Publications by authors named "Tasha-Cate Carter"

Reading disabilities (RD) are the most common neurocognitive disorder, affecting 5% to 17% of children in North America. These children often have comorbid neurodevelopmental/psychiatric disorders, such as attention deficit/hyperactivity disorder (ADHD). The genetics of RD and their overlap with other disorders is incompletely understood.

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Background: Children with chronic medical conditions often experience limited opportunities for social experiences due to frequent hospitalizations and medical appointments. Computer technology can provide valuable opportunities for social inclusion through online communities. However, moderation has been shown to be an important component of safe and successful use.

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Reading disabilities (RD) have been linked and associated with markers on chromosome 6p with results from multiple independent samples pointing to KIAA0319 as a risk gene and specifically, the 5' region of this gene. Here we focus genetic studies on a 2.3 kb region spanning the predicted promoter, the first untranslated exon, and part of the first intron, a region we identified as a region of open chromatin.

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Reading disabilities (RDs) have been associated with chromosome 6p with recent studies pointing to two genes, DCDC2 and KIAA0319. In this study, markers across the 6p region were tested for association with RD. Our strongest findings were for association with markers in KIAA0319, although with the opposite alleles compared with a previous study.

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A locus on chromosome 1p34-36 (DYX8) has been linked to developmental dyslexia or reading disabilities (RD) in three independent samples. In the current study, we investigated a candidate gene KIAA0319-Like (KIAA0319L) within DYX8, as it is homologous to KIAA0319, a strong RD candidate gene on chromosome 6p (DYX2). Association was assessed by using five tagging single nucleotide polymorphisms in a sample of 291 nuclear families ascertained through a proband with reading difficulties.

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The N-methyl-d-aspartate glutamate receptors (NMDAR) act in the CNS as regulators of the release of neurotransmitters such as dopamine, noradrenaline, acetylcholine, and GABA. It has been suggested that a weakened glutamatergic tone increases the risk of sensory overload and of exaggerated responses in the monoaminergic system, which is consistent with the symptomatology of schizophrenia. We studied two silent polymorphisms in GRIN1.

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