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Expanded CAG/CTG repeats in bipolar disorder: no correlation with phenotypic measures of illness severity

Craddock, Nicholas John, McKeon, P., Moorhead, S., Guy, Carol, Harrison, D., Mynett-Johnson, L., Claffey, E., Feldman, E., McGuffin, P., Owen, Michael John and O'Donovan, Michael Conlon 1997. Expanded CAG/CTG repeats in bipolar disorder: no correlation with phenotypic measures of illness severity. Biological psychiatry 42 (10) , pp. 876-881. 10.1016/s0006-3223(96)00516-1

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The hypothesis that expanded trinucleotide repeats (TNRs) contribute to the pathogenesis of bipolar disorder has received strong support from recent studies showing that, on average, bipolar patients carry larger repeat sequences of the TNR motif CAG/CTG than do controls. It has been postulated that intergenerational expansion of a TNR may be responsible for the tendency for age of onset to become earlier in younger generations (anticipation) observed in some bipolar pedigrees, and that length polymorphism may account for variability in clinical phenotype. We have used the method of repeat expansion detection to examine these predictions in a sample of 133 Caucasian DSM-III-R bipolar I probands from the British Isles. We found no evidence to support the notion that CAG/CTG TNR genes are major determinants of phenotypic severity or age at onset in the population examined, and conclude that for most cases of bipolar disorder TNR genes may operate as susceptibility genes rather than as single genes of major effect.

Item Type: Article
Date Type: Publication
Status: Published
Schools: Medicine
MRC Centre for Neuropsychiatric Genetics and Genomics (CNGG)
Neuroscience and Mental Health Research Institute (NMHRI)
Subjects: R Medicine > R Medicine (General)
R Medicine > RZ Other systems of medicine
Publisher: Elsevier
ISSN: 0006-3223
Last Modified: 17 Apr 2019 20:50

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