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Blocking inflammation in the brain prevents progression of Alzheimer's
If the inflammatory processes in the brain are stopped, the progression of Alzheimer's disease may be stopped. In a recent study, British scientists at the University of Southampton have shown that blocking brain inflammation in mice with Alzheimer's disease significantly slows disease progression. So far, the detectable inflammatory events in the brain of Alzheimer's patients have been interpreted as a consequence of the disease. It is becoming increasingly clear that these are more of a cause of the neurodegenerative disease. This new finding also opens up promising approaches for the treatment of the previously incurable disease.
The scientists of the University of Southampton have found in their studies in mice that the blocking of a receptor, which is responsible for the regulation of immune cells and thus for the inflammatory reactions in the brain slows the progression of the disease. While it was originally thought that Alzheimer's disease causes the immune response in the brain, the current study shows that inflammation in the brain is the driving force in the development of the disease, the researchers report. "The results suggest that reducing the inflammation could slow the progression of the disease," the university said. The study was published in the journal "Brain".
The inflammatory processes in the brain (green microglial cells) play a key role in the development of Alzheimer's disease. (Photo: University of Southampton) Microglia numbers in the brain of Alzheimer's patients increased
As part of their study, the researchers first examined tissue samples from the brains of healthy people and patients with Alzheimer's disease. They compared the samples of participants of the same age and counted the number of a certain type of immune cells, the so-called microglia. The scientists found that these were significantly more abundant in the brains of Alzheimer's patients than in healthy people. In addition, the activity of the molecules to regulate the number of microglia correlated with the severity of the disease. Based on these results, the scientists then examined the same immune cells in specific mice that had been bred to develop features of Alzheimer's disease. Here, the scientists tested whether blocking the receptor CSF1R, which is responsible for the regulation of microglia, can improve the animals' cognitive abilities. One group of mice were given oral doses of an inhibitor blocking CSF1R, and then the microglial numbers were evaluated. The comparison with the numbers in untreated mice showed that blocking the receptor resulted in a very significant decrease in microglial numbers. In addition, the inhibitor prevented loss of nerve cell communication sites and the treated mice showed less memory and behavioral problems compared to untreated mice, the University of Southampton reports.
Hope for an effective treatment method
The Director of Science Programs at the British MRC (Medical Research Council), Dr. Rob Buckle, commenting on the study's recent findings, said: "It is becoming increasingly clear that inflammation is a major player in a number of neurodegenerative diseases and the new study begins to decode the underlying biological processes." Diego Gomez-Nicola of the University of Southampton emphasized that science was about to clearly demonstrate the role of inflammatory processes in the development of Alzheimer's disease. The research director of Alzheimer Research UK, dr. Simon Ridley, added: "This work, looking at the role of the immune system in Alzheimer's disease, suggests that blocking the action of the CSF1R protein could help to limit the harmful effects of inflammation, thus providing protection against symptoms such as memory loss "The next step, working with industry partners, is to develop and test safe and appropriate medicines to see if this works for people. It is important that a certain number of microglia be preserved, as they are needed for the normal functioning of the immune system in the brain. The blocking of CSF1R therefore only had to reduce excess microglia. The research team hopes that current results can contribute to the development of effective treatment for Alzheimer's disease. (Fp)