PubMed · 5579204
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S Krauss. 1971-06-05. Post-hypoglycaemic encephalopathy.. https://doi.org/10.1136/bmj.2.5761.591-c
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OBJECTIVE: To investigate the relationship between two HTR2C gene polymorphisms, that is C-759T and G-697C polymorphisms, and attention deficit hyperactivity disorder (ADHD) comorbid or not comorbid learning disorder (LD). METHODS: Blood samples were taken from 189 trios with probands of ADHD comorbid LD (ADHD+LD) and 299 trios with probands of ADHD not comorbid LD (ADHD-LD). DNA was extracted and PCR was performed to amplify the fragments containing both C-759T and G-697C polymorphisms. Aci I was used to detect different alleles of the two polymorphisms. Allele- based and haplotype- based TDT analysis were used to test the association of the two polymorphisms of HTR2C gene and ADHD-LD and ADHD+LD. RESULTS: -759C(chi(2)=6.961, P=0.008), -697G(chi(2)=8.346, P=0.004), as well as -759C/-697G haplotype were over- transmitted(chi(2)=9.000, P=0.002 7), while haplotype -759T/-697C was under- transmitted(chi(2)=7.784, P=0.005 3) to probands with ADHD-LD. No biased transmission of any allele and haplotype were found in families with probands of ADHD+LD. CONCLUSION: ADHD-LD and ADHD+LD are different at the level of HTR2C gene polymrohisms of C-759T and G-697C. HTR2C is related to ADHD-LD, while not related to ADHD+LD.
We completed fine mapping of nine positional candidate regions for attention-deficit/hyperactivity disorder (ADHD) in an extended population sample of 308 affected sibling pairs (ASPs), constituting the largest linkage sample of families with ADHD published to date. The candidate chromosomal regions were selected from all three published genomewide scans for ADHD, and fine mapping was done to comprehensively validate these positional candidate regions in our sample. Multipoint maximum LOD score (MLS) analysis yielded significant evidence of linkage on 6q12 (MLS 3.30; empiric P=.024) and 17p11 (MLS 3.63; empiric P=.015), as well as suggestive evidence on 5p13 (MLS 2.55; empiric P=.091). In conjunction with the previously reported significant linkage on the basis of fine mapping 16p13 in the same sample as this report, the analyses presented here indicate that four chromosomal regions--5p13, 6q12, 16p13, and 17p11--are likely to harbor susceptibility genes for ADHD. The refinement of linkage within each of these regions lays the foundation for subsequent investigations using association methods to detect risk genes of moderate effect size.