Scientists from Wile Cornel Medical College have found that the Mutation named ApoE3-R136s weakens inflammatory signals in the immune cells of the brain. This reduces the risk of memory and attention deficit during Alzheimer's disease. The results of the study were published in the Momunitive magazine.
The version of the APOE3 GENER R136s is also known as the "Mutation of Crystcher". It was first discovered by a Colombian woman who descended from her hereditary family of early Alzheimer's disease. Despite the large number of amyloid shields in his brain, he did not develop a memory deficit or other typical signs of the disease, even at the age of 70.
In order to understand the principle of action of this mutation, researchers have imported it into laboratory mice, which had a predisposition to the accumulation of the Tau Protein, which is one of the main pathological features of Alzheimer's disease. It turned out that the mutation protects the brain from the decay of synapses, the occurrence of the clusters of the protein of the Tau Protein.
The defense mechanism turned out to block the immune signal route called CGAS-Sting. This route is usually active during viral infections, but in case of Alzheimer's disease, it operates chronically and too, causing inflammation and damaging brain cells. The Mutation of the Mutation weakens this reaction, reducing the inflammatory background of the brain tissue.
Pressure of CGAS-Sting has had a similar effect, reducing inflammation and slow down degenerative processes. According to the study, the mutation, the mutation, cannot be introduced into a person, but the impact on this immune path can become a new therapeutic strategy.
The group now studies whether this mechanism operates in other neurodegenerative diseases. The study confirms the main role of inflammation in the development of Alzheimer's disease and indicates the need to take into account the genetic characteristics of patients when choosing treatment tactics.
Translation of: Euromedia24.com
