Alzheimer’s disease could be caused by the deactivation of what are known as “presenilin genes”. Using mice as a model for the study of Alzheimer’s in humans, a scientific team headed by the researcher Carlos Saura, from the Universitat Autònoma de Barcelona, has discovered that when these genes mutate and stop working they cause neuro-degeneration and memory loss, giving rise to what in humans would be Alzheimer’s. The discovery, published in Neuron, is totally unexpected, since up till now it was thought that the alteration that caused Alzheimer’s was exactly the opposite, that is to say, an excess of presenilin activity.
Since 1995 it has been known that family hereditary Alzheimer’s is caused mainly by mutations in presenilin genes, but it was thought that the alteration of these genes caused Alzheimer’s due to an increase in their activity. Research by doctor Carlos Saura, of the Neuroscientific Institute (l’Institut de Neurociències (IN)) at the Universitat Autònoma de Barcelona, using mice, genetically modified to decrease the activity of presenilin genes, has shown that these genes take part in the process of memory consolidation and neuron survival, but in a different way to that expected.
The results, published in the journal Neuron last April, show that the absence of activity of these genes in mice, used as a model for the study of Alzheimer’s in humans, causes symptoms very similar to those observed in persons suffering from Alzheimer’s: progressive memory loss and neuro-degeneration. The authors suggest that mutations in presenilins could be a cause of Alzheimer’s, mainly due to loss of functionality.
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