A decade ago, University at Buffalo researchers shed some light on an enduring neuroscience mystery: How exactly does a mutated huntingtin protein (HTT) cause Huntington’s disease?
They found that HTT is something like a traffic controller inside neurons, moving different cargo along neuronal highways called axons in concert with other proteins key for cellular function and survival. Reduce the amount of non-mutant HTT and you’ll create the neurological equivalent of traffic jams and roadblocks.
Now, the researchers have learned more about what can control the traffic-controlling HTT.
They found that two specific signaling proteins, GSK3ß and ERK1, were expressed more in the neurons of Huntington’s disease patients, so they prevented them from functioning in the neurons of fruit fly larvae that have…