Zic deficiency in the cortical marginal zone and meninges results in cortical lamination defects resembling those in type II lissencephaly. (1/8)

Ethnically diverse causes of Walker-Warburg syndrome (WWS): FCMD mutations are a more common cause of WWS outside of the Middle East. (2/8)

Midbrain-hindbrain involvement in lissencephalies. (3/8)

Neurons generated from APP/APLP1/APLP2 triple knockout embryonic stem cells behave normally in vitro and in vivo: lack of evidence for a cell autonomous role of the amyloid precursor protein in neuronal differentiation. (4/8)

GPR56-related bilateral frontoparietal polymicrogyria: further evidence for an overlap with the cobblestone complex. (5/8)

G protein-coupled receptor 56 and collagen III, a receptor-ligand pair, regulates cortical development and lamination. (6/8)

Cobblestone lissencephaly: neuropathological subtypes and correlations with genes of dystroglycanopathies. (7/8)

Identification of mutations in TMEM5 and ISPD as a cause of severe cobblestone lissencephaly. (8/8)