peptide, which deposits itself on the senile plaques and causes direct toxic effects on neurons. The gene codifying the Tau protein synthesis is located on chromosome 17. The mutations in this gene caused an irreversible phosphorylation of the protein that impedes its normal function and makes easy its autoaggregation, forming this way the neurofibrillar tangles. Although it is still under study, it is accepted that the amyloid-beta deposit is one of the first causes of the disease; however, the unique correlation established between the intensity of the disease and the pathological injuries is observed in the neurofibrillar tangles.

Palabras clave : ALZHEIMER DISEASE [genetics]; ALZHEIMER DISEASE [etiology]; TAU PROTEINS; AMYLOID BETA PROTEIN PRECURSOR; CHROMOSOMES, HUMAN, PAIR 17; CHROMOSOMES, HUMAN, PAIR 21.

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