An experimental drug can reduce the toxic changes in tau proteins known to damage neurons in brains with Alzheimer’s disease, researchers from Yale School of Medicine and Johns Hopkins University report. While much research related to Alzheimer’s disease has concentrated on identifying ways to reduce the buildup of amyloid plaques — which form when sticky protein fragments known as amyloid beta collect in the brain — the new study focuses on slowing harmful changes in a molecule called tau, which can lead to tangles and neuronal degeneration. In particular, the phosphorylation of tau, in which phosphate groups are added to the tau peptide, is a key early event that triggers neurological damage, the researchers found. The research suggests that inflammatory processes in the aging brain contribute to the phosphorylation of tau in the common, late-onset form of Alzheimer’s disease. “We were able to reduce the phosphorylation of tau by restoring regulatory actions that are lost with age and inflammation,” said senior author Amy Arnsten, the Albert E. Kent Professor of Neuroscience at Yale School of Medicine and professor of neurobiology and psychology in Yale’s Faculty of Arts and Sciences. “The mechanism of protection is different from other approaches undertaken so
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