The two AZD-8055 web directions of simultaneous motion. Recently it has been suggested that a deficit in the processing of global motion only occurs in a sub-group of individuals, which might explain why performance on random-dot tasks is heterogeneous (Amitay et al., 2002; Ramus et al., 2003; White et al., 2006). Approximately 10?7 of poor readers classified as dyslexic and 4 of controls have a deletion on intron 2 of the DCDC2 gene (Meng et al., 2005; Wilcke et al., 2009). Studies have shown that individuals with this genotypic deletion (hereafter referred to as DCDC2d) have altered white Bayer 41-4109 mechanism of action matter tracts in brain regions implicated in reading (e.g. Darki, Peyrard-Janvid, Matsson, Kere, Klingberg, 2014). Interestingly, morphological changes have also been reported in extrastriate visual areas such as V5/MT (Morrone et al., 2011). Cicchini et al. (2015) administered a motion discrimination task to groups of poor readers with and without DCDC2d. The results showed that poor readers with the deletion had more profound impairments than those without DCDC2d. However, the latter performed significantly worse than controls, which suggests that factors other than genotypic variation areR. Johnston et al. / Brain and Cognition 108 (2016) 20?contributing to the inter-subject variability in coherence thresholds amongst poor readers. An interesting question is whether a deficit in the processing of global motion is causal to developmental dyslexia. There is evidence to suggest that this might be the case (e.g. Gori, Seitz, Ronconi, Franceschini, Facoetti, 2015) but these findings have not been replicated. Olulade, Napoliello, and Eden (2013) investigated whether motion-related activity in V5/MT differs between children with dyslexia and controls matched either in chronological- or reading-age. Significant differences would be expected for both types of comparison if causality were present (Goswami, 2014). Poor readers’ activity in V5/MT was significantly lower than that of chronological- but not reading-age matched controls. An eight-week phonological based intervention was then undertaken, which lead to significant improvements fpsyg.2017.00209 in poor readers’ scores on standardised measures of reading ability and increased neural activity in right V5/MT. Taken together, these findings imply that motion processing impairments are a consequence rather than the proximal cause of developmental dyslexia. Recent studies have suggested that the process of reading acquisition has an influence on the development of early visual areas (Carreiras et al., 2009; Dehaene, Cohen, Morais, Kolinsky, 2015; Szwed, Ventura, Querido, Cohen, Dehaene, 2012). The finer details of this hypothesis are still being worked out (see Grainger, Dufau, Ziegler, 2016) but it could explain why some poor readers’ coherence thresholds are higher than those of good readers on random-dot global motion tasks. In summary, it appears that some individuals with dyslexia have a deficit on tasks involving global motion perception (Conlon, Lilleskaret, Wright, Power, 2012; Conlon, Lilleskaret, Wright, Stuksrud, 2013; Cornelissen et al., 1995; Everatt, Bradshaw, Hibbard, 1999; Hansen et al., 2001; Hill Raymond, 2002; Olulade et al., 2013; Pellicano Gibson, 2008; Qian Bi, 2014; Raymond Sorensen, 1998; Ridder, Borsting, SART.S23503 Banton, 2001; Talcott et al., 2000, 2003; Wilmer, Richardson, Chen, Stein, 2004; Witton et al., 1998). However, the underlying nature of the perceptual deficit is unknown, a sit.The two directions of simultaneous motion. Recently it has been suggested that a deficit in the processing of global motion only occurs in a sub-group of individuals, which might explain why performance on random-dot tasks is heterogeneous (Amitay et al., 2002; Ramus et al., 2003; White et al., 2006). Approximately 10?7 of poor readers classified as dyslexic and 4 of controls have a deletion on intron 2 of the DCDC2 gene (Meng et al., 2005; Wilcke et al., 2009). Studies have shown that individuals with this genotypic deletion (hereafter referred to as DCDC2d) have altered white matter tracts in brain regions implicated in reading (e.g. Darki, Peyrard-Janvid, Matsson, Kere, Klingberg, 2014). Interestingly, morphological changes have also been reported in extrastriate visual areas such as V5/MT (Morrone et al., 2011). Cicchini et al. (2015) administered a motion discrimination task to groups of poor readers with and without DCDC2d. The results showed that poor readers with the deletion had more profound impairments than those without DCDC2d. However, the latter performed significantly worse than controls, which suggests that factors other than genotypic variation areR. Johnston et al. / Brain and Cognition 108 (2016) 20?contributing to the inter-subject variability in coherence thresholds amongst poor readers. An interesting question is whether a deficit in the processing of global motion is causal to developmental dyslexia. There is evidence to suggest that this might be the case (e.g. Gori, Seitz, Ronconi, Franceschini, Facoetti, 2015) but these findings have not been replicated. Olulade, Napoliello, and Eden (2013) investigated whether motion-related activity in V5/MT differs between children with dyslexia and controls matched either in chronological- or reading-age. Significant differences would be expected for both types of comparison if causality were present (Goswami, 2014). Poor readers’ activity in V5/MT was significantly lower than that of chronological- but not reading-age matched controls. An eight-week phonological based intervention was then undertaken, which lead to significant improvements fpsyg.2017.00209 in poor readers’ scores on standardised measures of reading ability and increased neural activity in right V5/MT. Taken together, these findings imply that motion processing impairments are a consequence rather than the proximal cause of developmental dyslexia. Recent studies have suggested that the process of reading acquisition has an influence on the development of early visual areas (Carreiras et al., 2009; Dehaene, Cohen, Morais, Kolinsky, 2015; Szwed, Ventura, Querido, Cohen, Dehaene, 2012). The finer details of this hypothesis are still being worked out (see Grainger, Dufau, Ziegler, 2016) but it could explain why some poor readers’ coherence thresholds are higher than those of good readers on random-dot global motion tasks. In summary, it appears that some individuals with dyslexia have a deficit on tasks involving global motion perception (Conlon, Lilleskaret, Wright, Power, 2012; Conlon, Lilleskaret, Wright, Stuksrud, 2013; Cornelissen et al., 1995; Everatt, Bradshaw, Hibbard, 1999; Hansen et al., 2001; Hill Raymond, 2002; Olulade et al., 2013; Pellicano Gibson, 2008; Qian Bi, 2014; Raymond Sorensen, 1998; Ridder, Borsting, SART.S23503 Banton, 2001; Talcott et al., 2000, 2003; Wilmer, Richardson, Chen, Stein, 2004; Witton et al., 1998). However, the underlying nature of the perceptual deficit is unknown, a sit.
