A University of Houston psychology professor is challenging the notion that dyslexia, or specific reading disorder, stems from a single faulty gene in the brain, suggesting instead that it is caused by an overall brain network vulnerability. The insight reshapes understanding of one of the world’s most common learning disorders, which affects up to 20% of the world’s population — nearly 780 million people who face lifelong challenges with reading.
Using computers and large biology databases, Elena Grigorenko, Hugh Roy and Lillie Cranz Cullen Distinguished Professor of Psychology, reviewed four decades of research covering the genetics of specific reading disorder. Her team systematically cataloged candidate genes reportedly associated with dyslexia and reading-related processes and published the findings in Journal of Speech, Language, and Hearing Research.
“Our findings challenge the notion of the existence of reading-specific genes, suggesting instead that dyslexia reflects the disruption of ancient evolutionary neural mechanisms operating within human-specific brain architecture,” reports Grigorenko.
“The identification of developmental expression transitions and functional networks provides insight into how genetic variation might impact reading development and offers potential targets for future clinical approaches to the identification and remediation of reading difficulties,” said Grigorenko.
The findings collectively provide valuable insights into the genetic bases of reading disability while raising important questions about the nature of it as a specific neurodevelopmental condition rather than an outcome of brain development processes.
Developmental process
People began reading about 3000 BCE in Mesopotamia, following the development of cuneiform, the most ancient of writing systems. But it turns out humans were all set up for the task, because the genes associated with reading are evolutionarily ancient, millions of years old.
The evolutionary conservation of the reading disorder genes across species and their expression across multiple brain regions further support viewing dyslexia as part of a broader neurodevelopmental spectrum rather than an isolated condition,” said Pavel Dobrynin, research scholar in Grigorenko’s GENESIS lab (Genetic and Neurobehavioral Systems: Interdisciplinary Studies) and the paper’s first author.
The study identified two functionally distinct groups among the 175 genes currently known to be associated with reading difficulties.
“The first group is active early in fetal development, helping build the brain’s physical architecture—its wiring and structure,” said Grigorenko. “The second group switches on later, around the 24th week of pregnancy, and supports synaptic signaling—how brain cells communicate with each other.”
This suggests there may be at least two developmental origins for reading difficulties: one related to how the brain is built, and another to how it functions — a process that has gone on for millions of years.
“Interestingly, a number of these genes sit near stretches of DNA that evolved rapidly in humans compared to other species. The genes themselves are ancient, but how and when they’re switched on may be uniquely human,” Dobrynin said.
