Blocking receptor in brain’s immune cells counters Alzheimer’s in mice, study finds

A Stanford study:

Blocking receptor in brain’s immune cells counters Alzheimer’s in mice, study finds

Brain cells called microglia chew up toxic substances and cell debris, calm inflammation and make nerve-cell-nurturing substances. New research shows that keeping them on the job may prevent neurodegeneration. 

http://med.stanford.edu/news/all-news/2014/12/blocking-receptor-in-brains-immune-cells-counters-alzheimers.html

KEY TERMS

• microglia: a defense cell which regulates brain health, sort of like an immune cell
• EP2: a receptor on microglia
• PGE2: binds to EP2, causing microglia overstimulation and deterioration, which may ultimately lead to brain inflammation (means: prostaglandin E2)
• Aspirin: provides upstream help by preventing certain enzymes from forming molecules which then get converted into PGE2
• A-beta: microglia control the brain levels of this protein...can form clusters toxic to nerve cells--Alzheimer’s plaques

KEY TAKEAWAY

Brain immune system health (via microglia) seems to decline over time. Researchers have found a rather preliminary (in my opinion), but promising, way to restore microglial fitness by silencing microglia receptor EP2, which, when overstimulated, causes microglia deterioration. Researchers have not fully explored the consequences of doing this, it seems (?)

NOTES

Researchers increased the load of A-beta levels in brain cells with and without EP2 receptors and found several different results:

1. Young brain cells did just fine with increased A-beta loads
2. Older brain cells struggled with increased A-beta loads...perhaps as a result of less fit microglia
3. When researchers silenced receptor EP2 on older brain cells, microglial fitness increased

Researchers noted increased EP2 signaling seemed to occur at the same time as microglial production of inflammation, decreased A-beta munching, and so forth.

Previous work in the same lab showed an increase in inflammation when EP2 binded to PGE2.

(Via)