The "invisible hat" will not allow Alzheimer's disease to develop?
An international team of scientists, led by Professor Jochen Herms from Ludwig-Maximilian University of Munich, has demonstrated that microglial cells are not only the direct culprits of neuronal death characteristic of Alzheimer's disease, but also destroy neurons under the action of signaling proteins secreted by them.
Microglia is a specialized class of glial (auxiliary) cells of the central nervous system, which are phagocytes that destroy infectious agents and destroy nerve cells. Excessive activation of microglia can lead to pathological processes and, in particular, to the death of neurons, which is believed to be one of the pathological mechanisms of neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease, dementia caused by AIDS, and some others.
Alzheimer's disease affects about 1.2 million people in Germany alone, and about 18 million in the world. Unfortunately, these figures are expected to increase in the near future, especially in developed countries – due to an increase in the average age of the population. Progressive dementia (dementia) in Alzheimer's disease occurs due to the death of brain neurons associated with the formation of insoluble protein aggregates - beta-amyloid plaques. In the vicinity of these plaques, a large number of microglial cells are detected, which monitor signs of degradation of surrounding tissues using complex molecular processes. This fact led scientists to the idea that the possible purpose of aggregation of microglial cells near beta-amyloid plaques is their destruction.
With the help of the latest microscopy methods, Professor Herms' group managed to directly look into the brains of living mice with a model of Alzheimer's disease, additionally genetically modified so that they produced fluorescent forms of proteins specific to neurons and microglia cells. By conducting long-term (up to several months) monitoring of labeled cells, the researchers for the first time visualized the loss of neurons in the brain tissues of living mice. Scientists found that the death of neurons was preceded by activation of microglia.
Professor Herms believes that the damaged nerve cells surrounding the plaques secrete chemical signals that lead to an indirect attack of these neurons by microglial cells, and the role of the signaling molecule is played by the protein fractalikin interacting with receptor proteins on the surface of microglial cells.
In support of Herms' hypothesis, removal of this receptor using genetic techniques prevented the loss of neurons, despite the absence of changes in the formation of amyloid plaques.
According to Professor Herms, the results obtained open up a promising direction in the development of drugs for Alzheimer's disease, the effect of which will be based on slowing the rate of loss of brain neurons due to disruption of the interaction between neurons and microglia.
The article by Martin Fuhrmann et al. "Microglial Cx3cr1 knockout prevents neuron loss in a mouse model of Alzheimer's disease" was published online on March 21 in the journal Nature Neuroscience.
Daria Chervyakova
Portal "Eternal youth" http://www.vechnayamolodost.ru / based on ScienceDaily: Dangerous Custodians: Immune Cells as Possible Nerve-Cell Killers in Alzheimer's Disease.
24.03.2010