DCDC2 and reading disability

The search for a genetic basis for disabilities took another step when Yale University researchers announced that they have identified alterations of a gene—DCDC2—in roughly 20% of individuals identified as having dyslexia. The researchers argue that this disruption leads to problems in the parts of the brain used in reading. Ultimately, they suggest that this discovery can be used to identify individuals at risk for Learning Disabilities in reading.

The researchers also found that a genetic alteration in DCDC2 leads to a disruption in the formation of brain circuits that make it possible to read. This genetic alteration is transmitted within families.

“These promising results now have the potential to lead to improved diagnostic methods to identify dyslexia and deepens understanding of how the reading process works on a molecular level,” said lead author Jeffrey R. Gruen, M.D., associate professor in the Pediatrics Department at Yale School of Medicine.

Although I find the discovery exiting, I have only been able to locate a press release about it. The published version will be more revealing, and I look forward to reading it. In the meantime and based on the incomplete report, I have two comments.

  1. I note that Gruen and his colleagues (way numerous and including many of the major figures in research about the genetics of Learning Disabilities) are describing an anomoly present for only one fifth of the population of individuals with dyslexia. There must be other ways that the circuits are disrupted, no?
  2. Research on the effects of instruction (some of it conducted by Sally Shaywitz, who’s a co-author on the forthcoming paper, too) show that explicit instruction in fundamental decoding helps many people overcome their difficulties with reading and that fMRI scans of their brains begin to look more like the scans of brains for people who read well. It will be worthwhile to investigate whether the 20% with this genetic marker are among the responders or non-responders to good reading instruction.

Much previous work has sought a genetic basis for dyslexia. A great deal of the most influential work has been done by a group of scientists—espcially John DeFries, Richard Olson, Bruce Pennington, and their colleagues (all co-authors on the paper with Gruen)—at the Institute for Behavioral Genetics at the University of Colorado. But, others have also been in the fray. For example, Finish scientists reported in 2003 that they had identified a gene—DYX1C1 near the DYX1 locus in chromosome 15q21—in which translocation might be associated with dyslexia.

Link to Yale press release. Links to the Institute for Behavioral Genetics and for Finish work (first author Mikko Taipale). List (incomplete) of links to news sources’ coverage:

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