Angiotensin converting enzyme gene insertion/deletion polymorphism: Case-control association studies in schizophrenia, major affective disorder, and tardive dyskinesia and a family-based association study in schizophrenia
Autor: | Kyra Kanyas, Fabio Macciardi, Bernard Lerer, Shmuel Hirschmann, Joseph Zislin, Baruch Shapira, Michael Schlafman, Ilan Modai, Boris Finkel, Yami Shapira, Adnan Hamdan, Arturo G. Lerner, Ronnen H. Segman, Osnat Karni, Uriel Heresco-Levy |
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Rok vydání: | 2002 |
Předmět: |
Male
Oncology Dyskinesia Drug-Induced medicine.medical_specialty Psychosis Candidate gene Genotype Peptidyl-Dipeptidase A Tardive dyskinesia Gene Frequency Internal medicine mental disorders Humans Medicine Bipolar disorder Alleles Genetics (clinical) Psychiatric genetics Sequence Deletion Family Health Genetics Polymorphism Genetic biology Mood Disorders business.industry Angiotensin-converting enzyme DNA Transmission disequilibrium test medicine.disease Mutagenesis Insertional Dyskinesia Case-Control Studies Schizophrenia biology.protein Female medicine.symptom business |
Zdroj: | American Journal of Medical Genetics. 114:310-314 |
ISSN: | 1096-8628 0148-7299 |
DOI: | 10.1002/ajmg.10255 |
Popis: | Angiotensin converting enzyme (ACE) is a candidate gene for psychiatric disorders. We examined the frequency of a functional insertion/deletion (I/D) polymorphism in the 16th intron of the ACE gene (located on chromosome 17q23) in groups of patients with schizophrenia (n = 104 and 113), major depression (n = 55), and bipolar disorder (n = 87) compared to healthy control subjects (n = 87). There was no evidence for allelic or genotypic association of the polymorphism with any of the disorders or with tardive dyskinesia (TD) in patients with schizophrenia. In a sample of nuclear families (n = 61) made up of one or more patients with schizophrenia recruited with their parents, there was no evidence for biased transmission of ACE I/D alleles. Particularly in the case of schizophrenia, these findings do not support an association of the ACE I/D polymorphism with the phenotypes examined. © 2002 Wiley-Liss, Inc. |
Databáze: | OpenAIRE |
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