LMNB1 and Ataxia: Transgenic mice, where lamin B1 cDNA overexpression was specifically targeted to oligodendrocytes (Plp-LMNB1), the cell types that produce CNS myelin, were normal at birth but exhibited profound age dependent motor dysfunction including ataxia and forelimb paralysis by about 8 months of age, reminiscent of the late age dependent onset of the human disease (Figure 2A).