TY - JOUR
T1 - The DCDC2 intron 2 deletion impairs illusory motion perception unveiling the selective role of magnocellular-dorsal stream in reading (Dis)ability
AU - Gori, Simone
AU - Mascheretti, Sara
AU - Giora, Enrico
AU - Ronconi, Luca
AU - Ruffino, Milena
AU - Quadrelli, Ermanno
AU - Facoetti, Andrea
AU - Marino, Cecilia
PY - 2015/6/1
Y1 - 2015/6/1
N2 - Developmental dyslexia (DD) is a heritable neurodevelopmental reading disorder that could arise from auditory, visual, and cross-modal integration deficits. A deletion in intron 2 of the DCDC2 gene (hereafter DCDC2d) increases the risk for DD and related phenotypes. In this study, first we report that illusory visual motion perception - specifically processed by the magnocellular-dorsal (M-D) stream - is impaired in children with DD compared with age-matched and reading-level controls. Second, we test for the specificity of the DCDC2d effects on the M-D stream. Children with DD and DCDC2d need significantly more contrast to process illusory motion relative to their counterpart without DCDC2d and to age-matched and reading-level controls. Irrespective of the genetic variant, children with DD perform normally in the parvocellular-ventral task. Finally, we find that DCDC2d is associated with the illusory motion perception also in adult normal readers, showing that the M-D deficit is a potential neurobiological risk factor of DD rather than a simple effect of reading disorder. Our findings demonstrate, for the first time, that a specific neurocognitive dysfunction tapping the M-D stream is linked with a well-defined genetic susceptibility.
AB - Developmental dyslexia (DD) is a heritable neurodevelopmental reading disorder that could arise from auditory, visual, and cross-modal integration deficits. A deletion in intron 2 of the DCDC2 gene (hereafter DCDC2d) increases the risk for DD and related phenotypes. In this study, first we report that illusory visual motion perception - specifically processed by the magnocellular-dorsal (M-D) stream - is impaired in children with DD compared with age-matched and reading-level controls. Second, we test for the specificity of the DCDC2d effects on the M-D stream. Children with DD and DCDC2d need significantly more contrast to process illusory motion relative to their counterpart without DCDC2d and to age-matched and reading-level controls. Irrespective of the genetic variant, children with DD perform normally in the parvocellular-ventral task. Finally, we find that DCDC2d is associated with the illusory motion perception also in adult normal readers, showing that the M-D deficit is a potential neurobiological risk factor of DD rather than a simple effect of reading disorder. Our findings demonstrate, for the first time, that a specific neurocognitive dysfunction tapping the M-D stream is linked with a well-defined genetic susceptibility.
KW - DCDC2
KW - dorsal pathway
KW - illusory motion perception
KW - reading (dis)abilities
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U2 - 10.1093/cercor/bhu234
DO - 10.1093/cercor/bhu234
M3 - Article
C2 - 25270309
AN - SCOPUS:84930334532
VL - 25
SP - 1685
EP - 1695
JO - Cerebral Cortex
JF - Cerebral Cortex
SN - 1047-3211
IS - 6
ER -