GPC4 and amyotrophic lateral sclerosis: Together, these findings show that GPC4/6 alterations in patient tissues resemble those identified in the Drosophila models of TDP-43 proteinopathy and suggest that glypican function may also be altered at neuromuscular synapses in ALS, consistent with a recent report of GPC4/6 reduction in SOD1 mice [7].