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2018, Número 4

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Rev Med Inst Mex Seguro Soc 2018; 56 (4)


Enzimas degradadoras de amiloide en la Enfermedad de Alzheimer: de las moléculas a la terapia genética

Chin-Chan M, Maldonado-Velázquez MG, Mex-Álvarez R, Garma-Quen PM, Cobos-Puc L

Idioma: Español
Referencias bibliográficas: 85
Paginas: 387-394
Archivo PDF: 632.54 Kb.


RESUMEN

La enfermedad de Alzheimer (EA) es la principal forma de demencia en adultos mayores a nivel mundial. En el año 2010 se estimó que 35.6 millones de personas padecen esta enfermedad y se proyectó que esta cifra se triplicará para el año 2050. De acuerdo con la hipótesis amiloide, la producción y agregación del péptido beta amiloide (A-beta) es el agente inicial en el desarrollo de la EA. El péptido A-beta se genera a partir del procesamiento proteolítico de la proteína precursora de amiloide (APP), y su degradación depende de un grupo de proteínas colectivamente conocidas como enzimas degradadoras de amiloide (EDA), las cuales se reducen durante el envejecimiento y particularmente en la EA. La terapia genética consiste en la restauración de la expresión genética de una proteína deficiente para tratar una enfermedad. La restauración o sobreexpresión cerebral de las EDA reduce los niveles y agregados de A-beta, y mejora el aprendizaje y la memoria en modelos animales de la EA. En la presente revisión se describe el papel de las EDA en la regulación de los niveles de A-beta, así como su uso potencial en la terapia genética contra la EA.


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