A study is predicated on the idea that a number of anti-inflammatory drugs might work well as Alzheimer's disease (AD) treatments.

The Sanders-Brown Centre on Ageing at the University of Kentucky's Linda Van Eldik, PhD, released an article in PLOS ONE.

This investigation focused on the p38 protein. This protein has been investigated in numerous labs as a potential target for the creation of drugs to treat neuroinflammatory diseases like Alzheimer's.

In order to halt the synthesis of p38 in the main immune cell type in the brain, the microglia, Van Eldik and her team employed genetic approaches.

They investigated whether this might affect the trajectory of amyloid plaque production, a crucial aspect of AD pathology, in experimental models.

The proportion of microglia around the plaques was reduced, despite the fact that the plaques themselves were unaffected.

This finding suggests that microglial p38 reduction may have an impact on how these microglia interact with various components of AD pathogenesis.

P38 inhibitors, which are now undergoing clinical development and have produced positive results in recent human clinical trials, are among the classes of anti-inflammatory medications.

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.

The findings reported by the Van Eldik lab indicate that early inhibition of p38 may be able to alter interactions between brain immune cells and AD pathology, and they suggest that long-term suppression of p38 does not cause noticeable adverse effects.