A review spanning four decades of genetic research suggests that dyslexia may result from disruptions across broader brain networks rather than a single faulty gene. The findings, published in the Journal of Speech, Language, and Hearing Research, offer new perspectives on one of the world’s most common learning disorders, which affects up to 20% of the global population.
Researchers at the University of Houston used computational tools and large-scale biological databases to catalogue genes associated with dyslexia and reading-related processes systematically. Lead author Elena Grigorenko, Distinguished Professor of Psychology, noted that the findings challenge the idea of reading-specific genes, proposing instead that dyslexia reflects disruption of evolutionarily ancient neural mechanisms operating within human-specific brain architecture.
The study identified 175 genes currently linked to reading difficulties, which fall into two functionally distinct groups. The first group is active early in foetal development, contributing to the brain’s physical structure and wiring. The second group becomes active later, around the 24th week of pregnancy, and supports synaptic signalling how brain cells communicate. This pattern suggests at least two developmental origins for reading difficulties: one related to brain structure and another to brain function.
First author Pavel Dobrynin highlighted that many of these genes are evolutionarily ancient, conserved across species, and expressed in multiple brain regions. However, some sit near DNA stretches that evolved rapidly in humans, indicating that how and when these genes are activated may be uniquely human.
The researchers suggested that their findings support viewing dyslexia as part of a broader neurodevelopmental spectrum rather than an isolated condition, though further research is needed to clarify clinical implications.
Source: Medical Xpress / University of Houston (Journal of Speech, Language, and Hearing Research, 2025)
