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chapter 14.doc

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PHSI 208
Neil Hibbert

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Molecular genetics  it does not appear that the genetic predisposition to s is transmitted by a single gene; several multi or polygenic models remains viable.  Hunt for s related genes has proven more difficult than expected for several reasons including 1) lack of preciseness in defining the boundaries of the clinical phenotype 2) absence of biological tests that confirm diagnostic categorization 3) clinical heterogeneity and the complex nature of s  Alternative strategies for s vulnerability gene identification were and are needed. S research turned to the endophenotypic strategy . endophentoyupes are characteristics that reflect the actions of genes predisposing an indiv to a disorder even in the absence of a diagnosable pathology.  Imp cuz indiv endophenotypoe are determined by fewer genes than the more complex s phenotype. Thus the complexity of genetic analyses would be reduced  Possible role of many specific genes: serotonin type 2A receptor (5—HT2a) gene, dopamine DS receptor gene, and chromosomal region on chromosome 6,8, 13 and 22. also suggested that G protein signalling 4 a gene localized to chromosome 1q23 plays a role in s susceptibility  Increasing evidence for an overlap in genetic susceptibility including s and bipolar disorder Evaluation of the genetic data  s is not complete due to genetics  S is defined by beh: it is a phenotype and thus reflects the influence of both genetics and enviro  Genetics predispose ppl to it and ten you need stress to bring it out Biochemical factors  best researched factors :dopamine Dopamine activity  excess dopamine leads to s is based on the fact that drugs used to treat s reduce dopamine activity but produce side effects remsnling the symp of Parkinson’s disease  Parkinson’s is known to be caused in part by low levels of dopamine in a particular nerve tract of the brain.  As time went on assumption that excess dopamine led to s was not true cuz the major metabolites of dopamine homovanillic acid (HVA) was not found in greater amounts in patients with s  Research on the antipsychotics mode of action suggest that the dopamine receptors are a more likely locus of disorder than the level of dopamine itself  excess dopamine receptors may not be responsible for all the symp of s; in fact they appear to be related to mainly to positive symp  amphetamines worsen positive symp and lessen negative one. Amtipsyhcotics lessen positive symmp but there effect on negative symp is less clear; some studies show no benefit while others show a reduction in negative symp  prefrontal cortex is thought to be esp relevant to the negative symp of s the under activity in this part of the brain may also be the cause of negative symp in s  antipsychotics do not have major effects on the dopamine neurons in the prefrontal cortex they are ineffective treatments for negative symp evaluation of the dopamine theory  dopamine theory isn’t complete theory of s other neurotransmitters  glutamate a transmitter that is widespread in the human brain may also play a role. Low levels of this have been found in cerebrospinal fluid of ppl with s  street drug PCP can induce psychotics states including both positive and negative sump in normal ppl. Interferes with one of glutamates receptors schizophrenia and the brain: structure and function  search for brain abnormality that causes s began as early as the syndrome was identified. Enlarged ventricles  this implies a loss of sub cortical brain cells. Structural problems in sub cortical temporal limbic areas such as the hippocampus and the basal ganglia and in the prefrontal and temporal cortex  CT and MRI scans reveal that esp males have enlarged ventricles. Research also
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