Boosting the immune system could offer a new way of treating Alzheimer's Disease, according to a new study.
Researchers at the Stanford University School of Medicine have discovered that the mass die-off of nerve cells in the brains of affected patients could be due to failings in another set of brain cells known as microglia, which resemble those of the immune system.
"Microglia are the brain's beat cops," said Katrin Andreasson, professor of neurology and neurological sciences and the study’s senior author. "Our experiments show that keeping them on the right track counters memory loss and preserves healthy brain physiology."
A study conducted on mice revealed blocking the action of a single molecule on the surface of microglia restored the cells' ability to perform their functions. This reversed memory loss and various other Alzheimer’s-like features in the animals.
Microglia guard the brain against invading bacteria and viruses, combat inflammation, and dispose of dead cells and molecular debris strewn among living cells - including clusters of a protein called A-beta, which can aggregate into Alzheimer's plaques.
If microglia cease to function, this can lead to a build-up of A-beta in the brain, inducing toxic inflammation.
The study provided strong evidence that this deterioration in function was due to the heightened signaling activity of a single molecule that sits on the surface of microglial and nerve cells.
Previous research has shown that this molecule, a receptor protein called EP2, has a strong potential to cause inflammation when activated by binding to a substance called prostaglandin E2, or PGE2.
As microglia are difficult to obtain, the researchers used close relatives - immune cells called macrophages.
They discovered that, when placed in a dish with soluble A-beta clusters, macrophages from young mice performed strongly. However, cells from older mice showed a big increase in EP2 activity, leading to a greater number of inflammatory molecules and fewer A-beta-digesting enzymes.
Blocking microglial EP2 activity significantly improved these animals' performance on two kinds of standard memory tests, the team observed.
Studies have suggested that aspirin can be effective in preventing Alzheimer's onset. This may be due to its role in blocking enzymes that lead to the production of PGE2, which triggers EP2 action. However, further research is needed in this area.
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