Experiments removing Ephexin5 protein prevented deficits in animal models of the memory–robbing disease.
In experiments with a protein called Ephexin5 that appears to be elevated in the brain cells of Alzheimer’s disease patients and mouse models of the disease, Johns Hopkins researchers say removing it prevents animals from developing Alzheimer’s characteristic memory losses.

In a report on the studies, published online March 27 in The Journal of Clinical Investigation, the researchers say the findings could eventually advance development of drugs that target Ephexin5 to prevent or treat symptoms of the disorder.

“Ephexin5 is a tantalizing pharmaceutical target because in otherwise healthy adults, there’s very little present in the brain,” says Gabrielle L. Sell, a graduate student at the Johns Hopkins University School of Medicine. “That means shutting off Ephexin5 should carry very few side effects,” adds Sell, who works with Seth S. Margolis, PhD, assistant professor of biological chemistry and neuroscience.

Their work with Ephexin5 grew out of a paradox about one of Alzheimer’s disease’s defining features, the development of thick plaques in the brain composed of a protein called amyloid beta. Stemming the production of this protein is currently the major focus of efforts to develop new Alzheimer’s treatments, explain Sell and Margolis, but it isn’t the amount of amyloid beta in patients’ brains that correlates best with the severity of symptoms; rather, it’s the loss of so–called excitatory synapses, a type of cellular structure forged between two brain cells.