Large immune cells in the brain may slow the progression of Alzheimer’s disease. That’s according to a study published today in natural aging.
The brain’s own immune cells are called microglia and are found in the central nervous system. They are big eaters that kill viruses, damaged cells and infectious agents they come across. It has long been known that microglial cells can be activated in different ways in several neurological diseases such as Alzheimer’s and Parkinson’s. Depending on how they are activated, they can both promote and slow the development of the disease. Researchers from Lund University and the Karolinska Institutet have just shown that a certain type of microglial cell activation triggers inflammatory protective mechanisms in the immune system:
“Most people probably think that inflammation in the brain is bad and that you have to suppress the inflammatory system when you’re sick. But inflammation doesn’t just have to be negative,” says Joana B. Pereira, a researcher at Lund University and Karolinska. Institutet who is the 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 disease increases. However, when the protein is activated, it may instead be protective. Namely, the TREM2 receptor appears to detect residual products of cell decay in the brain, causing it to fire. When TREM2 is activated in people with Alzheimer’s disease, researchers found that fewer thread-like structures formed by tau protein accumulate in brain cells.
“This in turn means that the development of the disease is slower and the deterioration of the patient’s cognitive abilities is slowed down,” says Oskar Hansson, professor of neurology at Lund University and chief physician at the University Hospital. from Skåne.
In some animal studies, it has been previously observed that microglial cells can eat tau proteins and thus clean up what is abnormal in the brain. Oskar Hansson thinks this might be behind what is also happening in this research study, which is being conducted in humans. Oskar Hansson also thinks the results of the study are particularly interesting, given that several pharmaceutical companies are currently developing antibodies capable of activating TREM2 in particular, and he hopes for a future method of treating Alzheimer’s disease.
“In addition to trying to find therapies to reduce beta-amyloid and tau proteins, I see this as a third treatment principle. Perhaps in the future, patients will be able to receive a cocktail of drugs that, in addition to reducing beta-amyloid, also stimulate TREM2 and thus slow the progression of the disease,” concludes Oskar Hansson.
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Material provided by Lund University. Note: Content may be edited for style and length.
