The brain’s over-eating immune cells may slow the progression of Alzheimer’s disease. This is demonstrated by a currently published study. Nature Aging.
The brain’s own immune cells are called microglia and are found in the central nervous system. They are big eaters that kill any viruses, damaged cells and infectious agents they encounter. It has long been known that microglial cells can be activated in different ways in many neurological diseases such as Alzheimer’s and Parkinson’s diseases. Depending on how they are activated, they can both sustain and slow disease development. Researchers from Lund University and Karolinska Institutet have now shown that a certain type of activation of microglial cells triggers inflammatory protective mechanisms in the immune system:
“Most people probably think that inflammation in the brain is a bad thing and that in case of illness you should block the inflammatory system. But inflammation doesn’t just have to be negative,” says researcher Joana B. Pereira of Lund University and Karolinska. Institute, first author of the study.
One of the proteins found on the surface of microglial cells is TREM2. When an unusual mutation occurs in this protein, the risk of developing Alzheimer’s increases. However, when the protein is activated it may instead be protective. That is, the TREM2 receptor seems to cause the degraded cells in the brain to be triggered by sensing their residual products. When TREM2 was activated in Alzheimer’s patients, the researchers found that there was less accumulation of thread-like structures formed by the protein tau in brain cells.
“This means that the development of the disease is slower and the deterioration in the patient’s cognitive abilities slows down,” says Oskar Hansson, MD, professor of neurology at Lund University and senior doctor at Skåne University Hospital.
Some animal studies have previously observed that microglial cells can clear abnormalities in the brain by eating tau proteins. Oskar Hansson believes that this may be behind what happened in this human research study. Oskar Hansson also thinks the results of the study are particularly interesting given that several pharmaceutical companies have developed antibodies that can specifically activate TREM2, and he hopes for a future treatment for Alzheimer’s disease.
“Besides trying to find treatments that will reduce beta-amyloid and tau proteins, I see this as a third principle of treatment. Maybe in the future patients can receive a cocktail of drugs that increase proteins as well as reduce beta-amyloid. TREM2 will slow the course of antibodies and thus the disease,” he concludes. Oscar Hansson.
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