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Erik Jönsson poster abstract
Association study and meta-analysis of
a DRD3 gene Ser9Gly variant and schizophrenia
Erik G Jönsson1*, Lena Flyckt2, Edgar
Burgert3, Marc-Antoine Crocq4, Kaj Forslund1, Marja Mattila-Evenden1,
Gunnar Rylander1, Marie Åsberg1, Vishwajit L Nimgaonkar5,
Gunnar Edman6, Lars Bjerkenstedt1, Frits-Axel Wiesel6, Göran
C Sedvall1
1Department of Clinical Neuroscience,
Psychiatry Section, Karolinska Institutet, SE-171 76 Stockholm,
Sweden, tel +46 8 51772626, telefax +46 8 346563, email erikj@ks.se;
2Jakobsberg - Karolinska Psychiatric Clinic, Stockholm, Sweden;
3Institute of Human Genetics, University of Freiburg, Freiburg,
Germany; 4Centre Hospitalier, 68250 Rouffach, France; 5Departments
of Psychiatry and Human Genetics, University of Pittsburgh School
of Medicine, Western Psychiatric Institute and Clinic, Pittsburgh,
PA 15213, USA; 6Department of Psychiatry, Karolinska Institutet,
Danderyds hospital, Danderyd, Sweden; 7Department of Neuroscience,
Psychiatry, Uppsala University Hospital, Uppsala, Sweden
There is considerable controversy about a
putative association between schizophrenia and a Ser9Gly variant
in the first exon of the dopamine D3 receptor gene (DRD3).
Two meta-analyses published in 1998 suggested
association (odds ratios 1.2). We previously reported lack of association
in a Swedish sample. In the present study additional subjects were
added to the case-control sample. Patients with schizophrenia (n=156)
and control subjects (n=463) were assessed for the DRD3 Ser9Gly
variant.
No significant difference between patients
and controls were found, but there was an association between DRD3
Ser9Gly variation and response to anti-psychotic drugs. In an updated
meta-analysis of all case-control studies comprising more than 8500
subjects the associations between DRD3 Ser9Gly homozygosity (c2=6.85,
df=1, p<0.01; odds ratio 1.13, 95% confidence interval 1.03-1.23)
persisted.
Reasons for the discrepancies between prior
studies are discussed.
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