With the passage of time and the advent of drastic changes in the generic lifestyle of the common man, many aged individuals are coming under the trap of several diseases, with Alzheimer being the most common one. Biomedical science is continuously working towards new and effective ways of treating Alzheimer’s with gradual developments in the field of neurogenetics. Generally, in the bodies of old people, proteins undergo a cycle of malformation and degradation over a period of time. This is mainly dependent on genetics and mental lifestyle. These changes in protein structures lead to a class of diseases called proteinopathy.
Recently, Morsani College of Medicine (University of South Florida) conducted a study and concluded that one of the causes of dementia is the gathering of tau tangles, which happens because of the secretion of a protein named as β-arrestin2. They disrupt the process of eradication of tau from the brain, which is a neurotoxin. Furthermore, studies also indicated that the component responsible for various dementias, neurotic disorders, and degradation of cognitive abilities could be strategically blocked towards frontotemporal lobar degeneration (FTLD) so that tau clearance can smoothly take place. This neurodegeneration can be prevented by blocking β-arrestin2 oligomers.
People in the age group 45-65 are prone to dementias such as Alzheimer’s and FTLD because of emaciation in the side/front areas of the brain. The former one is characterized by the accumulation of the protein – amyloid-beta (Aβ) or amyloid plaques. This results in neuron deaths, which worsens the condition of the patient. However, some studies also found that accumulation of tau is related to cognitive malfunction as well as ill effects of amyloid plaques. Apart from this, it was noticed that current medications for dealing with Aβ are inefficient for treatments.
Moreover, AD pathogenesis has a relationship with the GPCRs (G Protein-Coupled Receptors) according to the research conducted in the past few years. However, it is unclear how these GPCRs influence neurodegeneration and AD pathogenesis. Previous studies show that β-arrestin2 enhances the production rate of amyloid-beta. This drives researchers to work more on this domain because of direct correlation. β-arrestin2 is a very interesting protein because the monomers of β-arrestin2 help in receptor regulation, but when they are clogged, it results in oligomerization. As of now, scientists need to study more about the intricacies of β-arrestin2 oligomers.
The abnormal tau can also be reduced by a dose of Hsp90 inhibitors. The degradation is regulated as Hsp90 helps the formation of complexes that have a multi-component form. Some researchers also assert that genopathy is one of the few ways to treat neurodegeneration. This is generally done by introducing some molecule specific inhibitors such that tau tangles are cleared without any hindrance. Another effective treatment could be blocking oligomerization of β-arrestin2 so that FTLD-tau can also be prevented.
The conclusion of the studies suggests that the key factor causing this neural problem is beta-arrestin 2, which is responsible for clots that form tau-tangles, leading to Alzheimer’s disease, cognitive dysfunction, and other related disorders.
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