Potential Alzheimer's Disease Drug Target Identified

In findings with the potential to provide a therapy for Alzheimer's disease patients where none now exist, a researcher at the University of California, San Diego and colleagues have demonstrated in mice a way to reduce the overproduction of a peptide associated with the disease. The study, which showed substantial improvement in memory in an animal model of Alzheimer's disease, was led by Vivian Y. H. Hook, Ph.D., professor of the Skaggs School of Pharmacy and Pharmaceutical Sciences and professor of neurosciences, pharmacology and medicine at the UCSD School of Medicine, together with American Life Science Pharmaceuticals of San Diego. The study will be published in the March 21 edition of the Journal of Biological Chemistry, online March 14.

A hallmark sign of Alzheimer's disease, seen during autopsy of a patient's brain, is the accumulation of amyloid plaque deposits composed primarily of the neurotoxic beta-amyloid (Aβ) peptide which is believed to be a major factor in the cause of the disease. The Aβ peptides are "cut" out from a larger protein called the amyloid precursor protein (APP) and bind together to form plaques in brain regions responsible for memory. One drug strategy to fight Alzheimer's disease is to reduce production of Aβ."We discovered two chemical compounds that inhibit a new enzyme target, leading to reduced production of beta amyloid and improved memory in a mouse model of Alzheimer's disease," said Hook.