Recently, researchers have said that, the predictable narrative of how Alzheimer’s occurs should be upturn by their work. According to the argument of these researchers, they believe development of Alzheimer’s is caused by a very precise form of 2 proteins, which show a critical role in the occurrence of the disease, and these forms must be measured prions, a version of possibly infectious proteins, which replicate themselves by turning their brethren to their misfolded form. Basically, people dealing with Alzheimer’s have their brain filled with rigid along with clumped deposits of the amyloid proteins’ tau and beta, called as tangles and plaques respectively.
It has been noted since so long, that if these deposits are stopped, especially plaques, from occurring or tear them apart, Alzheimer’s can be delayed or prevented. But in recent years, this theory has taken a beating, as anti-amyloid drug has failed multiple times, trial after trial in human beings suffering with Alzheimer’s to slow down the illness. Reportedly, the recent study was conducted by researchers from the University of California, San Francisco, who are arguing by saying that it is not the last stages of amyloid tau and beta, which are causing the disease: it is the prior, like prion types of both proteins playing the role of real culprit.
In this theory, tangles and plaques are importantly just the ‘dead’, sluggish remains of tau and amyloid beta prions. As per one of the researchers, who is also a biochemist and neurologist Stanley B. Prusiner, whose Noble award-winning effort recognized that an entire class of infrequent but generally fatal brain disorders are caused by prions, like scrapie in sheep and Creutzfeldt-Jacob illness in humans. These diseases, caused by prions are essentially, distorted and misfolded type of a protein, which is naturally formed in several mammal species, also known as prion protein.