Alzheimer’s disease is characterized by the overproduction of plaques formed by beta-amyloid, which can be contrasted through the use of proteins belonging to the family of alpha-secretase. In a trial performed by MIT, some rats with an overproduction of beta-amyloid (with consequent behavioural and cognitive alterations very similar to the ones in Alzheimer’s disease) have been matched with some rats with an overproduction of SIRT1 (a molecule stimulating the production of alpha-secretase and slowing oxidative processes and ageing). Children have presented less plaques of beta-amyloid than their parents and have resulted protected against memory deficiency and against the loss of cognitive capability. On the contrary, when sick mice were matched with mice without SIRT1 overproduction, it was seen that the offspring presented more plaques of beta-amyloid and more cognitive damages than their parents.
A new path for the struggle against Alzheimer’s dementia is open: the stimulation of SIRT1 production. It is not the case of easy enthusiasm: we neither know the negative effects of SIRT1, nor whether in humans it is a practicable way. But the first step has been done.
