In July, we learned that microglia can stop working and that they may be implicated in Alzheimer's. We don't often hear the word "microglia" in everyday parlance. So, a quick refresher may be in order. Microglia are an immune cell resident in the brain and spinal column. They are macrophages which surround and consume cellular trash such as dead cells, pathogens and anything that doesn't register as healthy cells that belong there. Some macrophages can increase inflammation and others have anti-inflammation properties. Microglia decrease inflammation.
The study in July indicated that microglia may stop working and allow for a build up of detritus in the Central Nervous System which then allowed for Amyloid Beta to reach critical levels. The theory which resulted is that by blocking a receptor called EP2, the microglia could be bumped back into work.
A new study from a different lab has been released. This study examined post-mortem human brains and found an increase in the microglia count in the brains which had Alzheimer's. More microglia would indicate that the bodies were trying to clear the debris and trying to reduce the inflammation. The resulting theory is that by blocking a different receptor, CSF1R, fewer microglia will be produced and there will be an improvement in memory and cognition.
Both studies hope to find a drug which will help reduce Alzheimer's symptoms. The first study looked at genetically engineered mice and the second looked at, I presume, human brains. However, it did use a drug which prevented the production of the receptor in mice brains as well.
Maybe I'm wrong but these two studies seem contradictory. Increase microglia vs decrease microglia. Either way, their results with mice need to be proven in humans before we can determine if either are correct.