The team zeroed in on a protein known as p38. Upon halting the production of this protein in brain immune cells, researchers found a decrease in the concentration of these cells around amyloid plaques—a primary AD pathology component—implying the possibility of altering interactions with AD elements.

Researchers at the University of Kentucky´s Sanders-Brown Center on Aging tested its effects in a mouse model in AD´s early phase to determine whether it would alter the trajectory of formation of amyloid plaque, one of the components of the disease.

While the plaques themselves were not affected, the amount of microglia in proximity to these plaques was decreased, suggesting that suppression of microglial p38 may affect their interactions with aspects of AD pathology.

Some classes of anti-inflammatory drugs include p38 inhibitors, which are currently under clinical development and have shown encouraging results during recent human clinical trials.

However, it is still not clear when during the disease process these p38 inhibitors should be administered and whether long-term suppression of p38 is harmful.

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