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Edwin H. Cook

Researcher at University of Illinois at Chicago

Publications -  339
Citations -  61045

Edwin H. Cook is an academic researcher from University of Illinois at Chicago. The author has contributed to research in topics: Autism & Heritability of autism. The author has an hindex of 102, co-authored 337 publications receiving 54518 citations. Previous affiliations of Edwin H. Cook include University of Chicago & University of Illinois at Urbana–Champaign.

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Mutation screening and transmission disequilibrium study of ATP10C in autism.

TL;DR: A family-based association study was conducted for 14 markers in 115 autism trios, suggesting ATP10C is unlikely to contribute strongly to susceptibility to autism in these families, but the possible functional role of the nonsynonymous SNPs and the functional implications of the SNPs identified from 5' flanking region and intron 2 splicing region may be evaluated in further studies.
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Family-based association study of the serotonin transporter gene polymorphisms in Korean ADHD trios.

TL;DR: The result suggests that future studies should include more polymorphic markers and subjects to thoroughly investigate a potential association between SLC6A4 and ADHD in the Korean population, and that low heterozygosity in these markers would be expected to reduce the power of association.
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Variation in ITGB3 has sex-specific associations with plasma lipoprotein(a) and whole blood serotonin levels in a population-based sample.

TL;DR: Variation in ITGB3 in addition to Leu33Pro could contribute to susceptibility to CVD and serotonin in a sex-specific manner, and the results suggest that variation in IT GB3 and its relationship to intermediate phenotypes associated with CVD in the same population is suggested.
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Fluoxetine effects on cerebral glucose metabolism.

TL;DR: Parametric mapping for use in PET studies of glucose metabolism represents a significant new tool for studying drug effects in humans and revealed regional effects of fluoxetine shown by decreased metabolism in the amygdaloid complex, hippocampal formation and ventral striatum, and by increased metabolism centered in the right superior parietal lobe.