Alzheimer's, heal yourself!
The amyloid protein that causes Alzheimer's disease itself slows down its development
Kirill Stasevich, Compulenta
The cure for Alzheimer's disease lies in the same protein that causes it: one of the fragments of the beta-amyloid precursor protein suppresses the work of the enzyme responsible for the pathogenic modification of the same protein.
Brain tissue affected by Alzheimer's disease;
amyloid plaques are highlighted in blue and pink. (Photo by Simon Fraser.)
Alzheimer's syndrome (like many other neurodegenerative diseases) begins with the accumulation of protein deposits in the neurons of the brain. Some protein molecules suddenly acquire an alternative spatial conformation, become insoluble and precipitate, which gradually poisons the nerve cell. In the case of Alzheimer's syndrome, one of these proteins is the precursor of beta-amyloid, or ARP.
The reasons for the appearance of pathogenic proteins may be different, but in the case of alzheimer's, the enzyme beta-secretase is often pointed to as one of the main culprits. Naturally, beta-secretase has its own important functions, but among other things, it also splits the precursor of beta-amyloid so that one of the resulting fragments begins to behave badly, forming characteristic amyloid plaques in the brain.
However, the precursor of beta-amyloid has another way of splitting, which does not threaten the development of the disease. And now researchers from the University of South Florida (USA) have found out that another protein fragment formed during "healthy" cleavage helps slow down the production of harmful fragments by beta-secretase – simply because it binds to the enzyme and does not allow it to harm.
In experiments with cell cultures and transgenic mice (a report on them appeared in the journal Nature Communications), a reduced level of a "healthy" fragment of the ARP protein stimulated the accumulation of amyloid deposits and the appearance of amyloid plaques. According to the authors, Alzheimer's syndrome may just occur due to a disturbed balance of different cleavage products of the beta-amyloid precursor. At the same time, a reduced level of the fragment suppressing beta-secretase is not necessary at all: the enzyme itself can mutate in such a way that it loses the ability to bind to the suppressing fragment. Accordingly, we can talk about new areas of work for those who develop drugs against Alzheimer's syndrome: you either need to learn how to increase the level of the fragment that inhibits the work of dangerous beta-secretase, or replace it with a synthetic retarder molecule that will bind to a dangerous enzyme.
Prepared based on the materials of the University of South Florida:
USF researchers find that Alzheimer’s precursor protein controls its own fate.
Portal "Eternal youth" http://vechnayamolodost.ru12.04.2012