We are one step closer to knowing how Alzheimer’s disease originates. This brings us closer to finding a cure

We are one step closer to knowing how Alzheimer’s disease originates.  This brings us closer to finding a cure

Alzheimer’s disease is the most common cause of decreased cognitive ability. It is a neurodegenerative disorder that usually affects people over 65 years of age with impairment of language, memory, comprehension, attention, judgment and reasoning.

In the same way that occurs with obesity, Alzheimer’s disease has many polymorphisms that you can inherit, making this disease a fairly high heritability, estimated to be between 60 and 80%.

Knowing the strong genetic component allows us to determine the pathophysiological processes of Alzheimer’s disease and identify new biological characteristics, new diagnostic markers and therapeutic targets through translational genomics. For that very reason, the characterization of genetic risk factors in Alzheimer’s disease is a maxim.

Despite this, there is still a lot of information about Alzheimer’s disease that is unknownTherefore, increasing the size of the sample in the studies is an objective within the studies themselves in order to discover new risk factors.


What is the new study

The European Alzheimer and Dementia Biobank consortium conducted a two-stage genome-wide association study with a large Spanish collaboration with a total of 111,326 clinically diagnosed Alzheimer’s cases and 677,663 controls. From this information, collected a new data set of 20,464 diagnosed Alzheimer’s cases and 22,244 controls (people who do not have this disease) from 15 European countries.

What this new study tells us

This meta-analysis (which is a study carried out with information from many other previous studies), identified 75 loci (which are places where several genes are located) independent for Alzheimer’s disease and related dementias, of which 33 had been previously reported and 42 corresponded to new signals at the time of this meta-analysis.

In addition, some genetic alterations have been observed that affect the following points:

  1. Microglia cells: They are a type of neuronal support cell present in the central nervous system whose main function is to act as an immune cell. A smaller number of these cells greatly increases the chances of suffering from Alzheimer’s.
  2. Regulation of TNF-α signaling: It seems that there would be a increased signaling of this peptide, so there would be an increase in pathologies (in this case Alzheimer’s) that depends, in part, on beta-amyloid and tau proteins.
  3. APOE: Having at least one gene APOE e4 increases the risk of developing Alzheimer’s disease Alzheimer’s two to three times. If you have two genes APOE e4, the risk is even higher, approximately eight to twelve times.
  4. Beta-amoloid catabolism: In the study they found a gene association that regulated the catabolic process of amyloid precursor protein and the level of gene expression in microglia.
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These analyzes removed ambiguities related to the involvement of tau-binding proteins and beta-amyloid peptide metabolism, which are the most well-known proteins in Alzheimer’s disease.


Many new research approaches were developed to systematically characterize Links between amyloid-beta metabolism, tau, and genetic risk factors in Alzheimer’s disease.

By applying a genetic risk score (i.e., how much of an impact each gene has on disease) derived from all the significant genome-wide variants discovered in this study, we have identified an association with the risk of Alzheimer’s disease with patients with mild cognitive impairmentsomething that could be avoided with a high probability of success by exercising and maintaining a good diet.

It has also been shown that, in addition to the known risk variants, the new risk variants identified in the present study are significantly associated with the progression of Alzheimer’s.

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