An experimental cancer drug was used to clear away errant inflammatory cells in a mouse model for Alzheimer's, demonstrating potential for improving cognition even though it had no impact on the amyloid beta clusters many believe cause the memory-wasting disease.
A group of investigators at the University of California, Irvine, used a drug called pexidartinib--or PLX3397, now in mid- and late-stage cancer studies--in the animal study, which targeted microglia, inflammatory cells that are spurred by concentrations of amyloid beta. The drug inhibits signaling of microglial surface receptors, known as colony-stimulating factor 1 receptors, which is required for the proliferation of the inflammatory cells.
Once the inflammatory cells were swept away, the investigators noted a reduction in neuron death and an improvement in memory and cognition in the mice. And the fact that they could do that without having an impact on amyloid beta is likely to further fuel the long, ongoing debate over triggers for Alzheimer's.
The main role for microglia in healthy tissue is providing an immune response in the central nervous system. But the researchers say that in a diseased state like Alzheimer's they become go "rogue," causing inflammation.
"Our findings demonstrate the critical role that inflammation plays in Alzheimer's-related memory and cognitive losses," said Kim Green, an assistant professor of neurobiology & behavior. "While we were successful in removing the elevated microglia resulting from beta-amyloid, further research is required to better understand the link among beta-amyloid, inflammation and neurodegeneration in Alzheimer's."
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