Alzheimer's disease and interferon
Interferon turned out to be the driver of Alzheimer's disease
Svetlana Maslova, Hi-tech+
Scientists have found that type I interferon provokes the development of the main symptom of dementia — cognitive impairment. Blocking this molecule has demonstrated the ability to reverse symptoms. Now it is necessary to assess the potential of a promising treatment strategy for a person.
The most common form of dementia, Alzheimer's disease, leads to a gradual impairment of cognitive functions — memory, concentration, learning. Scientists do not fully understand all the mechanisms that lead to these problems. A new work by a team from Baylor College of Medicine reveals one of them: researchers have found that the inflammatory molecule interferon type I (IFN-I) begins to be abnormally produced in the brain in Alzheimer's disease and is a driver of cognitive impairment.
Article by Roy et al. Concerted type I interferon signaling in microglia and neural cells promotes memory impairment associated with amyloid β plaques is published in the journal Immunity – VM.
The current understanding of the nature of Alzheimer's disease is that amyloid and tau proteins that are toxic to neurons may be less of a problem compared to a pronounced inflammatory reaction in the brain. In previous studies, scientists have found that certain types of amyloid plaques activate immune cells in the brain, microglia, which then begin to produce interferon. This, in turn, triggers a cascade of inflammatory reactions leading to the loss of synapses — a key "tool" for communication of neurons.
Now the study shows that type I interferon plays a crucial role in this process.
Subsequent experiments demonstrated the potential of blocking interferon receptors (IFNAR) in mouse models of Alzheimer's disease — cognitive symptoms in old laboratory animals were reversed, even despite the preservation of amyloid plaques.
Scientists have also discovered different functions of interferon signals for different types of brain cells. This means that the complete mechanism of synapse loss requires coordinated actions of different cells.
Further research will allow the development of new therapeutic strategies targeting type I interferon as a potential treatment for human Alzheimer's disease. Currently, only symptomatic treatment is available to patients, which has very limited effectiveness.
Portal "Eternal youth" http://vechnayamolodost.ru