Earlier today I had the privilege of attending* the annual Sluckin Memorial Lecture given by eminent Oxford neuroscientist and academic blogger Professor Dorothy Bishop. Dorothy’s theme was ‘Developmental dyslexia and other neurodevelopmental disorders: Distinct syndromes or part of normal variation?‘. There was much in the talk worthy of blogging here, but since I’ve got a stack of final year dissertations to mark I will, for the moment, limit myself to reflections on one point that she raised.
As with many conditions in the genomic era, there is a desire to find the underlying genetic ’cause’ for dyslexia. This search is not without justification. For example, classic comparison of monozygotic twins (“identical” twins, i.e. same genetics, notwithstanding any epigenetic influences) and dizygotic twins (“non-identical twins”, no more genetically related than any brother or sister) strongly implies that there is a genetic component to dyslexia.
There is stronger evidence than this, particularly for a correlation between dyslexia and the catchily name gene DCDC2. A 2005 paper in the Proceedings of the National Academy of Science, a “Premier League” academic journal, showed a link between specific mutations in this gene and reading disability. A subsequent paper by Tom Scerri and colleagues (including Dorothy) found that a particular Single Nucleotide Polymorphism (a SNP, i.e. a particular base change difference in the DCDC2 gene) was associated with 31% of dyslexics. It was also found in 23% of the control (i.e. non-dyslexic) group, but nevertheless the difference the two is statistically significant (p = 0.005). Continue reading