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)

By means of enzyme immunoassay techniques to detect the presence of antibody to cytomegalovirus, the cerebrospinal fluid of 178 patients with schizophrenia, 17 patients with bipolar disorders, and 11 other psychiatric patients was compared with that of 79 neurological patients and 41 normal control subjects. The cerebrospinal fluid of 20 of the schizophrenic patients and 3 of the patients with bipolar disorders showed significant increases in immunoglobulin M antibody to cytomegalovirus; no difference was found in patients on or off psychotropic medications.
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PMID:Cytomegalovirus antibody in cerebrospinal fluid of schizophrenic patients detected by enzyme immunoassay. 628 83

The peroxidase-antiperoxidase method was employed to search for evidence of cytomegalovirus (CMV) or herpes simplex virus (HSV) antigen in the brains of 25 patients with a diagnosis of schizophrenia, 25 nonschizophrenic neuropsychiatric patients, and 16 nonpsychiatric control subjects. Brain specimens from patients with acute CMV and herpes encephalitis served as positive controls. Although early results with low-titer CMV antisera suggested immunoreactivity in specific brain regions of a small number of schizophrenic and control cases, the present studies with high-titer anti-CMV IgG did not give a positive immunoperoxidase reaction in sections from the basal forebrain, hypothalamus, or midbrain. Scattered neurons in the lateral vestibular nucleus and hippocampus showed questionable staining with CMV IgG in one schizophrenic patient and none in control subjects. No schizophrenic or control cases demonstrated an immune reaction to HSV antisera.
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PMID:A search for cytomegalovirus and herpes viral antigen in brains of schizophrenic patients. 633 38

The goal of these studies was to determine whether neonatal viral exposure leads to a deficit in information processing in adulthood. To accomplish this, rats were infected neonatally with rat cytomegalovirus, and acoustic startle responses were measured when rats were 120 days old. Acoustic startle was elicited by using a 118-decibel (dB) white noise alone or after a prepulse 10 dB above background (65 dB); responses were measured after an injection of saline or the dopamine agonist apomorphine. Response amplitudes after the pulse alone were not significantly altered by either viral exposure or apomorphine. Responses of animals exposed to the prepulse before the pulse were approximately 10% of that after the pulse alone and did not differ between control or virus-exposed animals injected with saline. Animals injected with apomorphine exhibited a greater startle response than animals injected with saline, and control and virus-exposed rats injected with apomorphine differed in the magnitude of their responses. Apomorphine attenuated responses after the prepulse, and virus-exposed animals exhibited more than twice the attenuation than non-virus-exposed animals. Analysis of prepulse inhibition, calculated from the acoustic startle data, indicated that although viral exposure alone did not significantly affect information processing, when virus-injected rats were exposed to apomorphine, a significant 38% decrease in prepulse inhibition was apparent. Findings demonstrate that rats infected neonatally with rat cytomegalovirus exhibit a deficit in sensorimotor gating upon dopamine stimulation, supporting a possible link between viral infection and schizophrenia.
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PMID:Neonatal cytomegalovirus exposure decreases prepulse inhibition in adult rats: implications for schizophrenia. 1044 Aug 92

Although there have been many studies surveying the prevalence of specific viral antibodies in a large cohort of patients with schizophrenia, changes in antibody levels during the course of acute illness have not been fully investigated. We conducted a preliminary study investigating levels of antibodies to 5 herpesviruses (herpes simplex virus type 1, cytomegalovirus, Epstein-Barr virus, varicella-zoster virus and human herpesvirus type 6) and 6 other viruses (measles, rubella, mumps, influenza A and B and Japanese encephalitis viruses) in paired sera of 8 patients with acute onset or exacerbation of schizophrenia. Assay for specific immunoglobulin M (IgM) antibody was also performed for herpesviruses and mumps. Neither any relevant change in antibody levels nor appearance of specific IgM antibody was observed for any of the viruses in any of the patients investigated. It is unlikely that the active infection or reactivation of these viruses has direct causal relationship to schizophrenia in these patients.
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PMID:No changes in paired viral antibody titers during the course of acute schizophrenia. 1047 57

We experienced two cases of infectious mononucleosis-like syndrome associated with human herpesvirus 6 (HHV-6). One of the patients had been under medication for depression and the other one for schizophrenia. Both of them were taking carbamazepine for more than a week along with the other drugs. The manifestation of the symptoms of those two were almost same, such as high fever, generalized eruption, liver dysfunction, lymph-adenopathy, and existence of atypical lymphocytes. Serological tests for EB virus, cytomegalovirus and herpes simplex virus showed no significant change while the tests for HHV-6 showed increased titers of IgG antibody during the courses. We also examined HHV-6 DNA by real time quantitative PCR tests for HHV-6, and they appeared significantly high in the peripheral blood samples.
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PMID:[Two cases of infectious mononucleosis-like syndrome associated with human herpes-virus 6]. 1213 54

Herpes simplex virus (HSV), Epstein-Barr virus (EBV), cytomegalovirus (CMV), and human herpesvirus-6 (HHV-6) are viruses capable of establishing latency. All of these infect the CNS and have been detected in human postmortem brains. Toxoplasma gondii is a protozoan organism which can reactivate in the brains of previously infected immunocompromised individuals. To screen for the presence of herpesviruses and T. gondii in postmortem orbital frontal brain samples from patients with schizophrenia, affective disorders, and controls, we used nested-polymerase chain reaction (n-PCR)/sequencing. We identified HHV-6B sequences in 2/51 postmortem brain samples but no sequences from other herpesviruses. We did not detect sequences of T. gondii in the postmortem brains. Additional studies including ones directed at the sensitive detection of viral nucleic acids in multiple brain regions should be directed at confirming or excluding a role for viruses and protozoa in the etiology of these disorders.
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PMID:Herpesviruses and Toxoplasma gondii in orbital frontal cortex of psychiatric patients. 1250 39

