2 May 2003. In today's Science, researchers report that
mutations in the protein dynein-the motor that drives the
transport of large molecules from the synaptic terminal back to
the neuron’s cell body-can lead to forms of neurodegeneration
reminiscent of motor neuron diseases such as amyotrophic lateral
sclerosis (ALS). This is not the first evidence implicating
axonal transport in neurodegenerative disease. Loss or
interference with the protein dynactin, a component of the motor
complex, has previously been shown to result in poor retrograde
transport and the complete loss of axons in mice (see ARF
related news story). Axonal transport is also implicated in
Alzheimer’s (see ARF related news story; also ARF story). Now, a
multinational collaboration led by Elizabeth Fisher at the
National Hospital for Neurology and Neurosurgery in London,
U.K., reports that Legs at odd angles (Loa) and Cramping 1
(Cra1), two chemically-induced mutations that cause progressive
loss of locomotor function, are actually point mut