HOUSTON, Feb 8 – A University of Houston psychology professor is challenging long-held assumptions about dyslexia, arguing the condition stems not from a single faulty gene but from vulnerabilities across broader brain networks.

Elena Grigorenko, Hugh Roy and Lillie Cranz Cullen Distinguished Professor of Psychology, reviewed four decades of genetic research into specific reading disorder, commonly known as dyslexia. Her team catalogued 175 candidate genes linked to reading difficulties and published the findings in the Journal of Speech, Language, and Hearing Research.

“Our findings challenge the notion of reading-specific genes, suggesting instead that dyslexia reflects disruption of ancient evolutionary neural mechanisms within human brain architecture,” Grigorenko said.

The study suggests dyslexia, which affects up to 20% of the global population, may arise from two developmental pathways: one involving early fetal brain wiring and another tied to later synaptic signaling.

Pavel Dobrynin, first author and research scholar in Grigorenko’s GENESIS lab, said the genes associated with reading are evolutionarily ancient but show unique human activation patterns. “The genes themselves are ancient, but how and when they’re switched on may be uniquely human,” he said.

The findings raise questions about whether dyslexia should be viewed as a distinct neurodevelopmental disorder or part of a broader spectrum of brain development processes.