Viruses and beta-amyloid
Herpes corona became the germ of Alzheimer's disease in mice
Viral particles gave rise to the aggregation of amyloid, the molecules of which stuck to their surface
Polina Loseva, "The Attic"
An international group of scientists has found an explanation for why herpes often accompanies the appearance of amyloid plaques in the brain. It turned out that viral particles work as a crystallization center, triggering the adhesion of beta-amyloid molecules. Another widespread virus affecting the human respiratory system may have a similar property.
Many scientists consider infection, bacterial or viral, to be one of the causes of the development of Alzheimer's disease. The suspects include, for example, the herpes virus: its presence in the human body correlates with the subsequent appearance of amyloid plaques in the brain – clusters of improperly folded beta-amyloid protein molecules. They accumulate in the nervous tissue and lead to the death of neurons and the destruction of connections between them. However, exactly how infectious agents provoke the appearance of amyloid plaques is not very clear.
In his article (Ezzat et al. The viral protein corona directs viral pathogenesis and amyloid aggregation), published in the journal Nature Communications, a group of researchers put forward a new assumption: viral particles can serve as one of the triggering factors. Being unable to reproduce outside the cells, they nevertheless actively interact with the environment, traveling through the intercellular space. Proteins from blood and tissue fluid adhere to them, forming a protein crown.
Drawing from the press release of Stockholm University Coat of proteins makes viruses more infectious and links them to Alzheimer's disease – VM.
In a conversation with the press service of Stockholm University, the lead author of the study, Karim Ezzat, compared this process to dipping a tennis ball into a bowl of cereal with milk. "The ball is instantly covered with sticky particles," Ezzat described, "which remain on it when you take it back out." It is possible that beta-amyloid molecules turn out to be part of the protein crown, which thus receive a support for aggregation.
In vitro experiments have confirmed that herpes particles catalyze (that is, accelerate) the growth of amyloid aggregates and do this the more actively the cleaner the solution. In blood serum containing many different proteins, amyloid aggregates grow much slower in the presence of the virus – probably due to competition for binding to the surface of the particle.
By itself, the idea that infections can contribute to the development of Alzheimer's disease is far from new. The search for candidates continues, among them there are not only the herpes virus, but also bacteria. Infection is usually considered as one of the reasons for the release of beta-amyloid by cells: it is believed that it can act as a defense against the pathogen. Now, scientists note that regardless of whether the infection causes the production of beta-amyloid, viral particles can additionally provoke its aggregation. If this is the case, then almost 70% of people on the planet who secretly or openly carry the herpes virus are at risk of developing Alzheimer's disease.
In addition, the researchers found similar properties in another common pathogen – respiratory syncytial virus. During the first two years of life, it infects 90% of children, and subsequently manifests itself in the form of weak local symptoms of a cold. The particles of this virus also accelerated the aggregation of amyloid in vitro, but another one – islet amyloid polypeptide, which occurs in the pancreas and is associated with the development of type 2 diabetes (insulin-dependent). So we can be significantly indebted for our age-related diseases to viruses, whose neighborhood we most often do not suspect.
Portal "Eternal youth" http://vechnayamolodost.ru