SMA is caused by a deficiency of the survival of motor neuron (SMN) protein. This is also reported to be an exacerbating factor in the development of ALS.
They show that:
Mutant SOD1 alters the sub-cellular localization of the SMN protein, preventing the formation of nuclear ‘gems’ by disrupting the recruitment of the protein to Cajal bodies. Overexpressing SMN in mutant SOD1 mice, a model of familial ALS, alleviates this phenomenon, and significantly mitigates the loss of motor neurons in the spinal cord.