Mutations in CLN6 (ceroid-lipofuscinosis neuronal protein 6) cause variant late-onset neuronal ceroid lipofuscinosis (vLINCL), a childhood neurodegenerative disorder (CLN6). Alterations in neurite maturation resulting from a loss of CLN6 interaction with protein CRMP2, which has been implicated in controlling axon number and outgrowth, may contribute to this neuronal pathology []. A link between CLN6 expression and biometal homeostasis has been suggested [].
