Mouse Study Reveals Blocking Receptor in the Brain’s Immune Cells Reverses Alzheimer’s

Mouse Study Reveals Blocking Receptor in the Brain’s Immune Cells Reverses Alzheimer’s

shutterstock_183116927A Stanford University School of Medicine study recently published in the Journal of Clinical Investigation, entitled “Prostaglandin signaling suppresses beneficial microglial function in Alzheimer’s disease models,” indicate that microglia impairment may be under the cause of Alzheimer’s disease.

The cause of Alzheimer’s disease (AD) is assumed to arise from an over accumulation of amyloid plaques (AB42), which trigger inflammation and tau hyperphosphorylation, leading to synaptic and neural loss. This process ultimately causes the cognitive decline found in AD patients.

Microglia, are the immune cells of the central nervous system responsible for maintaining normal neural function. However, recent evidence shows that in Alzheimer’s disease, microglial functions are progressively impaired, causing synaptic and neuronal loss.

In order to understand the underlying molecular mechanisms that may be implicated in the microglial dysfunction found in AD patients, a team of researchers led by Katrin Andreasson, MD, Professor of Neurology and Neurological Sciences at Stanford University, evaluated mice models that recapitulate microglial responses to AB peptides.

Results determined that blocking the action of a single molecule (a gene that encodes PGE2 receptor EP2) found on the surface of microglia works as a potential strategy to restore healthy microglial ability and memory loss, to suppress toxic inflammation, and to prevent other Alzheimer’s disease symptoms.

In a recent press release, Katrin Andreasson, the study’s senior author, said about the results, “Microglia are the brain’s beat cops. Our experiments show that keeping them on the right track counters memory loss and preserves healthy brain physiology.”

“The microglia are supposed to be, from the get-go, constantly clearing A-beta, as well as keeping a lid on inflammation,” Andreasson said. “If they lose their ability to function, things get out of control. A-beta builds up in the brain, inducing toxic inflammation.”

“We’d previously observed that if we bioengineered mice so their brain cells lacked this receptor, there was a huge reduction in inflammatory activity in the brain,” Andreasson concluded in the press release.

Findings from this study are encouraging in a preventive progression perspective for AD, since, more than indicating that the receptor EP2 suppresses the beneficial microglia functions, the researchers found that the inhibition of the Eps immune pathway may restore healthy microglial function, which can have important therapeutic implications in the future.

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