Our results hence show a double dissociation denoting that defective phonological perception can be compensated for by the right auditory cortex, whereas phonological production (as probed by naming tasks) cannot, presumably because it relies on an extended strongly lateralized network encompassing left-hemispheric inferior prefrontal (BA44/45) and parietal (BA40)

cortices (Morillon et al., 2010 and Price, 2010). It ensues that those participants who compensate JQ1 order well with the right auditory cortex, e.g., dyslexic subjects 9, 5, 11, appear impaired only on tasks requiring a transfer of phonological material to the left-lateralized speech production system. Conversely, those who are strongly impaired in tasks requiring phonological analysis are not necessarily impaired in phonological output if phonological processing remains globally

Screening Library manufacturer left-lateralized, e.g., dyslexic subjects 23, 24, 31, 46, etc. As reading relies on phonological input, storage, and output processes, this dissociation could explain why the asymmetry measure does not correlate with reading fluency in the dyslexics group (Figure 4A). Altogether, our results suggest that a single oscillation entrainment anomaly in the left auditory cortex, the absence of specific resonance in the 25–35 Hz window, may have distinct behavioral effects depending on how it is individually compensated for. These findings are hence consistent with the notion that dyslexics exhibit different profiles of phonological deficit (Wagner and Torgesen, 1987 and Wolf et al., 2002). What determines individual trajectories of neural compensation, however, remains unexplained by the current data. Oscillatory anomalies in dyslexics were observed over a large part of the language network. Such a broad distribution is in line with widespread morphological

anomalies as, for instance, ectopias, which have been observed in dyslexia both postmortem and using brain imaging (Démonet et al., 2004, Eckert, 2004 and Galaburda et al., 1985). At a mechanistic level, neocortical Thymidine kinase oscillation anomalies are compatible with the function of the genes that have been incriminated in dyslexia. These genes typically control neuronal migration, axonal guidance, and the spatial organization of cortical layers (Galaburda et al., 1985 and Rosen et al., 2007), which may all contribute to the generation of periodic interactions across excitatory and inhibitory cortical neuronal populations (pyramidal cells and interneurons) (Börgers and Kopell, 2005), and across cortical layers (Roopun et al., 2008). Our results also suggest that genetic variants associated with specific oscillatory phenotypes might be good candidates for the susceptibility to dyslexia.