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Academia Mexicana de Neurología, A.C.

2012, Número 3

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Rev Mex Neuroci 2012; 13 (3)


Acción protectora de la proteína tau en la enfermedad de Alzheimer

Luna-Muñoz J, Zamudio S, De la Cruz F, Minjarez-Vega B, Mena R

Idioma: Español
Referencias bibliográficas: 62
Paginas: 160-167
Archivo PDF: 361.74 Kb.


RESUMEN

Las marañas neurofibrilares (MNF) están constituidas por la proteína tau, la cual se encuentra anormalmente ensamblada en la enfermedad de Alzheimer (EA). Las MNF representan una acumulación masiva de filamentos helicoidales apareados (FHA). La hiperfosforilación y la proteólisis endógena o truncación son los eventos postraduccionales más importantes en los FHA. A pesar de que la mayoría de estudios han considerado la hiperfosforilación como un evento clave en la patogénesis de la EA, algunos estudios han evidenciado contradicciones en cuanto a la toxicidad de las MNF hiperfosforiladas. Más aún, estos mismos estudios sugirieron que la proteína tau hiperfosforilada tiene de hecho una función protectora como respuesta a la acumulación de un fragmento truncado de la proteína tau en el Glu391. Este fragmento de 90-92 aminoácidos es denominado como «núcleo» mínimo del FHA. Se ha demostrado que este núcleo es altamente tóxico y, al parecer, responsable de la muerte de las neuronas en la EA. En esta revisión abordamos ambos eventos postraduccionales: la hiperfosforilación y truncación, enfocados principalmente a su efecto protector y tóxico de las diversas especies de la proteína tau en la EA.


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