Alterations in neural activation in the ventral frontoparietal network during complex magnocellular stimuli in developmental dyslexia associated with READ1 deletion
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View abstract on PubMed
Summary
This summary is machine-generated.A deletion in the DCDC2 gene (READ1d) affects brain activity in children with developmental dyslexia (DD). This genetic factor influences neural responses during visual tasks, particularly in those with reading difficulties.
Area Of Science
- Neuroscience
- Genetics
- Developmental Psychology
Background
- A deletion in the DCDC2 gene (READ1d) is linked to developmental dyslexia (DD) and impacts reading performance and brain function.
- Visual motion perception, processed by the magnocellular (M) stream, is a key endophenotype for DD.
Purpose Of The Study
- To investigate how the READ1d deletion affects neural activations in brain regions sensitive to M stream demands during reading proficiency changes.
- To explore the interaction between the READ1d deletion and reading performance on neural activity.
Main Methods
- Utilized fMRI with two M-eliciting visual tasks: full-field sinusoidal gratings and motion coherence sensitivity.
- Examined four groups: children with DD and typical readers (TRs), with and without the READ1d deletion.
Main Results
- Poor readers showed hyperactivation in the right polar frontal cortex during the sinusoidal gratings task, irrespective of READ1d status.
- A significant interaction between READ1d and reading performance was observed in the left frontal opercular area during the 15% coherent motion task.
Conclusions
- The READ1d deletion moderates genetic vulnerability to altered neural activation in ventral attentive and salient networks.
- These alterations are evident in individuals with poor reading proficiency when processing relevant visual stimuli.
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