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Family‐based association studies of α‐adrenergic receptor genes in chromosomal regions with linkage to bipolar affective disorder
Author(s) -
Jamra Rami Abou,
Schumacher Johannes,
Golla Astrid,
Richter Carola,
Otte Andreas C.J.,
Schulze Thomas G.,
Ohlraun Stephanie,
Maier Wolfgang,
Rietschel Marcella,
Cichon Sven,
Propping Peter,
Nöthen Markus M.
Publication year - 2003
Publication title -
american journal of medical genetics part b: neuropsychiatric genetics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.393
H-Index - 126
eISSN - 1552-485X
pISSN - 1552-4841
DOI - 10.1002/ajmg.b.20145
Subject(s) - gene , linkage disequilibrium , genetics , biology , β2 adrenergic receptor , receptor , exon , allele , haplotype , agonist
Several lines of evidence suggest an involvement of the noradrenergic neurotransmitter system in the pathogenesis of bipolar affective disorder (BPAD). Three genes for α‐adrenergic receptors (ADRA) are located in chromosomal regions that showed evidence for linkage: The α 1c ‐adrenergic (ADRA‐1C) receptor gene on 8p21, the α 2a ‐adrenergic (ADRA‐2A) receptor gene on 10q25, and the α 2c ‐adrenergic (ADRA‐2C) receptor on 4p16. In a BPAD sample of 120 parent‐offspring triads, we genotyped a 492 Cys/Arg variant in exon 2 of the ADRA‐1C gene, a ‐1291 G/C variant in the 5′UTR of the ADRA‐2A gene, and a STR marker (adra2c1) in the 5′UTR of the ADRA‐2C gene. Using the Transmission Disequilibrium Test (TDT), no significant differences in transmissions were observed for any of the three ADRA genes. © 2003 Wiley‐Liss, Inc.