Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036341 (schizophrenia)
 60,220 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Conflicting views as to the form and content of delusions among African psychotics, notably the influence of cultural factors in the preliterate, led us to devote special attention to this area in a recent study of Bantu psychiatric patients. Our sample was drawn chiefly from Baragwanath Hospital serving the South Western Townships of Johannesburg, and smaller samples were drawn from mental hospitals, mental health society clinics, an old age home, and a middle class township in the Witwatersrand area. The degree of systematization and fixity of delusions in the sample as a whole, and in schizophrenia and manic-depressive psychosis in particular, were assessed. On the side of delusion content, cultural features such as witchcraft, animals as instruments of witchcraft, familiars, and ancestor worship are described. In conclusion, the relationship of cultural content of delusion to class, education and income are evaluated, with special attention to the influence of an early tribal background in our urban professional group, as illuminating the general issue reflected in our title.
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PMID:Universal and cultural features in the delusions of a black urban group. 123 71

Previous studies have yielded evidence for a locus conferring susceptibility to schizophrenia and schizophrenia spectrum disorders on chromosome 6p24-22 in a sample of multiply affected Irish families. We tested for linkage between highly polymorphic chromosome 6p24-22 markers and narrowly defined schizophrenia in a sample of 19 Southern African Bantu-speaking families, a population known to have diverged in the last 2000 years. There is no evidence to support the linkage of markers in this region of chromosome 6 to schizophrenia in this population.
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PMID:No evidence for linkage of chromosome 6p markers to schizophrenia in southern African Bantu-speaking families. 884 Mar 89

Previous studies have demonstrated possible linkage between chromosome 22 and one of the hypothesized schizophrenia susceptibility genes. Interpretation of these data, however, is not straightforward: although not significant at the level traditionally accepted to demonstrate linkage, reported lod scores were greater than should have occurred by chance for an unlinked marker based on simulation studies. Further, these studies used sample populations which were either of mixed nationality and ethnicity, or mixed ethnic ancestry from one country. We therefore tested for linkage between highly polymorphic chromosome 22 markers and schizophrenia in a sample of southern African Bantu-speaking black families, a population known to have diverged within the last 2,000 years. We also tested one candidate locus, the gene for the soluble form of catechol-O-methyl transferase (COMT) located at 22q11, which has been suggested as the cause of psychiatric symptoms observed in velo-cardio-facial syndrome (VCFS, including DiGeorge syndrome), and which is known to be functionally as well as genetically polymorphic. There is no evidence to support the linkage of markers on chromosome 22 to susceptibility to schizophrenia in this population, using either parametric or nonparametric analysis.
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PMID:No evidence for linkage of chromosome 22 markers to schizophrenia in southern African Bantu-speaking families. 895 Apr 8

Both direct and indirect evidence implicate excitatory amino acid neurotransmission in the aetiology of schizophrenia. The data are particularly suggestive for N-methyl-D-aspartate (NMDA) neurotransmission. Four of the six genes coding for subunits of the neural NMDA receptor have been mapped. We have studied segregation and allele sharing of markers in these four regions in a sample of southern African Bantu-speaking families multiply affected with DSM-III-R schizophrenia. This population was chosen because anthropological and linguistic data suggest that it has diverged from a small initial population within the past 1000 years, making shared genetic aetiology more likely. We find positive LOD score maxima of 0.876 at a marker D9S1838 on chromosome 9q34.3 near the NMDAR1 central subunit gene, 0.758 at marker D17S784 on chromosome 17q25 near the NMDAR2C potentiating subunit gene, and 0.453 at marker D12S77 near the NMDAR2B gene on chromosome 12p12 when analysing affected samples only. Only the region of NMDAR2A, on chromosome 16p13, can be excluded in this population. There is evidence of increased allele sharing on chromosomes 9p34.3 and 17q25 using APM. Multipoint allele-sharing analysis using GENEHUNTER does not reject possible effects on chromosome 9q34.3, but does not support any involvement of chromosome 17q25. We propose that the NMDA receptor may be involved in the genetic predisposition to schizophrenia in this population through covariation in several of the subunits, which is consistent with the genetic models of the inheritance of the disease.
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PMID:A linkage study of the N-methyl-D-aspartate receptor subunit gene loci and schizophrenia in southern African Bantu-speaking families. 928 63

