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Perhaps, a remedy for multiple sclerosis has been found
Last reviewed: 22.11.2021
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Each medal has in fact two sides, and in every villain there is always something good. Therefore, probably, it is not surprising that beta-amyloid proteins managed to become the heroes of the day.
Beta-amyloid - this incorrectly packaged protein fragment, which is supposedly responsible for the death of brain cells in Alzheimer's disease - has been able to reverse the symptoms of another incurable autoimmune disease, multiple sclerosis (MS). In any case, in mice.
With multiple sclerosis, the cells of the immune system mistakenly attack the myelin sheath of nerve fibers, which plays the role of an electrical signal insulator. Myelin sheath increases the rate at which electrical impulses spread through the nervous system. Without isolation, communication is disrupted within the nervous system, nerve impulses become entangled or even inhibited, leading to physical and cognitive problems. Starting his research, Lawrence Steinman of Stanford University (USA) was confident that he would be able to show that beta-amyloids significantly increased the damage caused by autoantibodies of multiple sclerosis. After all, beta-amyloids are toxic to neurons (as it seems) and generally prefer to accumulate where the myelin sheath is destroyed.
But life is full of surprises, it easily refutes even the most seemingly solid beliefs. When scientists injected beta-amyloid into the "cavity" of the body of mice, whose immune system was preparing to tear all myelin sheaths, causing complete paralysis, the seemingly imminent death suddenly receded, eliminating the threat of early paralysis, and the functions of the nervous system began to recover!
The experiment was repeated several times, but the result did not change. Moreover, a careful study showed that injections of beta-amyloid reduce the level of circulating immune-signal molecules involved in the formation of inflammation. Thus, scientists conclude that beta-amyloid, apparently, is able to fight with multiple sclerosis, muffling the autoimmune reaction, the "black mark" of this disease.
And what's next? Have we finally found a cure for multiple sclerosis? Not so simple. Although the authors of the paper did not find any evidence that the beta-amyloid introduced into mice is able to accumulate in the brain of animals, the state regulators are likely to fall into a state of shock from the mere thought that it is proposed to use proteins, which are believed to be a disease Alzheimer's. Especially after other research groups have managed to state that beta-amyloid somehow gets from the blood into the brain.
Understanding this, scientists have already begun to look for workarounds, to lay straws. It may be possible to avoid the need for beta amyloids themselves. Thus, it was found that amyloid-like protein alpha-crystallin B, present in large quantities in the lens of the eye, has the same effect on multiple sclerosis. With all resemblance to beta-amyloid, this protein appears to be harmless. But even now it's too early to rejoice - because what works on mice does not necessarily help people. Ahead is a long way. But there is hope!
And now let us ponder a bit about why the "hostile" amyloid turned out to be the means that humanity is hopelessly searching for a very long time. First, we can assume that the amyloid removes the "erroneous" inflammation around the nerve fibers, pushing the immune system to action (for example, it can simply irreversibly block the immune-signal molecules that cause inflammation). Remember, scientists have mentioned that the amyloid itself likes to concentrate in places of attack (inflammation) of the immune system on the nervous tissue? Maybe it's not for nothing? Maybe this is his destiny?
Secondly, the other day there was information that one of the factors of the onset of Alzheimer's disease is an autoimmune mechanism that causes a thickening of the blood vessels of the brain and, as a consequence, the accumulation of amyloids in them. However, it remains unclear why the wrong amyloids generally appeared. Now, looking at the results obtained at Stanford, I would like to assume that both these news are related and the formation of "wrong" amyloids may not be a symptom of the disease, but an attempt by the body to restore order in the economy by protecting itself from an enraged immune system. In fact, no one knows exactly how dangerous amyloid plaques are, just they always have Alzheimer's, but that does not mean that they are the cause of the disease. It may well be (and now for such reasoning, it seems to us, there are all grounds) that these plaques are the consequences of the organism's struggle with something like autoantibodies that destroy the brain. It even sounds more logical ...
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