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)

The in vivo frequency of mutants resulting from mutation at the hprt locus in human T-lymphocytes was determined with a cloning assay. T-lymphocytes were obtained from 14 individuals diagnosed with schizophrenia and 5 controls. No significant difference in mutant frequency was observed between the 2 groups. In addition, DNA-repair capacity was measured with the unscheduled DNA synthesis technique in lymphocytes from 7 individuals diagnosed with schizophrenia and 7 controls. Repair capacity was determined following treatment with MMS, MNNG, and 20 J/m2 ultraviolet light. No significant differences in DNA repair were observed between the patient and control groups in response to any of the 3 DNA-damaging agents. These results argue against differences between normal and schizophrenic individuals with respect to in vivo mutant frequency or their capacity to repair DNA lesions induced by MMS, MNNG, or ultraviolet radiation.
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PMID:DNA repair and mutant frequency in schizophrenia. 171 95

Interest in genetic marker studies of schizophrenia has been considerably enhanced by the advent of recombinant DNA technology, which has dramatically increased the number of available markers. In the present paper, we review studies that have been carried out using classical markers as well as the more recent molecular studies. The problems that arise when schizophrenia is studied in this way are discussed and attempts are made to account for some of the conflicting findings in this area.
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PMID:DNA and classical genetic markers in schizophrenia. 182 8

Genetic studies of alcoholics, their families and controls have given credence to the idea that genetic influences in alcoholism exist, and set the stage for efforts to identify alcoholism-susceptibility genes (Devor and Cloninger, 1989). My purpose is not to review the genetics of alcoholism, but rather to review the genetic approaches that have been successful in identifying the genes responsible for genetic conditions such as muscular dystrophy and cystic fibrosis. In these disorders our current knowledge of the basic biochemical defect was derived directly from the cloning of the gene that is defective in the disorder. The cloned gene provides DNA probes for carrier identification and prenatal diagnosis, while knowledge of the basic defect allows new and direct investigation of potential therapeutic strategies. The genetic approach is much less definitive when it comes to the study of polygenic or multifactorial disorders such as schizophrenia or Alzheimer's disease. In the case of alcoholism the problem is exacerbated not only by environmental factors but also by phenotypic and genetic heterogeneity. The lack of a clear inheritance pattern means that plausible modes of inheritance must be invoked and tested on families with multiple affected members. Direct segregation analysis may not be possible and the less informative analysis of sib-pairs may be the method of choice. Ultimately, however, it should be possible to identify and clone those genes that play a major role in determining susceptibility to alcoholism. Once cloned, the protein products can be identified, and study of their function should lead to new understanding of the complex biological processes involved in this disorder.
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PMID:Molecular genetic approaches to the study of individual risk in alcoholism. 184 36

Several psychophysiological abnormalities associated with schizophrenia have been proposed as genetic trait markers of vulnerability to the disorder. Smooth pursuit eye tracking dysfunction and abnormal long latency event-related potentials are the most promising candidates. Both are independent of the effects of psychotropic medication or mental state at the time of testing, and twin studies demonstrate that each has a high level of heritability. Having recorded smooth pursuit eye tracking and event-related potentials in 20 high-density schizophrenic families, we find abnormalities in one or both measures in most of the families studied. The abnormalities, when present, occur in the family members with schizophrenia and other forms of functional psychosis, and they have a bimodal distribution with approximately half the nonschizophrenic relatives also showing eye tracking dysfunction and/or abnormal event-related potentials. Some of these relatives had psychiatric symptoms; others were normal. Our results suggest that psychophysiological examination can help to clarify the boundaries of schizophrenia spectrum disorder. By helping to decide the phenotypic status of nonschizophrenic family members, this should increase the power of DNA linkage studies.
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PMID:Auditory P300 and eye tracking dysfunction in schizophrenic pedigrees. 192 59

