Embryonic PI3K-Yap activity regulates apical adhesion and proliferation of neural progenitors lining the lateral ventricular surface, to maintain the smooth, non-folded mouse brain and to prevent developmental hydrocephalus.

FGF signaling is crucial for gyrus formation, proliferation of outer radial glial cells and expansion of upper layers of the cerebral cortex in gyrencephalic mammals.

Introducing a hominoid-specific gene into mice induces cortical folding.

Cortices from 11 primate species share the same archetypal fractal shape, indicating a universal mechanism for primate and mammalian cortical folding, and suggesting novel shape biomarkers for brains.

Expression of human-specific gene ARHGAP11B in the developing ferret neocortex leads to an increase in abundance of neural progenitor cells, which results in neocortex expansion.

A diverse assortment of mRNAs are present in projection axons in the adult forebrain and their translation is associated with new memory formation.

Combining phylogenetic and functional approaches, it is shown that the protein sequence, the proliferative activity, and a regulatory element of TRNP1 co-evolve with brain size and folding.

Fetal Zika virus’ direct infection of the brain causes neuroanatomical pathology that tracks with the brain development, following a caudal-to-rostral trajectory, even in individuals who do not develop microcephaly.

Genome-wide transcriptional profiling and genetic analyses reveal conserved mechanisms underlying the generation of neocortical basal radial glia and cerebellar Bergmann glia.

The provided framework based on biological models and clinical literature can aid in the optimization of visual cortical prostheses through computational or behavioral simulation experiments, serving as a flexible tool for computational, clinical, and behavioral neuroscientists working on visual neuroprosthetics.