Polyglutamines stop traffic: axonal transport as a common target in neurodegenerative diseases

In this issue of Neuron, two papers provide evidence that polyglutamine (polyQ) proteins disrupt axonal transport. Gunawardena et al. show that normal levels of huntingtin are required for proper axonal transport in Drosophila. In addition, expression of expanded polyQ proteins disrupts axonal transport in larval neurons. Szebenyi and colleagues find that polyQ proteins directly inhibit fast axonal transport using axoplasm from the squid giant axon and suggest that axonal transport defects may be a common feature of polyQ disease pathogenesis.