Genetics & Schizophrenia
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According to McGuffin et al. (1995), at the beginning of this century schizophrenia was already considered to have a genetic component. However, this was disputed during the 1960s by the word of R.D. Laing and others, who considered schizophrenia as primarily environmental, and as representing an adaptive response to a crazy-making culture. In looking carefully at the research, however, the current consensus is that there is clearly a genetic component to schizophrenia, although the exact method of transmission has not been identified. The intent in the following pages is to explore some of the research, looking at problems, methods, and future directions, along with the current state of knowledge. There are many problems associated with the study of schizophrenia, not the least of which it appears to be a complex syndrome that actually includes more than one disease. Clinical observation has supported the possibility that there are several different symptom "dimensions," each of which may result from a different pathophysiologic process. Pharmacologic investigation, genetic research, brain imaging, and other types of studies have indicated that schizophrenia cannot be associated with any one cause (Flaum, 1996). This makes it difficult to study and obtain results that are definitive. For example, simply in looking at genetic research, it is apparent that the disorder is probably genetically co
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taken into affect. This is helpful because it reinforces the genetic linkage and also indicates that unstable trinucleotide repeat DNA is also involved in some way (this being associated with the anticipation effect).
This is further supported by the work of a group under Gargus at the University of California, Irvine (Travis, 1997) which found a link between schizophrenia and a gene with a repeating nucleotide sequence on chromosome 22. In their study, which involved chromosome mapping of a region of chromosome 22, they discovered that schizophrenics had a longer CAG repeat, or stutter. This repeat had already been associated with several other neurodegenerative disorders. Still, as Travis reported, it has been difficult to obtain consistently replicable results for any of the gene studies and any of the reported linkages between gene segments and schizophrenia.
For example, researchers had previously hypothesized that an abnormality in glutamatergic function was of etiologic importance in schizophrenia. However, using a linage study of 23 English and Icelandic families with multiple cases of schizophrenia, researchers reported no significant connection between the GLUR6 glutamate receptor locus and schizophrenia (Chen et a
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Some common words found in the essay are:
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Approximate Word count = 2874
Approximate Pages = 11 (250 words per page)
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