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Rev Med Inst Mex Seguro Soc. 2018 Nov 30;56(4):387-394.

Amyloid-degrading enzymes in Alzheimer´s disease: from molecules to genetic therapy

[Article in Spanish; Abstract available in Spanish from the publisher]

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Universidad Autónoma de Campeche, Facultad de Ciencias Químico Biológicas, Cuerpo Académico Ciencias de la Salud y Biotecnología. Campeche, Campeche, México


in English, Spanish

Alzheimer’s disease (AD) is the main form of dementia in elderly population worldwide. By 2010 it was estimated that 35.6 million of people were living with this disease, and it was projected that this figure will triple by the year 2050. According to amyloid hypothesis, production and aggregation of amyloid beta (A-beta) peptide is the initial step in AD development. A-beta peptide is generated through proteolytic processing of amyloid precursor protein (APP); whereas its degradation depends on the action of a group of proteins collectively known as amyloiddegrading enzymes (ADE), which are reduced during aging and particularly in AD. Genetic therapy consists in the restoration of the genetic expression of a deficient protein to treat a disease. Brain restoration or overexpression of ADE reduces the levels and aggregates of A-beta, and improves learning and memory in animal models of AD. In this review we will describe the role of ADE in the regulation of A-beta levels, as well as its potential use in genetic therapy against AD.


Alzheimer Disease; Plaque, Amyloid; Genetic Therapy


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