There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

Abstract

We have previously reported reduced serum levels of soluble intercellular adhesion molecule-1 (sICAM-1) in schizophrenic patients. A single-nucleotide polymorphism (SNP) of the ICAM-1 gene was described at position 241. The G-->A SNP results in a nonsynonymous amino acid exchange of the ICAM-1 protein, and the A allele was shown to be also associated with several immunological disorders like rheumatoid arthritis. We investigated 70 schizophrenic patients and 128 unrelated healthy control persons regarding the relationship between the serum levels of sICAM-1 and the ICAM-1 G214A polymorphism. We were able to replicate our previous finding of reduced sICAM-1 levels in schizophrenia. Healthy control persons carrying the polymorphic A allele showed markedly lower sICAM-1 serum levels than carriers of the homozygous GG wild type (p < 0.004). In contrast, no significant difference in the sICAM-1 serum levels were seen regarding the G241A genotype distribution in schizophrenic patients. We hypothesize that the biochemical effect of the G241A SNP is masked in schizophrenic patients, indicating a disease-related mechanism leading to reduced levels of sICAM-1 in schizophrenia.

Related collections

Most cited references 27

Record: found
Abstract: found
Article: not found

Schizophrenia: genes and environment.

Ming Tsuang (2000)

The historical and genetic foundations of our current understanding of schizophrenia are reviewed, as are the present and future directions for research. Genetic epidemiological investigations, including family, twin, and adoption studies have confirmed the contributions of genetic and environmental determinants of schizophrenia. For example, identical twins show average concordance rates of only 50%; rates of 100% would be expected on the basis of genetic equivalence alone. Genetic factors may cause errors in brain development and synaptic connections. A broad range of environmental components may further damage the brain. Biological components may include pregnancy and delivery complications, such as intrauterine fetal hypoxia, infections, and malnutrition. Primarily nonbiological components may include psychosocial stressors, such as residence in an urban area and dysfunctional family communication. It is likely that the environmental factors interact with the genetic liability in a negative manner to produce disorders in the schizophrenic spectrum. Genetic and environmental components of the disorder are examined, as well as their interactions in producing either neurodevelopmental syndromes or schizophrenia itself. The implication of these findings for prevention and treatment are considered.

0 comments Cited 95 times – based on 0 reviews      Review now

Bookmark

Record: found
Abstract: found
Article: not found

Beneficial antipsychotic effects of celecoxib add-on therapy compared to risperidone alone in schizophrenia.

R. Engel, Norbert Müller, Michael Riedel … (2002)

Abnormalities in the immune system in schizophrenia have been described. However, important findings such as high levels of activating cytokines in the CSF and signs of CNS inflammation have been controversial. The authors conducted a trial of the new selective cyclooxygenase-2 inhibitor celecoxib, an immunomodulatory drug, in schizophrenic patients to evaluate its therapeutic effects. In a prospective, double-blind evaluation, 50 patients with an acute exacerbation of schizophrenia were randomly assigned to either risperidone plus celecoxib or risperidone plus placebo. After a washout period, 25 patients received 2-6 mg/day of risperidone plus placebo and 25 received risperidone plus 400 mg/day of celecoxib for 5 weeks. The treatment effect was calculated by analysis of covariance. There were no significant differences between groups in age, sex, duration or severity of disease or psychopathology, or risperidone dose or plasma level. Over 5 weeks, both groups of patients showed significant improvement in scores on the Positive and Negative Syndrome Scale and on all subscales. However, the celecoxib group showed significantly greater improvement in the total score. Additional treatment with celecoxib has significant positive effects on the therapeutic action of risperidone with regard to total schizophrenia psychopathology. Moreover, the fact that treatment with an immunomodulatory drug showed beneficial effects on schizophrenia symptoms indicates that immune dysfunction in schizophrenia is not just an epiphenomenon but is related to the pathomechanism of the disorder. However, a nonimmunological therapeutic effect of celecoxib mediated by the N-methyl-D-aspartic acid receptor has to be taken into account.

0 comments Cited 71 times – based on 0 reviews      Review now

Bookmark

Record: found
Abstract: found
Article: not found

Elevated interleukin 6 is induced by prostaglandin E2 in a murine model of inflammation: possible role of cyclooxygenase-2.

Preston T. J. A. Williams, Ashley R. P. Hinson, E Shacter (1996)

Injection of mineral oils such as pristane into the peritoneal cavities of BALB/c mice results in a chronic peritonitis associated with high tissue levels of interleukin 6 (IL-6). Here we show that increased prostaglandin E2 (PGE2) synthesis causes induction of IL-6 and that expression of an inducible cyclooxygenase, Cox-2, may mediate this process. Levels of both PGE2 and IL-6 are elevated in inflammatory exudates from pristane-treated mice compared with lavage samples from untreated mice. The Cox-2 gene is induced in the peritoneal macrophage fraction isolated from the mice. A cause and effect relationship between increased macrophage PGE2 and IL-6 production is shown in vitro. When peritoneal macrophages are activated with an inflammatory stimulus (polymerized albumin), the Cox-2 gene is induced and secretion of PGE2 and IL-6 increases, with elevated PGE2 appearing before IL-6. Cotreatment with 1 microM indomethacin inhibits PGE2 production by the cells and reduces the induction of IL-6 mRNA but has no effect on Cox-2 mRNA, consistent with the fact that the drug inhibits catalytic activity of the cyclooxygenase but does not affect expression of the gene. Addition of exogenous PGE2 to macrophages induces IL-6 protein and mRNA synthesis, indicating that the eicosanoid stimulates IL-6 production at the level of gene expression. PGE2-stimulated IL-6 production is unaffected by addition of indomethacin. Taken together with the earlier finding that indomethacin diminishes the elevation of IL-6 in pristane-treated mice, the results show that PGE2 can induce IL-6 production in vivo and implicate expression of the Cox-2 gene in the regulation of this cytokine.

0 comments Cited 41 times – based on 0 reviews      Review now

Bookmark

All references

Author and article information

Journal

PubMed ID:: 15756053

DOI:: 10.1159/000082364

ScienceOpen disciplines: Chemistry

Keywords: Adolescent,Adult,Amino Acid Substitution,genetics,immunology,Autoimmune Diseases,blood,Cell Adhesion,DNA Mutational Analysis,Down-Regulation,Female,Gene Frequency,Genetic Testing,Humans,Intercellular Adhesion Molecule-1,Macrophage-1 Antigen,Macrophages,Male,Middle Aged,Mutation,Polymorphism, Genetic,Schizophrenia

ICAM G241A polymorphism and soluble ICAM-1 serum levels: evidence for an active immune process in schizophrenia.

Read this article at

Abstract

Related collections

Karger: Endocrinology

Most cited references 27

Schizophrenia: genes and environment.

Beneficial antipsychotic effects of celecoxib add-on therapy compared to risperidone alone in schizophrenia.

Elevated interleukin 6 is induced by prostaglandin E2 in a murine model of inflammation: possible role of cyclooxygenase-2.

Author and article information

Journal

Comments

Comment on this article

Similar content 277

Cited by 10

Most referenced authors 250