Absence of a significant linkage between Na(+),K(+)-ATPase subunit (ATP1A3 and ATP1B3) genotypes and bipolar affective disorder in the old-order Amish
Authors
Philibert, Robert A.Cheung, D.
Welsh, N.
Damschroder-Williams, Patricia J.
Thiel, B.
Ginns, Edward I.
Gershenfeld, Howard K.
UMass Chan Affiliations
Brudnick Neuropsychiatric Research Institute, Department of PsychiatryDepartment of Pediatrics
Document Type
Journal ArticlePublication Date
2001-04-08Keywords
Bipolar DisorderCase-Control Studies
Cohort Studies
Ethnic Groups
*Genetic Linkage
Genetic Predisposition to Disease
Genotype
Humans
Nuclear Family
Protein Subunits
Sodium-Potassium-Exchanging ATPase
Statistics, Nonparametric
Neurology
Pediatrics
Psychiatry
Metadata
Show full item recordAbstract
Previous studies provide evidence for a genetic component for susceptibility to bipolar affective disorder (BPAD) in the old-order Amish population. El-Mallakh and Wyatt [1995: Biol Psychiatry 37:235-244] have suggested that the Na(+),K(+)-ATPase may be a candidate gene for BPAD. This study examines the relationship between BPAD in the old-order Amish cohort and the Na(+),K(+)-ATPase alpha1 and beta3 subunit genes (ATP1A3, ATP1B3). A total of 166 sibling pairs were analyzed for linkage via nonparametric methods. Suggestive levels of statistical significance were not reached in any stratification model for affective illness. Overall, the results do not support linkage of bipolar disorder to the Na(+),K(+)-ATPase alpha subunit gene (ATP1A3) and beta subunit gene (ATP1B3) in these old-order Amish families and they show that these Na(+),K(+)-ATPase subunit genes are not major effect genes (>or=fourfold increased genetic risk of disease) for BPAD in the old-order Amish pedigrees. We cannot exclude other genetic variants of the Na(+),K(+)-ATPase hypothesis for BPAD, whereby other loci may modifying Na(+),K(+)-ATPase activity.Source
Am J Med Genet. 2001 Apr 8;105(3):291-4. DOI: 10.1002/ajmg.1322DOI
10.1002/ajmg.1322Permanent Link to this Item
http://hdl.handle.net/20.500.14038/43523PubMed ID
11353452Related Resources
Link to Article in PubMedae974a485f413a2113503eed53cd6c53
10.1002/ajmg.1322