Alterations in CRMP2 activity have been implicated in a number of neurological diseases including Alzheimer’s disease, where aggregates of hyperphosphorylated CRMP2 have been found in neurofibrillary tangles, and have been hypothesized to contribute to the death of Cln6 mutant neurons in culture [7–11]. Here, DPYSL2 is linked to early-onset autosomal dominant Alzheimer disease.