Alzheimer's and immunity

Immune system protein is linked to the course of Alzheimer's disease

Anna Stavina, XX2 century, based on materials

Gardeners often cut the branches of overgrown trees and shrubs, and this stimulates healthy plant growth. Something similar happens in the brain – periodic "weeding" of the formed connections is useful while the brain is developing. But what if this process continues into adulthood? Researchers from Brigham and Women's Hospital used preclinical models and found that "clearing synapses" may play a role in the development of neurodegenerative diseases. The results of the study published in Science Translational Medicine (Shi et al., Complement C3 deficiency protects against neurodegeneration in aged plaque-rich APP/PS1 mice) contain new information about the relationship between the immune system and the onset of Alzheimer's disease.

As part of the new work, scientists focused on the so-called "Complement C3" (see Complement System) – this molecule participates in the immune response, which is activated in Alzheimer's disease. Previous studies have shown that C3 is also involved in the destruction of some synapses during brain development. But the loss of synapses is also observed in Alzheimer's disease, it is associated with cognitive impairments characteristic of this disease. However, it is still unknown whether blocking the complement cascade, the central part of which is complement C3, can protect against dementia and neurodegeneration in the late stages of Alzheimer's disease.

In a new study, scientists decided to study the effect of C3 deficiency on experimental animals with a model of Alzheimer's disease. It turned out that mice with a congenital deficiency of this protein are protected from age-related synapse loss. In addition, fewer markers of inflammation were found in the brains of animals.

Interestingly, in elderly mice, beta-amyloid plaques characteristic of Alzheimer's disease were present in large numbers, but their cognitive functions were preserved. The animals trained well and performed tasks despite the continued accumulation of beta-amyloid in the brain.

"The formation of beta-amyloid plaques in Alzheimer's disease begins many years before the first signs of memory loss appear. However, managing the immune system's response to the appearance of these plaques can be an excellent therapeutic approach," says one of the authors of the study, Cynthia Lemere from the Ann Romney Center for Neurological Diseases at Brigham and Women's Hospital. – We believe that in the later stages of the disease, neurodegeneration is caused not only and not so much by the presence of plaques, but by the immune response of the body."

Complement C3 is also associated with a number of other diseases, for example, stroke and macular degeneration (macular degeneration). Although the new study has certain limitations – the work of the immune system and life expectancy in mice and humans differ – the discoveries made in the course of work, coupled with the results of previous work, suggest that the control of the C3 complement signaling pathway may become a new therapeutic strategy to combat Alzheimer's disease.

Portal "Eternal youth" http://vechnayamolodost.ru  02.06.2017