This study evaluates the pathoplastic influences of ethnicity and culture on the symptoms of schizophrenia. A sample of 113 schizophrenics was evaluated using the Present State Examination (PSE) and Landmark's Manual for the Assessment of Schizophrenia. The subjects were 57 coloured and 56 black individuals. Six different tribes of Bantu, Negroid and Khoisan origin and with different language and cultural backgrounds were represented among the black subjects. Core symptoms remained basically the same in two groups, but the content of positive symptoms was found to be influenced by culture. However, no statistically significant differences in the presentation of negative symptoms were found in terms of quantity, but there were qualitative differences between the ethnic groups.
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PMID:A polydiagnostic approach to the differences in the symptoms of schizophrenia in different cultural and ethnic populations. 969 13

Several recent reports have provided evidence suggesting linkage of markers on chromosome 13q14.1-q32 to schizophrenia in families from England, Wales, Japan and the USA, but not in Chinese families. We tested for linkage between markers in this region and schizophrenia in a sample of 16 families multiply affected with schizophrenia drawn from the Bantu-speaking black population of South Africa. Twelve markers spanning 76 cM of chromosome 13q were examined in these analyses, including 10 markers covering the most positive region in the studies of the English, Welsh and Chinese families, and two additional markers yielding the largest positive LOD scores in the American study. The map of markers used was D13S126-14.6cM-D13S119-12.2cM-D13S144-10.+ ++2cM-D13S160-7.9cM-D13S121-6.3cM -D13S71-1.6cM-D13S122- 4.9cM-D13S128-8.9cM-D13S770-1.4cM-D13S7 79-2.2cM-D13S64-7.4cM-D13S173. Parametric two-point analysis yields strongly negative LOD scores across the region D13S71-D13S64 under all models, and D13S71-D13S173 under a recessive model, when analysing either the whole sample or affected individuals only. ALOD maxima are 0.0 when allowing for heterogeneity for all markers in this subset. Under recessive modelling, the ALOD maximum is 0.717, theta = 0.0, alpha = 0.45, for D13S126 when analysing all samples. Affected-only analysis of this marker yields a maximum LOD score of 0.645, theta = 0.1, and an ALOD maximum of 0.697, theta = 0.0, alpha = 0.55. Non-parametric multipoint analysis of these markers provides no support for excess sharing of alleles identical by descent, although D13S119 and D13S770 show some evidence for excess sharing of alleles identical by state.
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PMID:Failure to exclude a possible schizophrenia susceptibility locus on chromosome 13q14.1-q32 in southern African Bantu-speaking families. 980 Feb 16

Recent reports have strongly linked markers near the alpha-7 nicotinic cholinergic receptor subunit gene on human chromosome 15q13-q14 to a sensory gating deficit common in schizophrenics, and have shown positive though non-significant results linking this region to the primary phenotype of schizophrenia in a sample of North American families. We therefore tested for linkage between markers in this region of chromosome 15q and schizophrenia in a sample of 15 multiply affected and 5 single case families with schizophrenia drawn from the Bantu-speaking black population of South Africa. An initial replication using markers from the original study gave an affected-only LOD score maximum of 1.08 under a recessive model at Theta=0.00 for D15S1360, a dinucleotide polymorphism found on the same YAC as the alpha-7 receptor gene. Nonparametric affected-only multipoint analysis gave a Z-score of 1. 29, P=0.098, for D15S1360, and Z=1.45, p=0.075 for D15S118. We then increased the resolution of the map with an extended set of 20 markers. Again, two peaks were observed, with NPL scores of 1.81, p=0.037, at D15S1043 and 1.79 at D15S1360 and 1.80 at D15S1010, both p=0.037. Transmission disequilibrium testing of data from D15S1360 gave an allele-wise and genotype-wise chi(2) of 6.59, 2 df, p=0.037. Haplotype transmission disequilibrium testing using a restricted allele and haplotype set from D15S1043 and D15S1360 gave a global chi(2) of 10.647, 4 df, P=0.007, and a maximum chi(2) of 6.567, 1 df, P=0.004 for excess transmission of the 1.2 haplotype into affected offspring. Am. J. Med. Genet. (Neuropsychiatr. Genet.) 96:196-201, 2000.
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PMID:Haplotype transmission disequilibrium and evidence for linkage of the CHRNA7 gene region to schizophrenia in Southern African Bantu families. 1089 97