Evolution of the mammalian neocortex (isocortex) has been a persisting problem in neurobiology. While recent studies have attempted to understand the evolutionary expansion of the human neocortex from rodents, similar approaches have been used to study the changes between reptiles, birds, and mammals. We review here findings from the past decades on the development, organization, and gene expression patterns in various extant species. This review aims to compare cortical cell numbers and neuronal cell types to the elaboration of progenitor populations and their proliferation in these species. Several progenitors, such as the ventricular radial glia, the subventricular intermediate progenitors, and the subventricular (outer) radial glia, have been identified but the contribution of each to cortical layers and cell types through specific lineages, their possible roles in determining brain size or cortical folding, are not yet understood. Across species, larger, more diverse progenitors relate to cortical size and cell diversity. The challenge is to relate the radial and tangential expansion of the neocortex to the changes in the proliferative compartments during mammalian evolution and with the changes in gene expression and lineages evident in various sectors of the developing brain. We also review the use of recent lineage tracing and transcriptomic approaches to revisit theories and to provide novel understanding of molecular processes involved in specification of cortical regions. J. Comp. Neurol. 524:630–645, 2016. © 2015 The Authors. The Journal of Comparative Neurology Published by Wiley Periodicals, Inc.

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Understanding the architectural principle that shapes the topology of the human connectome at its multiple spatial scales is a major challenge for systems neuroscience. This would provide key fundamental principles and a theory for browsing brain’s networks, to ultimately generate hypothesis and approach to which extent key structures might impact different brain pathologies. In this work, we propose the hypothesis that the centrality of the different brain nodes in the human connectome is a product of their embryogenic age, and accordingly, early-born nodes should display higher hubness, and viceversa for late-born nodes. We tested our hypothesis by identifying and segmenting eighteen macroregions with a well-known embryogenic age, over which we calculated nodes’ centrality in the structural and functional networks at different spatial resolutions. First, nodes’ structural centrality correlated with their embryogenic age, fully confirming our working hypothesis. However, at the functional level, distinct trends were found at different resolutions. Secondly, the difference in embryonic age between nodes inversely correlated with the probability of existence and the weights of the links. This indicated the presence of a temporal developmental gradient that shapes connectivity and where nodes connect more to nodes with a similar age. Finally, brain transcriptomic analysis revealed high association between embryonic age, structural-functional centrality and the expression of genes related to nervous system development and synapse regulation. Furthermore, the spatial expression of genes causally related to major neurological diseases was highly correlated with spatial maps of region centrality. Overall, these results support the hypothesis that the embryogenic age of brain regions shapes the topology of adult brain networks. Our results show two key principles, “preferential age attachment” and “older gets richer” on the wiring of the human brain, thus shedding new light on the relationship between brain development, transcriptomics, node centrality, and neurological diseases.