Please use this identifier to cite or link to this item: http://hdl.handle.net/1959.13/32429
- Gene profiling in the amygdala in schizophrenia
Bowden, N. A.;
Scott, R. J.;
Tooney, P. A.
- There is a genetic component involved in the development of schizophrenia, however the genes involved remain unknown. The amygdala is one brain region that has been implicated in the pathogenesis of schizophrenia. To investigate gene expression changes in the amygdala in schizophrenia, microarray studies were performed on post-mortem tissue from the NSW Tissue Resource Centre. Arrays consisting of DNA oligos from 19,000 genes were used to identify genes whose expression were consistently and significantly altered in the amygdala from seven subjects with schizophrenia when compared to seven subjects with no history of psychiatric illness, matched for age, gender and post-mortem interval. This study identified 132 genes whose expression was consistently up- or down- regulated (fold change greater than 1.5) in at least four of the seven matched pairs. Analysis of 5 genes by Realtime PCR has confirmed these array results. Western Blotting is now being used to identify whether the alterations in gene expression also effect protein expression. Some of the genes with altered expression have functions in cellular signaling and myelination of axons. The effect of antipsychotic drug treatments on these genes needs to be determined to ascertain if the dysregulation is due to the pathogenesis of schizophrenia or its treatment. In conclusion, these findings support arrays studies performed by other investigators showing changes in other brain regions of the expression of genes involved in cellular signaling and myelination of axons, implicating these processes in the pathophysiology of schizophrenia.
- XIIth World Congress of Psychiatric Genetics. Abstracts for the XIIth World Congress of Psychiatric Genetics (Presented in the American Journal of Medical Genetics Part B: Neuropsychiatric Genetics Vol. 130B Iss. 1) (Dublin, Ireland 9-13 October, 2004) p. 145-145
- Publisher Link
- John Wiley & Sons, Inc.
- Resource Type
- conference paper