![]() This region overlapped that highlighted in 3 genome scans for autism, a disorder in which inattention and hyperactivity are common, and physically mapped to a 7-Mb region on 16p13. (2002) used affected sib pair analysis in 203 families to localize the first major susceptibility locus for ADHD to a 12-cM region on chromosome 16p13 (maximum lod score 4.2 P = 0.000005). (2002) analyzed data from sib pairs selected for reading deficits and found suggestive bivariate linkage for ADHD and 3 measures of reading disability, indicating that comorbidity between reading disability and ADHD may be due at least in part to pleiotropic effects of a QTL on 6p (see DYX2, 600202, which maps to 6p21.3). Reading disability and ADHD frequently occur together. None exceeded genomewide significance thresholds. Qualitative trait maximum lod score analyses pointed to a number of chromosomal sites that may contain genetic risk factors of moderate effect. Under a strict diagnostic scheme, they could exclude all screened regions of the X chromosome for a locus-specific lambda-s of 2 or more in brother-brother pairs, demonstrating that the excess of affected males with ADHD is probably not attributable to a major X-linked effect. Allele-sharing linkage methods enabled them to exclude any loci with a lambda-s of 3 or more from 96% of the genome and those with a lambda-s of 2.5 or more from 91%, indicating that there is unlikely to be a major gene involved in ADHD susceptibility in the sample. (2002) performed the first systematic genomewide linkage scan for loci affecting ADHD in 126 affected sib pairs (ASPs). The correlation between ADHD symptoms and IQ was -0.3 (on average ADHD diagnosed children obtained an IQ score 9 points lower than comparison children).įisher et al. In a large population-based sample of 5-year-old twins (both monozygotic and dizygotic), they assessed twins individually on IQ tests, and data on ADHD symptoms were obtained from mothers' and teachers' ratings. (2004) found that 86% of the association between ADHD symptom scores and IQ, and 100% of the association between ADHD diagnosis and IQ was accounted for by genetic influences that are shared by ADHD and IQ. Zametkin and Ernst (1999) reviewed the diagnostic criteria, differential diagnosis, and treatment of ADHD. Smalley (1997) reviewed studies of the genetics of ADHD and autism ( 209850). The parents in this study continued to have symptoms as adults. (1990) reported that 28.6% of the biologic parents of hyperactive children also had a history of hyperactivity. This study was done in adults because of ethical considerations about exposing children to a radioactive tracer however, each of the 25 hyperactive adults was the biologic parent of a hyperactive child. ![]() Among the regions with greatest reduction were the premotor cortex and the superior prefrontal cortex. Glucose metabolism was significantly reduced in 30 of 60 specific regions of the brain. (1990) found that global cerebral glucose metabolism was 8.1% lower in adults with hyperactivity than in normal controls. By means of positron-emission tomography (PET) of the brain using (18F)-fluoro-2-deoxy-D-glucose, Zametkin et al. ![]()
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