Molecular genetics of schizophrenia

Mowry, B. J. and Nancarrow, D. J. (2001). Molecular genetics of schizophrenia. In: Clinical and Experimental Pharmacology and Physiology. Proceedings of the Australian Neuroscience Society Symposium on Schizophrenia. Australian-Neuroscience-Society Symposium on Schizophrenia, Melbourne, (66-69). January-February 2000. doi:10.1046/j.1440-1681.2001.03399.x

Author Mowry, B. J.
Nancarrow, D. J.
Title of paper Molecular genetics of schizophrenia
Conference name Australian-Neuroscience-Society Symposium on Schizophrenia
Conference location Melbourne
Conference dates January-February 2000
Proceedings title Clinical and Experimental Pharmacology and Physiology. Proceedings of the Australian Neuroscience Society Symposium on Schizophrenia   Check publisher's open access policy
Journal name Clinical and Experimental Pharmacology and Physiology   Check publisher's open access policy
Place of Publication Carlton, Australia
Publisher Blackwell Science Asia
Publication Year 2001
Sub-type Fully published paper
DOI 10.1046/j.1440-1681.2001.03399.x
ISSN 0305-1870
Volume 28
Issue 1-2
Start page 66
End page 69
Total pages 4
Language eng
Abstract/Summary 1. Schizophrenia is a chronic, disabling brain disease that affects approxmately 1% of the world's population. It is characterized by delusions, hallucinations and formal thought disorder, together with a decline in socio-occupational functioning. While the causes for schizophrenia remain unknown, evidence from family, twin and adoption studies clearly demonstrates that it aggregates in families, with this clustering largely attributable to genetic rather than cultural or environmental factors. Identifying the genes involved, however, has proven to be a difficult task because schizophrenia is a complex trait characterized by an imprecise phenotype, the existence of phenocopies and the presence of low disease penetrance, 2. The current working hypothesis for schizophrenia causation is that multiple genes of small to moderate effect confer compounding risk through interactions with each other and with non-genetic risk factors, The same genes may be commonly involved in conferring risk across populations or they may vary in number and strength between different populations. To search for evidence of such genetic loci, both candidate gene and genome-wide linkage studies have been used in clinical cohorts collected from a variety of populations. Collectively, these works provide some evidence for the involvement of a number of specific genes (e.g. the 5-hydroxytryptamine (5-HT) type 2a receptor (5-HT2a) gene and the dopamine D-3 receptor gene) and as yet unidentified factors localized to specific chromosomal regions, including 6p, 6q, 8p, 13q and 22q, These data provide suggestive, but no conclusive, evidence for causative genes. 3. To enable further progress there is a need to: (i) collect fine-grained clinical datasets while searching the schizophrenia phenotype for subgroups or dimensions that may provide a more direct route to causative genes; and (ii) integrate recent refinements in molecular genetic technology, including modern composite marker maps, DNA expression assays and relevant animal models, while using the latest analytical techniques to extract maximum information in order to help distinguish a true result from a false-positive finding.
Subjects C1
321021 Psychiatry
730104 Nervous system and disorders
730107 Inherited diseases (incl. gene therapy)
730211 Mental health
0606 Physiology
1115 Pharmacology and Pharmaceutical Sciences
Keyword Pharmacology & Pharmacy
Complex Traits
Linkage (genetics)
Molecular Genetics
Risk Factors
First-degree Relatives
Q-Index Code C1

Document type: Conference Paper
Collection: School of Biomedical Sciences Publications
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Created: Tue, 14 Aug 2007, 16:43:42 EST