A research project

Alzheimer disease (AD) is a neuron degeneration process that produces a progressive loss of memory and other intellectual functions, supposing a serious health, social and human problem.

Although it can’t be denied that there have been significant advances in the diagnostic methods and slight improvements in the treatment of some of the disease’s symptoms, it will not be possible to develop more rational diagnostic methods and therapies without first increasing our knowledge on the pathogenic mechanisms of the disease.

Currently the Association of Families of Alzheimer Patients (AFAL) is presenting in Spain a research project “Searching for susceptibility genes”, with the goal of finding pathogenic mechanisms that can define the approach.

The most characteristic pathology findings of AD are neuritic plaques and neurofibrillary tangles, as well as the loss of synapses and neurons.  The plaques are produced by the addition and deposit of the amyloid peptide in the extra cellular space, while neurofibrillary tangles are aggregated to the protein associated to tau microtubules, hyperphosphorylated and abnormally folded, inside the neurons.

Mutations have been found in three genes, the one of the precursor protein of the amyloid (APP) and those of the presenilin 1 and 2 (PSEN1 and PSEN2), which cause monogenic AD, transmitted in a dominant autosome way.  These mutations are responsible for only a small fraction of AD cases (around 1%).

Collaborated in this article: Ma. Jesús Morala del Campo

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