Investigation of complement C4B deficiency in schizophrenia.

Abstract

Several lines of evidence suggest that autoimmune mechanisms might contribute to the development of schizophrenia. Important factors involved in immune responses in man include the human leukocyte antigens and components of the complement system. In the present study we attempted to confirm a positive association between a homozygous deficiency in complement factor C4B and schizophrenia as previously reported. We also determined parental genotypes in a subset of our schizophrenic patients to test the hypothesis of a genetic mechanism depending on the mother's genotype. C4B deficiency was found in similar frequency among patients (n = 176) and controls (n = 145). There was also no increased frequency of C4B deficiency in the mothers of schizophrenic patients. Our study does not support a widespread or consistent association between a deficiency in complement component C4B and schizophrenia.

• Authors: R Schroers, M M Nöthen, M Rietschel, M Albus, W Maier, S Schwab, D Wildenauer, R Fimmers, P Propping, G Dewald
• Journal: Human heredity (Hum Hered) 1997 Sep-Oct Vol. 47 Issue 5 Pg. 279-82 ISSN: 0001-5652 [Print] Switzerland
• PMID: 9358016 (Publication Type: Comparative Study, Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Complement C4b
• endodeoxyribonuclease NlaIV
• Deoxyribonucleases, Type II Site-Specific

Topics

• Alleles
• Complement C4b (deficiency, genetics)
• Deoxyribonucleases, Type II Site-Specific
• Female
• Gene Frequency
• Genes (genetics)
• Genotype
• Homozygote
• Humans
• Male
• Polymorphism, Restriction Fragment Length
• Schizophrenia (immunology)
• Sequence Analysis, DNA