Inflammation Drives Tau Damage in Alzheimer's

A study published in Nature explored the role of the protein complex called the NLRP3 inflammasome in Alzheimer's and frontotemporal dementia (FTD), reports Medical News Today . The research characterized how tau protein changes under the influence of inflammation processes from the brain's immune system. Normally, tau proteins help stabilize the skeleton of the nerve cell or neuron, but in Alzheimer's and FTD, the proteins experience chemical changes that make them detach from the skeleton and clump to each other, eventually causing the cell to die. This effect is induced by a process called hyperphosphorylation, which changes the chemical composition and behavior of the protein molecules. Hyperphosphorylation involves the protein molecule's saturation with added phosphate groups, and the researchers discovered the NLRP3 inflammasome activates the enzymes that saturate the tau proteins with phosphate, so that they detach from the cell skeleton and clump. Earlier research had already identified NLRP3 inflammasome as a promoter of beta-amyloid protein accumulation. "Our results support the amyloid cascade hypothesis for the development of Alzheimer's," says University of Bonn Professor Michael T. Heneka. The implication is that the inflammasome is the missing link that bridges the disease processes of beta-amyloid and tau, and Heneka suggests these findings could lead to development of drugs that target tau pathology by altering the immune response.