Stanford University may have a cure for Alzheimer's disease

A drug which boosts the brain's immune response may prevent or cure Alzheimer's disease, scientists believe

Don't knock mice.  They're very similar to us.  Now excuse me, I'm off to eat some cheese.

Seems more like a possible forestalling than a cure.

Anything that can be done to help those with Alzheimers is a help for sure.

The study, published online Dec. 8 in The Journal of Clinical Investigation, illustrates the importance of microglia and could lead to new ways of warding off the onset of Alzheimer’s disease, which is predicted to afflict 15 million people by mid-century unless some form of cure or prevention is found. The study also may help explain an intriguing association between aspirin and reduced rates of Alzheimer’s.

Microglia, which constitute about 10-15 percent of all the cells in the brain, actually resemble immune cells considerably more than they do nerve cells.

“Microglia are the brain’s beat cops,” said Katrin Andreasson, MD, 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.”

The experiments began in a dish. Isolating viable microglia from the brain is quite difficult. But it’s easy to harvest large numbers of their close cousins, immune cells called macrophages. These cells circulate throughout the body and can be readily obtained from a blood sample. While not carbon copies of one another, microglia and macrophages share numerous genetic, biochemical and behavioral features.

When placed in a dish with soluble A-beta clusters, macrophages drawn from young mice responded calmly, producing recruiting chemicals and not ramping up production of inflammatory molecules. Notably, the output of A-beta-chewing enzymes in these young cells was robust. But macrophages from older mice acted differently: A-beta’s presence incited a big increase in EP2 activity in these cells, resulting in amped-up output of inflammatory molecules and reduced generation of recruiting chemicals and A-beta-digesting enzymes.

This early hint that age-related changes in EP2 action in microglia might be promoting some of the neuropathological features implicated in Alzheimer’s was borne out in subsequent experiments for which Andreasson’s team used mice genetically predisposed to get the mouse equivalent of Alzheimer’s, as well as otherwise normal mice into whose brains the scientists injected either A-beta or a control solution. In both groups of mice, the expected deleterious effects on memory and learning didn’t arise if EP2 within microglial cells was absent, as a result of a genetic manipulation. Blocking microglial EP2 activity significantly improved these animals’ performance on two kinds of standard memory tests: one that assesses how quickly a mouse forgets that it has encountered an object before, and another that rates the mouse’s ability to remember where a food reward is in a maze.