{Reference Type}: Journal Article
{Title}: Alterations in neural activation in the ventral frontoparietal network during complex magnocellular stimuli in developmental dyslexia associated with READ1 deletion.
{Author}: Mascheretti S;Arrigoni F;Toraldo A;Giubergia A;Andreola C;Villa M;Lampis V;Giorda R;Villa M;Peruzzo D;
{Journal}: Behav Brain Funct
{Volume}: 20
{Issue}: 1
{Year}: 2024 Jun 26
{Factor}: 3.95
{DOI}: 10.1186/s12993-024-00241-2
{Abstract}: <B>BACKGROUND: </B>An intronic deletion within intron 2 of the DCDC2 gene encompassing the entire READ1 (hereafter, READ1d) has been associated in both children with developmental dyslexia (DD) and typical readers (TRs), with interindividual variation in reading performance and motion perception as well as with structural and functional brain alterations. Visual motion perception -- specifically processed by the magnocellular (M) stream -- has been reported to be a solid and reliable endophenotype of DD. Hence, we predicted that READ1d should affect neural activations in brain regions sensitive to M stream demands as reading proficiency changes.<BR><B>METHODS: </B>We investigated neural activations during two M-eliciting fMRI visual tasks (full-field sinusoidal gratings controlled for spatial and temporal frequencies and luminance contrast, and sensitivity to motion coherence at 6%, 15% and 40% dot coherence levels) in four subject groups: children with DD with/without READ1d, and TRs with/without READ1d.<BR><B>RESULTS: </B>At the Bonferroni-corrected level of significance, reading skills showed a significant effect in the right polar frontal cortex during the full-field sinusoidal gratings-M task. Regardless of the presence/absence of the READ1d, subjects with poor reading proficiency showed hyperactivation in this region of interest (ROI) compared to subjects with better reading scores. Moreover, a significant interaction was found between READ1d and reading performance in the left frontal opercular area 4 during the 15% coherent motion sensitivity task. Among subjects with poor reading performance, neural activation in this ROI during this specific task was higher for subjects without READ1d than for READ1d carriers. The difference vanished as reading skills increased.<BR><B>CONCLUSIONS: </B>Our findings showed a READ1d-moderated genetic vulnerability to alterations in neural activation in the ventral attentive and salient networks during the processing of relevant stimuli in subjects with poor reading proficiency.