Genetic techniques were used to stop the production of p38 in the microglia in early-stage mouse models of AD, which is the major immune cell type within the brain. Then they tested the effects of this to determine if it would alter the trajectory of amyloid plaque formation. The team reports that while the plaques themselves were not affected the amount of microglia in proximity to the plaques was decreased, which suggests that suppression of microglial p38 may affect their interactions with certain aspects of Alzheimer’s disease pathology.
Currently, there are some classes of anti-inflammatory drugs that include p38 inhibitors under clinical development which have shown promising results during recent human clinical trials. But it is important to note that it is not clear at what phase during the disease process that these p38 inhibitors should be administered, or whether or not the long-term suppression of p38 is harmful. Findings from this study suggest that early inhibition might alter the interactions between microglia and Alzheimer’s disease pathology, and the researchers report that thus far long-term suppression of p38 does not appear to cause any noticeable adverse effects.
