Viral Alzheimer's
Alzheimer's disease can be caused by the herpes virus, scientists say
Biologists and physicians have found new hints that Alzheimer's disease can be directly caused or provoked by various pathogens, such as the herpes virus or microbes, according to an article published in the journal Neuron (Readhead et al., Multiscale Analysis of Independent Alzheimer's Cohorts Finds Disruption of Molecular, Genetic, and Clinical Networks by Human Herpesvirus).
"We didn't try to find anything like this – initially we were just checking whether any existing medications could help people with Alzheimer's disease. Suddenly, our algorithm began to find extremely unusual "patterns" in the data linking her to viruses." – says Joel Dudley from Icahn School of Medicine in New York (in a press release Unusually high levels of herpesviruses found in the Alzheimer's disease brain – VM).
The Silent Strangler
In September 2015, British doctors discovered, studying the brains of people who died from mad cow disease, that Alzheimer's disease can actually be transmitted from one person to another by "infecting" their nervous tissue with foreign prions.
Prions are "tangles" of tangled and improperly assembled protein molecules that accumulate in the nerve cells of sick people, and, as it turned out, are able to stimulate the appearance of beta-amyloid plaques in the neurons of healthy people when they enter their blood and brain.
This was the first time that doctors faced the fact that Alzheimer's disease can be contagious. As scientists discovered two years ago, some pathogenic bacteria can be the carrier and source of prions. In addition, biologists have found out that prions can be part of the immune system that protects cells from microbes and other pathogens.
Dudley and his colleagues found another hint of the contagiousness of Alzheimer's disease, and uncovered another of its pathogens – two specific strains of the herpes virus, studying how various drug molecules created to treat other diseases will affect the neurons of patients.
It helped them that recently all scientists involved in the study of Alzheimer's disease joined forces and began publishing all the data, including information on the levels of gene activity, in three large open databases. This allowed Dudley and his colleagues to quickly check which DNA regions associated with the accumulation of beta-amyloid plaques could be affected by thousands of existing drugs.
Uninvited guests
The further the scientists analyzed the data, the more it seemed to them that they were looking for a cure not for Alzheimer's disease, but for herpes – the stronger the drugs acted on the virtual brains of patients, the more they looked like antiviral drugs that prevented certain types of pathogens from "sticking" to cells and penetrating inside them.
This led Dudley and his team to check whether viruses were present in the brains of people suffering from Alzheimer's disease. As it turned out, large amounts or traces of two specific strains of the herpes virus – HHV-6A and HHV-7 - were present in the nervous tissue of its carriers. As a rule, the more viral particles were present in the brain, the more beta-amyloid was contained in its cells.
There were several reasons for this at once. First, cells produce these proteins to fight herpes and other viruses. Secondly, the virus itself provokes a similar reaction, enhancing the work of genes associated with the production of APP and beta-amyloid, and suppressing the synthesis of short RNA molecules that serve as a natural "brake" of innate immunity.
Dudley and his colleagues tested this idea by artificially suppressing the synthesis of one of these chains, miR-155, in the body of several mice predisposed to the development of Alzheimer's disease. This procedure accelerated the accumulation of beta-amyloid plaques in their neurons, which confirmed the suspicions of scientists.
As Dudley emphasizes, he does not believe that the herpes virus is the main and only cause of the development of Alzheimer's disease, however, changes in the work of neurons that occur during the fight against it serve as the main trigger for its development. Further experiments with HHV-7 and HHV-6, according to him, will help to understand how to stop this process, which is very important, given that almost all inhabitants of the planet are infected with herpes.
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