Richard Robitaille, PhD
Restoring In Vivo Glial Functions at Neuromuscular Junctions in ALS: A New Therapeutic Target
The communication between nerve cells and muscles is impaired in ALS and the neuromuscular synapses, nerve contacts that control muscle activity, are destroyed. The destruction of the neuromuscular synapse causes the disconnection between the nervous system and the muscles, leading to paralysis. Our current work will examine the contribution of specialized glial cells at the neuromuscular synapse as they ensure its stability and participate in its repair should injury arise. This research aims at restoring the properties of these glial cells so as to restore their normal function, preventing the destruction of the neuromuscular synapse and maintaining a better control of muscles by the nervous system. This work would also unravel novel avenues to understand the causes of ALS and lead to possible clinical applications.
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Gladstone Institutes, UCSF
Two recently discovered genes that have been associated with both familial and sporadic forms of ALS encode the related proteins TDP43 and FUS cause neuron death in ALS.
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