Theresa Bartels

Abstract Neurodegeneration shows regional and cell-type-specific patterns in ageing and disease1, but the underlying mechanisms for cell-type-specific neuronal losses remain poorly understood. Previous studies have shown that upper cortical layer thinning occurs in progressive human multiple sclerosis (MS) and that cortical layer 2 and layer 3 (L2/3) excitatory neurons (L2/3ENs) that express CUT-like homeobox 2 (CUX2) are selectively vulnerable to degeneration2.

Abstract Cortical GABAergic interneurons generated in the ventral developing brain travel long distances to their final destinations. While there are examples of interneuron migration in the neonatal human brain, the extent of postnatal migration across species and how it contributes to cortical interneuron composition remains unknown.

1 INTRODUCTION Myelin, the insulating sheath that surrounds neuronal axons, is produced by oligodendrocytes (OLs) in the central nervous system (CNS). It is an evolutionary innovation, which first appears in vertebrates above jawless fishes, enabling more rapid transmission of nerve impulses at reduced axon diameter (Stadelmann et al., 2019), both critical to house a larger number of neurons and hence greater brain complexity (Freeman and Rowitch, 2013).