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Alberto Pérez Mediavilla, Senior Associate Professor of Biochemistry and Molecular Biology, researcher senior in Neurosciences of Cima University of Navarra

The reality of Alzheimer's disease: progress and prevention

Sat, 21 Sep 2019 11:07:00 +0000 Published in La Razón

We are celebrating World Alzheimer's Day and, once again, there are no new developments in its treatment. It makes one envious to follow the advances that other colleagues are accumulating in the refinement and efficacy of therapies aimed at curing diseases such as cancer. There are several reasons for this. The main one is that, while in cancer the challenge is to "kill" the tumor cells, in Alzheimer's disease the challenge is to protect the neurons. Protect! From what? We know that two proteins are involved in this dementia: tau and beta amyloid. Over the past 20 years, the pharmaceutical industry has spent millions of euros designing treatments to neutralize the action of both proteins.

However, in this same 2019, virtually all clinical trials with this strategy have been stopped due to lack of efficacy. The reason most likely lies in the fact that the patients participating in these trials are in a "no-turnaround" phase. This shows that, unlike cancer, in Alzheimer's we do not have biomarkers to reliably identify the population at risk or already suffering from it without apparent external symptoms.

Another question revolves around this dementia: is there only one disease or several? In cancer, there is no single way of treating it, but several treatments depending on the tumor subject , its characteristics, the patient's genetic profile , etc. Similarly, we see that there is no single subject in Alzheimer's disease. For example, a very significant percentage of patients with diabetes subject 2 develop Alzheimer's following a very different pathway to that of other patients without the first pathology. This coexistence between diabetes subject 2 and neurodegenerative disease leads me to other questions related to prevention.

Can this dementia be prevented? As I said, one of the challenges is to know why neurons die. In this dementia the cause-effect relationships are not yet established, but we do know that in about 1% of patients there is a causality: the mutation in several genes that lead, irreducibly, to suffer from it. This is not the case in 99% of the remaining cases. A possible biomarker of this dementia could be diabetes subject 2. Therefore, preventing it with exercise and an adequate per diem expenses , can help us to protect ourselves against Alzheimer's disease. Prevention should be a priority. It is not necessary to wait for symptoms to appear, since "silent" Alzheimer's disease begins up to 20 years before they appear.