Memory, Cognition in Mice with Alzheimer’s Improve When Inflammatory Cells Reduced, Researchers Say

Memory, Cognition in Mice with Alzheimer’s Improve When Inflammatory Cells Reduced, Researchers Say
Researchers have successfully reduced the levels of inflammatory cells in the central nervous system linked to inflammation using pharmacological drugs. This decrease translated into improved memory, cognition, and neuronal survival in mouse models of Alzheimer’s disease. The research paper, “Eliminating microglia in Alzheimer’s mice prevents neuronal loss without modulating amyloid-β pathology,” was published in the journal Brain. Neuroinflammation, along with amyloid-β plaque and tau neurofibrillary tangle deposition, is considered a key hallmark of Alzheimer’s disease. This inflammation is attributed to reactive astrocytes and abnormally activated microglial cells, which in normal circumstances act as the main immune defenses in the central nervous system, but in Alzheimer’s patients, turn against healthy tissue and are present in high levels among amyloid plaques, suggesting a possible implication of these cells in Alzheimer’s development. In healthy mice, microglia depend on colony-stimulating factor 1 receptor (CSF1R) signaling for survival. Earlier research revealed that pharmacological inhibition of this receptor leads to the rapid elimination of most microglial cells in the central nervous system. Researchers at the University of California, Irvine (UCI), studied whether activated microglial cells in Alzheimer’s disease are also dependent on this receptor and, if so, how they contribute to disease development. Researchers treated mouse models of Alzheimer’s with a small molecule, pexidartinib (PLX3397), a selective CSF1R inhibitor that is currently in several Phase 2 on
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