"A considerable proportion of the variance in the liability to develop schizophrenia may be genetic, but segregation analysis, to establish a mode of transmission, has not produced a consistent result. One of these studies was carried out in Iceland and made use of the large family size and extensive genealogical information present in that country. Here we demonstrate genetic linkage of two DNA polymorphisms on the long arm of human chromosome 5 to schizophrenia in seven British and Icelandic families with multiple affected members. The results indicate the existence of a gene locus with a dominant schizophrenia-susceptibility allele. Inheritance of the allele in the families studied suggests that it may also predispose to psychiatric conditions such as schizophrenia spectrum disorders and a variety of other disorders. This report provides the first strong evidence for the involvement of a single gene in the causation of schizophrenia."
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PMID:Localisation of a susceptibility locus for schizophrenia on chromosome 5. 197 58

Disorders in the DNA repair in the human lymphocytes isolated from patients with Marfan's syndrome, homocystinuria, schizophrenia, and gout have been found. In this investigation criteria used estimating the DNA repair were the following: host cell reactivation (vaccinia virus reactivation) and its mutagenesis, DNA repair synthesis, resynthesis of DNA breakages. Lymphoblastoid interferon was used as a modulator of DNA repair activity. Pretreatment of normal human cells with interferon stimulated all steps of DNA repair. In human cells with disorders, interferon stimulated DNA repair (XP) in some cases but failed in others.
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PMID:DNA repair and human pathology. 209 26

We analysed six multiplex pedigrees of schizophrenia for linkage to two DNA probes mapping to the chromosome 5q11-q13 region where linkage to a gene for schizophrenia was recently reported. Analyses were conducted using three penetrance models and considering the affected state to be schizophrenia, the schizophrenia spectrum, and all psychiatric diagnoses. All analyses gave consistently negative lod scores. Although the region was not formally excluded, no evidence for linkage was found.
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PMID:The Iowa multiplex family study of schizophrenia: linkage analyses on chromosome 5. 214 Jul 77

The prediction of risk for mental illnesses that have a strong genetic basis has usually been carried out by employing empirically derived estimates of recurrence observed in family studies. Because systematic methods of mapping the human genome with DNA polymorphisms have been developed it is possible that prenatal prediction of certain mental illnesses may eventually become a more accurate method of risk prediction than the empirical method currently used. Recombinant DNA technology as used in genetic linkage studies can also specify a mode of genetic transmission and lead on to aetiological studies of the disorder. The latter will result from the molecular cloning and sequencing of the responsible genetic mutations. The use of recombinant DNA technology has enabled single-gene effects to be found in schizophrenia, manic depression and Alzheimer's disease. In highly selected families it is now possible to calculate the risk of developing certain mental illnesses by DNA testing before birth. Failure to find linkages in separate schizophrenia, manic depression and Alzheimer's disease family samples has also been reported, indicating that there is heterogeneity of linkage with genes at several distinct genetic loci that contribute susceptibility to very similar clinical disorders. Resolution of the degree to which there is heterogeneity of linkage and a further examination of the factors which influence the variable effects of the abnormal genes predisposing to mental illness will both be necessary before accurate risk prediction can become feasible.
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PMID:Recent advances in the genetics of psychiatric disorder. 233 24

Employing the appropriate technique the authors have examined lymphocytes of 26 patients suffering from schizophrenia of different types. The study has shown distinct disorders of DNA reparation associated with this disease, which is suggestive of deficiency or noncoordination of the enzymatic system explained by mutations in corresponding genes. Disorders of DNA reparation have until recently been known to be associated only with hereditary diseases.
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PMID:[Disordered DNA repair in the lymphocytes of patients with schizophrenia depending on the form of the course of the disease]. 245 40

In schizophrenia patients, the level of T-lymphocytes with cytogenetic aberrations is elevated, and the ability of these cells for PGA-blast-transformation and the interferon synthesis is reduced. The elevation of the lymphocytes ability for blast-transformation in the presence of the native preparation of DNA and for lysis of the erythrocytes proper is marked in these patients. The observed changes were especially marked in schizophrenia with an interrupted course.
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PMID:[Cytogenetic instability, the ability to produce interferon and immunoreactivity of blood lymphocytes in patients with schizophrenia]. 250 74


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