In recent years, a substance called beta amyloid has attracted great attention among scientists. β-amyloid is a normal protein in every human brain, but researchers are not sure why such proteins will coagulate and form deposits in patients with Alzheimer's disease, which is a typical feature of Alzheimer's disease.

Nowadays, more and more research evidence suggests that the toxic form of beta amyloid may not be present in sediments. Instead, the soluble version of this protein may be toxic. Recently, in a research report published in the international magazine JAMA Neurology, scientists from institutions such as Pacific Northwest National Laboratory in the United States have conducted an in-depth analysis of the toxicity characteristics of this soluble β-amyloid protein, which is a difficult problem to solve for now across the industry. The researchers used mass spectrometry to clearly observe the level of this soluble amyloid in the brain.

The researchers analyzed multiple proteins in more than 1,000 brain tissue samples, and then they conduct further researches on 148 brain tissue in which the presence of amyloid deposits was not detected. They found that individuals carrying high levels of soluble β-amyloid protein have a lower rate of cognitive decline than individuals with low levels of soluble β-amyloid protein, which supports the assumption that there is a toxic form of soluble beta amyloid in the brain. However, the classic features of Alzheimer's disease are not 100% related to the protein determinations performed by the researchers, because Alzheimer's disease also has other symptoms like neurofibrillary tangles and problems with contextual memory.

Ever since the first discovery of the association between β-amyloid plagues and dementia in 1906 by researchers Alois Alzheimer, researchers have always been exploring the exact role of β-amyloid plagues in the pathology of Alzheimer's disease, yet it is still unclear. In the first place, such plagues were considered to be occurring incidentally. But as multiple clinical trials aiming at clearing plaque in the brain all failed, scientists come to realize that the role of theseβ-amyloid plaques in the pathogenesis of the disease may need more researches.

In the study mentioned above, mass spectrometry was used, which actually could be employed as a universal tool to determine different forms of amyloid beta, not just insoluble sediments. Further investigations will be conducted later as to what role these beta amyloid proteins are playing in the development of a variety of neurodegenerative diseases, which hopefully would offer some new ideas and hopes for the development of novel therapies for the treatment of Alzheimer's.

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