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Etiología proteica de la enfermedad de Alzheimer

Miriam García Hernández, Clara Ortegón Salas

Resumen


En la Enfermedad de Alzheimer (EA), determinadas mutaciones alteran el procesamiento de la proteína precursora del amiloide (APP) conduciendo a una producción excesiva del β-amiloide (Aβ), que se agrega en fibrillas insolubles. Se desencadena así una respuesta local inflamatoria que, con el tiempo, los subsiguientes cambios bioquímicos y el estrés oxidativo conducen a la muerte neuronal y al desarrollo de placas neuríticas. La hiperfosforilación de la proteína tau constituye el paso clave para la formación de los ovillos neurofibrilares responsables de la demencia por interrupción de la transducción sináptica. Este trabajo se centra en las consecuencias de estas dos alteraciones y su relevancia en el mecanismo global de la Enfermedad de Alzheimer.

Palabras clave


β-amiloide; Proteína tau; Secretasas; Presenilinas; Priones;

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