Neurodegenerative conditions such as Parkinson’s disease and Alzheimer’s involve progressive neuronal loss due to disease-induced damage. An enzyme known as dual leucine-zipper kinase (DLK) plays a key role in this process, telling neurons that are damaged or unhealthy when they should cut their losses and self-destruct. Hence, sparing neurons from DLK is an attractive therapeutic strategy that could slow disease progression.

Past attempts to inhibit DLK’s action in human patients, however, led to unexpected side effects affecting the nervous system, suggesting that DLK also has beneficial effects on neurons and that blocking it indiscriminately is harmful. Now, in a new study published online April 3 in the journal Nature Communications, a group of scientists led by Gareth Thomas, PhD, Associate Professor of Neural Sciences in the Center for Neural Development and Repair at the Lewis Katz School of Medicine at Temple University, describes a more precise way to block DLK in damaged neurons, while preserving its function in healthy neurons.