Neurobiological systems in dyslexia.

Biological systems-level principles of the genetic landscape underlying the neurobiology of dyslexia provide a novel and heuristic theoretical framework for a new understanding of the disability. Dyslexia may result from reduced neuroplasticity and earlier peak of maturation of the posterior corpus callosum, temporoparietal region of the left hemisphere reading network, and temporoparietal region of the right hemisphere circuitry of attentional networks. This precocious abridgement of a typically prolonged maturation originates prenatally or in early childhood, driven by environmentally-guided epigenetic mechanisms as retrogressive, adaptive responses to stress. Epigenetics suggests the importance of identifying circumstances that influence reading-related maturational timing; and network control theory suggests an instructional orientation for enhancing plasticity. Thus, dyslexia may be an unexceptional genetic variation resulting from gene/environment interactions.