“Most people probably think that inflammation in the brain is something bad and that you should inhibit the inflammatory system in case of illness. But inflammation doesn’t just have to be negative,” explained Joana B. Pereira, a researcher at Lund University and Karolinska Institute.

A new study demonstrates that a certain type of activation of the brain’s own immune cells, microglia cells, triggers inflammatory protective mechanisms in the immune system. Microglia cells can either slow or drive disease progression in neurological diseases depending on how they’re activated. Researchers at Lund University and Karolinska Institute explored how these cells can be triggered to slow down Alzheimer’s disease.

The findings are published in the journal Nature Aging in an article titled, “Microglial activation protects against accumulation of tau aggregates in nondemented individuals with underlying Alzheimer’s disease pathology.”

“The role of microglia in tau accumulation is currently unclear but could provide an important insight into the mechanisms underlying Alzheimer’s disease (AD),” wrote the researchers. “Here, we measured the microglial marker soluble TREM2 and the disease-associated microglial activation stage 2 markers AXL, MERTK, GAS6, LPL, CST7, SPP1, and CSF1 in nondemented individuals from the Swedish BioFINDER-2 cohort who underwent longitudinal tau-positron emission tomography (PET), amyloid-PET, and global cognitive assessment.”

One of the proteins that sits 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 can instead be protective.

The TREM2 receptor seems to sense residual products of disintegrating cells in the brain, causing it to be triggered. When TREM2 is activated in people with Alzheimer’s, the researchers found that less of the thread-like structures formed by the protein tau accumulate in the 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,” said Oskar Hansson, MD, PhD, professor of neurology at Lund University and senior physician at Skåne University Hospital.

Hansson thinks that the results of the study are particularly interesting, given that several pharmaceutical companies are now developing antibodies that can activate TREM2 in particular, and he hopes for a future treatment method for Alzheimer’s disease.

“In addition to trying to find therapies to reduce the proteins beta-amyloid and tau, I see this as a third treatment principle. Perhaps in the future patients can receive a cocktail of drugs that, in addition to reducing beta-amyloid, also boost TREM2 antibodies and thus slow down the course of the disease,” concluded Hansson.

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