We investigated the levels of antibodies to infectious agents in the serum and cerebral spinal fluids (CSFs) of individuals with recent onset schizophrenia and compared these levels to those of controls without psychiatric disease. We found that untreated individuals with recent onset schizophrenia had significantly increased levels of serum and CSF IgG antibody to cytomegalovirus and Toxoplasma gondii as compared to controls. The levels of serum IgM class antibodies to these agents were not increased. Untreated individuals with recent onset schizophrenia also had significantly lower levels of serum antibody to human herpesvirus type 6 and varicella zoster virus as compared to controls. Levels of antibodies to herpes simplex virus type 1, herpes simplex virus type 2, and Epstein Barr virus, and did not differ from cases and controls. We also found that treatment status had a major effect on the levels of antibodies in this population. Individuals who were receiving treatment had lower levels of antibodies to cytomegalovirus and Toxoplasma gondii, and higher levels of serum antibodies to human herpesvirus type 6 as compared to untreated individuals. The level of antibodies to Toxoplasma and human herpesvirus type 6 measured in treated individuals did not differ from the levels measured in controls. In the case of cytomegalovirus, the levels of CSF antibodies in treated individuals did not differ from those of controls, while the level of serum IgG antibodies to CMV remained slightly greater than controls in this population. Our studies indicate that untreated individuals with recent onset schizophrenia have altered levels of antibodies to cytomegalovirus, Toxoplasma gondii, and human herpesvirus type 6 while the levels of these antibodies in treated individuals with recent onset schizophrenia are similar to those of controls. These findings indicate that infectious agents may play a role in the etiopathogenesis of some cases of schizophrenia.
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PMID:Antibodies to infectious agents in individuals with recent onset schizophrenia. 1499 72

Several lines of evidence suggest that cytomegalovirus (CMV) may play an aetiological role in schizophrenia. Epidemiologically, both have a worldwide distribution and an increased prevalence in lower socioeconomic groups. Studies have reported that some patients experiencing initial episodes of schizophrenia have increased levels of IgG antibodies against CMV, but not other herpes viruses, in their sera and CSF. Treatment with antipsychotic medications may result in a decrease in CMV antibodies, while treatment with anti-herpes virus and anti-inflammatory medications may reduce symptoms in some individuals with schizophrenia. There is also some overlap in the genes that are thought to operate in CMV infections and schizophrenia. The strongest argument against the role of CMV in schizophrenia is the absence of the traditional CMV neuropathological changes in the brains of individuals with schizophrenia; however, neuropathological studies of CMV have mostly been conducted in immune-compromised individuals. Further studies on CMV and schizophrenia are needed and may lead to improved treatments for schizophrenia.
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PMID:Cytomegalovirus and schizophrenia. 1704 25

Viral infection may be a risk factor for schizophrenia and has been associated with decreased cognitive functioning in patients. We report associations of SNPs at MICB (MHC class I polypeptide-related sequence B, chromosome 6p21) with cytomegalovirus and herpes simplex virus 1 seropositivity. We previously found associations with schizophrenia on chromosome 6p21 among patients seropositive for cytomegalovirus (CMV) and herpes simplex virus 1 (HSV1). To localize the associations further, we genotyped 26 SNPs spanning 100 kb in a sample of 236 Caucasian schizophrenia patients and 240 controls. Based on suggestive associations, we selected five SNPs at MICB to assay among two additional Caucasian samples that had been serotyped for CMV and HSV1: a case-control sample recruited in Baltimore (n=272 cases, 108 controls), and a case-parent trio sample recruited in Pittsburgh (n=221). Among Baltimore control individuals there were significant associations with antibody status for infectious agents: rs1051788 with HSV1 seropositivity (p=0.006) and rs2523651 with cytomegalovirus seropositivity (p=0.001). The former association was also detectable among the parents of cases recruited in Pittsburgh (p=0.024). Neither viral association was noted among the schizophrenia cases. With respect to schizophrenia risk, significant transmission distortion was noted at rs1051788 and rs1055569 among the case-parent trios regardless of antibody status (p=0.014 and 0.036 respectively). A similar trend for association with schizophrenia liability at rs1051788 in the Baltimore sample did not attain statistical significance. There are a number of explanations for the associations, including chance variation, as well as gene-virus interactions. Further replicate studies are warranted, as are functional studies of these polymorphisms.
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PMID:Polymorphisms in MICB are associated with human herpes virus seropositivity and schizophrenia risk. 1756 76

The infectious theory of psychosis, prominent early in the twentieth century, has recently received renewed scientific support. Evidence has accumulated that schizophrenia and bipolar disorder are complex diseases in which many predisposing genes interact with one or more environmental agents to cause symptoms. The protozoan Toxoplasma gondii and cytomegalovirus are discussed as examples of infectious agents that have been linked to schizophrenia and in which genes and infectious agents interact. Such infections may occur early in life and are thus consistent with neurodevelopmental as well as genetic theories of psychosis. The outstanding questions regarding infectious theories concern timing and causality. Attempts are underway to address the former by examining sera of individuals prior to the onset of illness and to address the latter by using antiinfective medications to treat individuals with psychosis. The identification of infectious agents associated with the etiopathogenesis of schizophrenia might lead to new methods for the diagnosis, treatment and prevention of this disorder.
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PMID:Are some cases of psychosis caused by microbial agents? A review of the evidence. 1826 2


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