Prolonged myelination in human neocortical evolution

TLDR

Nerve myelination supports conduction and varies across development, yet it is unclear whether the human neocortex’s protracted myelination is evolutionarily unique, a pattern that may relate to psychiatric vulnerability. The study quantified myelinated axon density and myelin protein expression across postnatal life in human and chimpanzee neocortex to elucidate the evolution of human cognition and behavior. The authors measured myelinated axon fiber length density and myelin protein expression in somatosensory, motor, frontopolar, and visual neocortical areas of 20 chimpanzees and 33 humans across postnatal development. Human neocortical myelination is developmentally protracted compared to chimpanzees, with a delayed maturation extending beyond late adolescence, implying that this human‑specific timing shift may influence vulnerability to psychiatric disorders.

Abstract

Nerve myelination facilitates saltatory action potential conduction and exhibits spatiotemporal variation during development associated with the acquisition of behavioral and cognitive maturity. Although human cognitive development is unique, it is not known whether the ontogenetic progression of myelination in the human neocortex is evolutionarily exceptional. In this study, we quantified myelinated axon fiber length density and the expression of myelin-related proteins throughout postnatal life in the somatosensory (areas 3b/3a/1/2), motor (area 4), frontopolar (prefrontal area 10), and visual (areas 17/18) neocortex of chimpanzees ( N = 20) and humans ( N = 33). Our examination revealed that neocortical myelination is developmentally protracted in humans compared with chimpanzees. In chimpanzees, the density of myelinated axons increased steadily until adult-like levels were achieved at approximately the time of sexual maturity. In contrast, humans displayed slower myelination during childhood, characterized by a delayed period of maturation that extended beyond late adolescence. This comparative research contributes evidence crucial to understanding the evolution of human cognition and behavior, which arises from the unfolding of nervous system development within the context of an enriched cultural environment. Perturbations of normal developmental processes and the decreased expression of myelin-related molecules have been related to psychiatric disorders such as schizophrenia. Thus, these species differences suggest that the human-specific shift in the timing of cortical maturation during adolescence may have implications for vulnerability to certain psychiatric disorders.