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)

This study replicates and extends earlier work by finding that low levels of platelet monoamine oxidase (MAO) activity correlate with sensation seeking, high ego strength, positive affect, and high leisure time activity levels, somewhat similar psychological correlates also being found for plasma amine oxidase activity. Although there are several ways in which a schizophrenia/MAO relationship may exist and still be congruent with the present data, these results pose difficulties for theories which link low MAO activity levels specifically to schizophrenia. Nothing in the present findings, however, is incongruent with the possibility of an association between low platelet MAO activity and bipolar affective disorder.
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PMID:Psychological correlates of monoamine oxidase activity in normals. 64 36

Two hundred eighty-five volunteers from a community college were screened on campus for accuracy of their smooth pursuit eye movements (SPEM) by electrooculograph (EOG). Those volunteers with the least and the most accurate SPEM were recalled to the laboratory for a comprehensive evaluation of clinical and demographic characteristics, family history, neurological status, and psychophysiological and biological measures, including SPEM [repeat EOG test and infrared (IR) test], an electroencephalogram, auditory and visual evoked potentials, reaction time (RT), the continuous performance task (CPT), platelet monoamine oxidase (MAO), plasma amine oxidase, and dopamine-beta-hydroxylase (DBH). Low-accuracy SPEM was associated with social isolation, inadequate rapport, eccentricity, and a variety of related schizotypal or schizophrenia-like characteristics, but not with generalized psychopathology or other demographic/medical/clinical history variables. Low-accuracy SPEM also was associated with neurological and psychophysiological abnormalities frequently observed in schizophrenic patients. These results suggest that impaired SPEM may reflect an underlying central nervous system dysfunction that is specifically associated with clinical and biological characteristics related to schizophrenia, even in the absence of overt schizophrenia.
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PMID:Clinical, psychophysiological, and neurological characteristics of volunteers with impaired smooth pursuit eye movements. 272 22

Plasma amine oxidase (PAO) activity has been implicated in the biology of schizophrenia. PAO activity is, in part, under genetic control, but its mode of inheritance has not been determined. To assess the genetic pattern of PAO activity and its relation to the transmission of schizophrenia, we studied 73 chronic schizophrenic probands and 217 first-degree relatives (siblings and parents). Single-major-locus hypotheses were tested by pedigree analysis methods for quantitative traits. The distribution of PAO activity indicated significant admixture. When the transmission probability model was used, the familial pattern of PAO activity was consistent with mendelian transmission; the environmental hypothesis was rejected. PAO activity was lower in schizophrenic patients than in unaffected relatives, but the mean reduction in enzyme activity was small (10.7%) and the two groups of subjects overlapped greatly in their PAO values. The difference between ill and well relatives was not statistically significant. However, schizophrenia spectrum disorders segregated with low PAO activity in families of low-activity probands, and a greater proportion of ill than well subjects clustered in the low PAO activity mode. The results are interpreted as follows: (1) The transmission of PAO activity may be determined in part by a single major autosomal gene. (2) Low PAO activity does not qualify as a major risk factor in the schizophrenic population at large; however, a relationship may exist between low PAO activity and the transmission of schizophrenia in families of patients with extremely low enzyme activity.
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PMID:Genetic analysis of plasma amine oxidase activity in schizophrenia. 386 44

Among 76 chronic schizophrenic patients, plasma amine oxidase activity was unrelated to paranoid/nonparanoid subtype, narrow/broad diagnostic criteria, prognosis, or age at onset. These clinical indices do not identify biological subtypes of schizophrenia with deviant plasma amine oxidase activity.
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PMID:Plasma amine oxidase and clinical features of schizophrenia. 402 99

The establishment of the new diagnostic category, Schizotypal Personality Disorder (SPD), has stimulated biological studies of patients with this disorder. Such studies offer the potential of better understanding the diagnosis and treatment of SPD as well as more clearly defining the boundaries of the schizophrenic disorders. SPD has been studied in the clinical setting, in family studies of schizophrenia, and in the biological high-risk paradigm. In most cases, biological variables associated with schizophrenia have been evaluated. Decreased activities of plasma amine oxidase and platelet monoamine oxidase have been associated with SPD in the families of schizophrenics and in "biological high-risk" studies. Smooth pursuit eye movement (SPEM) impairment has also been associated with SPD in a "biological high-risk" study of college students. Inferior backward masking performance has been demonstrated in SPD patients in the clinical setting. Other studies using psychophysiological measures have been applied to subjects with psychological characteristics similar to DSM-III SPD and found biological abnormalities similar to those reported in schizophrenia. These studies are consistent with the possibility that some individuals with SPD may share common psychobiological abnormalities with schizophrenic individuals and may sharpen our understanding of SPD and its relationship to schizophrenia.
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PMID:Biological markers in schizotypal personality disorder. 408 50

Activity levels of platelet monoamine oxidase (MAO) and plasma amine oxidase (PAO) were determined in eight chronic schizophrenic patients who had been treated with neuroleptic drugs for 3 months. The mean reduction in platelet MAO activity was 18.6%. The extent of decrease was statistically significant. The reduction in enzyme activity was unrelated to serum iron levels. PAO activity was unaltered. The implications for schizophrenia research are discussed.
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PMID:Neuroleptic drug effect on platelet monoamine oxidase and plasma amine oxidase in schizophrenia. 612 54

Plasma amine oxidase (PAO) activity was studied in 52 chronic schizophrenics, 130 first-degree relatives, and 36 normal control subjects. Enzyme activity was shown to be a heritable and stable characteristic. Age and sex effects were not present. Patients had lower PAO activity than did control subjects, although the difference fell short of statistical significance. Within families, reduced PAO activity was associated with schizophrenia spectrum disorders.
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PMID:Plasma amine oxidase and genetic vulnerability to schizophrenia. 683 Apr 6

Sedation is a common adverse effect of clozapine treatment, which may be partly related to clozapine binding to histamine receptors in the central nervous system. The objective of this study was to investigate whether single nucleotide polymorphisms (SNPs) in the histaminergic system are associated with sedation in clozapine-treated patients. The study population comprised 237 clozapine-treated, Finnish, Caucasian patients that were diagnosed with schizophrenia and 176 were genotyped using Illumina HumanCoreExome-12 BeadChip. Sedation levels were assessed using self-rating questions from the Liverpool University Neuroleptic Side Effect Rating Scale (LUNSERS). The relationships between 55 different SNPs in the histaminergic system and adverse sedation effects were examined. SNPs were analyzed separately, and in groups, to formulate a genetic risk score (GRS). A permutation test was performed to avoid type I errors. Eight linked SNPs (r2 = 1) in the HNMT gene were also associated with sedation according to the GLM, adjusted for age, gender and BMI (false-discovery-rate-adjusted p = 0.013). An association on a trend level between a GRS of four different SNPs (recessive histamine N-methyltransferase HNMT rs2737385, additive histamine receptor H1 rs1552498, dominant HRH1 rs17034063 and recessive amine oxidase, copper containing 1 AOC1 rs6977381) and sedation was found (permuted p-value = 0.066) in a generalized linear model (GLM) incorporating age, gender and body mass index (BMI; adjusted R2 = 0.22). Polymorphisms in genes encoding histamine receptors or enzymes related to histamine metabolism may explain individual variation in sedative effects experienced during clozapine treatment.
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PMID:Histaminergic gene polymorphisms associated with sedation in clozapine-treated patients. 2840 Jan 55