A recent study by Guido Marco Cicchini (IN-CNR) and Maria Concetta Morrone (University of Pisa) published in the prestigious Journal of Neuroscience sheds light on the genetic marker that is associated with specific visual deficit and may help early diagnosis of dyslexia, before beginning to read.
Dyslexia is a specific and severe reading impairment afflicting otherwise bright children. It is very common, affecting up to 10% of the population, two to three children in every class. It is known that 20% of dyslexics show alterations in a specific gene, DCDC2, but the role of this gene in dyslexia has been unclear. The new study shows that dyslexics with an alteration in the DCDC2 gene are blind to certain types of visual motion, motion that is highly salient to typical controls.
The authors compared two groups of dyslexics – one with and one without a specific deletion within the DCDC2 gene – to typical readers in a series of visual tests. All the subjects of the group of dyslexics with the gene deletion failed to detect the motion of finely patterned stimuli, although they were able to report the orientation of these stimuli with precision. While they could clearly see the visual stimulus, they could not report its motion, even at maximum contrast. On the other hand, the group of dyslexics without the specific deletion behaved more similarly to controls, showing only a mild motion deficit.
These results suggest that the reading deficit results not from higher intellectual dysfunction, but has a clear perceptual basis. It is still not fully understood why a deficit in motion perception should impact on reading, but the researchers have some very clear ideas. Eye movements are fundamental to reading, and these frequent scanning movements move and displace of the image continuously: failure to process this motion satisfactorily could interfere with the stable perception of the text page in the face of these continual eye movements. The results also point to an anomalous sparseness of motion detectors for fine patterns, consistent with DCDC2's role in modulating neuronal migration during development.
Dyslexia is generally diagnosed only after children have commenced school and show obvious difficulties in reading. However, the motion perceptual difficulties can be measured at a very early age in the subjects with alteration in DCDC2 gene, before schooling begins, allowing for prompt diagnosis and intervention.
The Italian research group is getting closer to their goal of defining a specific biomarker and specific therapies of dyslexia associated with specific genetic mutations. Their work clearly shows that tackling the problem of dyslexia, with its enormous cost to society, requires a concerted multidisciplinary approach to construct better diagnostic tools, and to begin to refine more effective therapies.