Bearing in mind the potential role of CRMP2 in regulating mitochondrial dynamics and given the ability of (S)-LCM to normalize mitochondrial morphology and motility under conditions of CRMP2 hyperphosphorylation, it is conceivable that (S)-LCM could be beneficial in treatments of neuropathologies with hyperphosphorylated CRMP2, such as Huntington’s and Alzheimer’s diseases. Here, DPYSL2 is linked to early-onset autosomal dominant Alzheimer disease.