These findings show that changes in the expression of LMNB1 inhibit proliferation and are potentially relevant in understanding the molecular pathophysiology of ADLD [32], suggesting the possibility that a distinct spectrum of “brain laminopathies” might eventually be mapped to missense mutations in LMNB, not in LMNA. Here, LMNB1 is linked to adult-onset autosomal dominant demyelinating leukodystrophy.