Possible Missing Link in Alzheimer's Pathology Identified

A study at the University of Alabama at Birmingham (UAB) in Science Translational Medicine appears to characterize a missing mechanism in Alzheimer's disease pathology, reports Scientific American . Accrual of beta-amyloid triggers a receptor that responds to norepinephrine, boosting the activity of an enzyme that activates tau and makes neurons more susceptible to it. "We really show that this norepinephrine is a missing piece of this whole Alzheimer's disease puzzle," says UAB Professor Qin Wang. She notes this can explain the failure of previous drug treatments, which mainly target the elimination of beta-amyloid. Whereas beta-amyloid alone only kills neurons in very high doses, the addition of norepinephrine means only 1 percent to 2 percent as much beta-amyloid is needed to destroy brain cells under lab conditions. Wang adds that the drug idazoxan — originally developed to treat depression — appears to target this same pathway, and she seeks to promote larger clinical trials of the medication as a treatment for early-stage Alzheimer's.