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October 8, 2019CNIC researchers open a new avenue in the prevention of this neurodegenerative disease with the use of oral anticoagulants
A common medicine that prevents the blood from being less viscous, transgenic mice with all the "ballots" to develop Alzheimer's and a board with a single den where they can take shelter when they feel threatened. With these elements, the National Center for Cardiovascular Research (CNIC) designed a curious experiment to test whether an oral anticoagulant could prevent memory loss by maintaining more fluid cerebral circulation and “clean” arteries.
The answer has been affirmative. The medication has managed to delay the onset of the disease and reduce other known symptoms. One year after treatment, they have not experienced memory loss, brain inflammation and vascular damage have decreased, and deposits of the amyloid beta protein, a typical sign of Alzheimer's, have been reduced.
The preliminary results of this pioneering research now open a hopeful door to the prevention and treatment of this serious disease that has erased the memories of more than 30 million people in the world. Although at the moment its effectiveness has only been demonstrated in mice, "the important thing is that this work begins a field of research in Alzheimer's disease that had been completely forgotten," says cardiologist Valentín Fuster, director of the CNIC and lead author of the investigation.
It is known that the brain and the heart go hand in hand in numerous diseases, and that the better the cardiovascular health, the less cholesterol, diabetes or hypertension there is, and the less risk of suffering from some type of dementia. But until now, research against this neurodegenerative problem had focused more on the brain, on preventing the formation of amyloid beta plaques and the destruction of neurons that cause the disease. «Alois Alzheimer himself, when describing the disease to which he gave his name, was the one who proposed in 1906 that Alzheimer's was a vascular problem, not of the brain parenchyma. What was said more than a century ago had been totally forgotten,” Fuster insists.
The CNIC team started from an idea, that this amyloid beta protein that destroys neurons is very thrombotic. "When it enters the brain, part of it is deposited in the vascular wall of the cerebral arteries and clots form," explains the cardiologist.




