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 pote
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