Researchers discover 'promising' genetic paths to treat Alzheimer's disease

Researchers from the Massachusetts Institute of Technology, in collaboration with Faculty of Medicine at Harvard University, were able to determine new pharmaceutical goals to treat or prevent Alzheimer’s disease by analyzing large multi -resource data, some of which were taken from people and others from fruit flies. The study, published in the journal “Nature Communications”, reached the disclosure of genetic and cellular pathways, which was not previously linked to Alzheimer’s, including a path related to the recovery of DNA, in a development that can pave the way for completely different therapeutic strategies from the traditional treatments. “amyloid” of the brain. In a part of his study, the team relied on a model of fruit flies, as the researcher Mail Fini, a professor of genetic pathology to Harvard, erased every reserved gene expressed in the neurons of flies, and then saw the effect of this on the timing of the incidence of nerve. Alzheimer’s disease, and this experiment led to the identification of about 200 genes that accelerate the occurrence of symptoms of nerve degeneration, some of which are known as the pre -protein genes of the amyloid, but others were not previously associated with Alzheimer’s. The researchers used new algorithms, which enabled these genes to link with cellular surgeries and certain functional pathways by combining flies -data with genetic data from human brain tissue for people with Alzheimer’s after death. “All the evidence suggests that Alzheimer’s is the result of the overlap of different roads, and for this reason, most current medicines may not have managed to treat it effectively. We will need a set of treatments that target different aspects of this complex disease,” says the lead author of the study, Ernest Frankl, a professor of the Department of Biological Engineering. Frankel adds that even if the ‘amyloid’ hypothesis is correct, it may not be sufficient to explain all cases. Therefore, the search for other factors may be the key to combating, or even reflecting the course of the disease. RNA modification focused on the two cells that the analysis showed that they were linked to Alzheimer’s disease. The first cut, called ‘RNA’, says that the loss of a Mepce or HNRNPA2B1 genetic loss increases the environment of neurons to damage due to the entangled ‘protein associated with the disease. This was confirmed by experiments on fruit flies and human neurons taken from stem cells. The Mepce gene produces a protein that contributes to the stabilization of a molecular complex in the cell nucleus called “7SK”, a complex that plays a role in regulating genes, ie to determine when and how genes are used within the cell. Through this organizational role, the Mepce gene contributes to maintaining a balance in genetic activity, especially those responsible for the growth and functions of neurons. The study, conducted by the Massachusetts Institute researchers, revealed that the lack or disruption of this gene activity increases the ability of nervous cells to affect the toxic “Tao” protein, which is one of the basic features of the development of Alzheimer’s disease, which indicates that this no important preventative role play against the nerve. While the HNRNPA2B1 Jin produces a protein, its most important function is to handle RNA in the cell nucleus as it is involved in processes such as transferring this acid from the core to cytoplasm and regulating how it is translated into protein. This protein is a substantial element in what is known as ‘controls to copies’, that is, how genetic information is used after being written in the form of an irrigated DNA. The researchers linked the imbalance of this gene and the poor ability of neurons to handle the pressure as a result of the presence of “Tao” tangles, making the process of nerve deficiency faster. This gene is a possible new treatment goal; Improving the activity or limiting its disruption can reduce the risk of infection or the development of Alzheimer’s disease. The path of DNA recovery, as for the second lane, known as the ‘DNA repair road’, in which the researchers focused on the genetic notch1 and CSNK2A1, known for their roles in regulating cell growth, but the new is to discover that their absence leads to the accumulation of DNA through two different mechanisms, which in turn lead to nervouseg. The researchers say that the Notch1 -no one of the most important genes that plays an important role in regulating and distinction of cell growth, that is, how stem cells turn into specialized cells that perform specific functions within the body. This gene work as part of the cellular “Nootpad”, a system of communication between cells that direct the cellular decisions process during the stages of the development of the fetus, as well as in the maintenance of tissues in adults. The Notch1 no contributes to the regulation of the growth and renewal of neurons, and it also plays a role in stabilizing the environment around the neurons. Recent studies indicate that the disruption of this gene can lead to the accumulation of damage to the DNA in the nerve cell, which makes it more vulnerable to damage and death, a mechanism that believes it contributes to the development of degenerative diseases such as Alzheimer’s. Although this gene was previously known for its role in the growth of cells and cancer, its association with DNA reforms within neurons is a new discovery, which opens the door for its focus in the investigation into Alzheimer’s treatments. CSNK2A1 has been coded to produce a sub -unit of an enzyme known as “kiniz, the second case of protein”, an enzyme responsible for adding phosphate groups to different proteins in the cell, a process known as “phosphorous”, and this process is essential to organize a large number of self -function, organize. The protection of neurons is characterized by this gene is that it is very active in most types of cells, and plays an important role in maintaining the stability of proteins and organizing their interaction. In recent years, research has discovered that CSNK2A1 can play an important role in the brain, especially in the protection of neurons against damage. In the new study, the researchers found that its disruption is linked to a defect in the process of repairing the DNA within the neurons, which exposes them to decline and death. After these goals have been set, researchers hope to work with other laboratories to investigate whether the medicines aimed at improving the health of neurons. Franklk, and other researchers, use the Alzheimer’s patients to generate neurons that can be used to judge such medication. The search for Alzheimer’s medicine will be largely accelerated when good and powerful experimental systems are available. He explains: “We approach a stage in which two many innovative systems meet, one of which is better experimental models that depend on stimulating stem cells, and the other the computer models that enable us to integrate large amounts of data. If these two systems are mature at the same time, I think we will reach some scientific breakthroughs.”