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Schizophrenia

Evidence of infectious cause

  1. Increased rate of schizophrenia for infants born during spring/winter – there is a 5-8% increased risk for schizophrenia among those born in the winter-spring months, when infectious diseases are more prevalent and at times when other infections (measles, varicella, poliomyelitis) show increased activity. 1)
  2. Co-infections – persistent co-infections are generally a sign of an immune system disabled by the Th1 pathogensThe community of bacterial pathogens which cause chronic inflammatory disease - one which almost certainly includes multiple species and bacterial forms.. It's telling to note that there remains no conclusive evidence for any single kind of virus or bacteria always present in patients with schizophrenia.2) That said, a number of viruses and bacteria have been identified or implicated in schizophrenic patients including:
    • Borna disease virus 3)
    • Helicobacter pylori 4)
    • herpes simplex virus 5)
    • retroviruses 6)
  • Prenatal infection and schizophrenia – According to Alan S. Brown of Columbia University, “Accumulating evidence suggests that prenatal exposure to infection contributes to the etiology of schizophrenia.” In a 2006 study, Brown showed that prenatal infections such as rubella, influenza, and toxoplasmosis are all associated with higher incidence of schizophrenia.7) Brown found a seven-fold increased risk of schizophrenia when mothers were exposed to influenza in the first trimester of gestation. This work was echoed by a 2009 paper by Sørensen et al. who showed that bacterial infections (upper respiratory tract and gonococcal infections) were associated with elevated risk of the disease.8)
  • Increased suceptibility to other probable infectious diseases - There is an increased prevalence of Sjogren's, hypothyreosis and rheumatoid arthritis in schizophrenia.9)

More evidence

From bacteriality:

Think about syphilis. In 1913, it was discovered that the disease resulted from infection with the bacterium Treponema pallidum. Soon, the disease was dubbed the “Great Imitator” because its symptoms often resembled those of other diseases, particularly in the later stages. I think syphilis should be called the “Great Illustrator,” because it’s a disease that imitates a whole spectrum of other diseases. This suggests that we should be actively looking for a pathogenic cause in these other diseases as well – especially since so many illnesses are still considered to be of unknown cause. Back in the day, the psychoses associated with syphilis and schizophrenia were grouped together into a single category of illness. But as soon as syphilis was found to have a bacterial cause, we separated syphilitic insanity from what is now called schizophrenia, and assumed that schizophrenia was not caused by infection. Rather than just separating the two diseases we should have actively pursued the hypothesis that schizophrenia also has an infectious cause. The information we can gain from these kinds of relationships is far more enlightening than any genetic data.

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Schizophrenia tied to a range of autoimmuneA condition or disease thought to arise from an overactive immune response of the body against substances and tissues normally present in the body ills

NEW YORK (Reuters Health) - Results of a study suggest that schizophrenia may be associated with a larger range of autoimmune diseases than previously suspected.

Schizophrenia affects about 1 percent of the population and can trigger delusions, paranoia, and hallucinations. It is very difficult to treat. A few autoimmune disorders are thought to play some role in schizophrenia.

Dr. William W. Eaton, of the Johns Hopkins University, Baltimore, and colleagues examined the association between schizophrenia and a range of autoimmune diseases using three databases.

Included in the analysis were 7704 subjects diagnosed with schizophrenia between 1981 and 1998 and their parents, and age- and sex-matched controls and their parents.

Subjects with a history of one or more autoimmune diseases had a 45 percent higher risk of schizophrenia, according to the authors. Schizophrenia patients had a higher prevalence of nine autoimmune disorders compared with comparison subjects.

Compared with the parents of controls, the parents of schizophrenic patients had a higher prevalence of 12 autoimmune diseases.

The autoimmune disorders – thyrotoxicosis, celiac disease, acquired hemolytic anemia, interstitial cystitis, and Sjogren's syndrome – occurred more often in schizophrenic patients and their parents compared with the controls and their parents.

“In future clinical studies, it may be interesting to search for a family history of autoimmune diseases … in patients with schizophrenia,” Eaton's team suggests. “Eventually, individual or family disease comorbidity may help to elucidate shared etiologic pathways.”

SOURCE: American Journal of Psychiatry March 2006.

Researchers discover a possible link to an infectious agent in the human genome.

From Newsday March 20, 2007

MELVILLE, N.Y. A team of Long Island scientists has scanned the entire human genome for evidence of genes that play a role in schizophrenia and has discovered a hot spot near two genes that regulate the immune system.

Dr. Anil Malhotra and Todd Lencz of the Zucker Hillside Hospital campus of the Feinstein Institute for Medical Research in Glen Oaks, N.Y., found that certain markers within these genes were more common in patients with schizophrenia than in those without a history of the mental illness. Their study will appear today in the journal Molecular Psychiatry.

A small group of scientists has long proposed that infectious agents might play a role in schizophrenia.

A finding supported by multiple studies is that toxoplasma, a cat parasite, is two times more common among patients than normal volunteers. One percent of the population suffers from schizophrenia, a serious mental illness that can cause hallucinations, delusions, apathy, dulled emotion and cognitive problems.

The Hillside study looked at genes from 178 chronic schizophrenia patients and 144 volunteers. For computer analysis, they put the DNA from each individual onto a gene chip that has 500,000 markers, numbers along the entire stretch of the human genome.

When they found markers overrepresented in the patient population studied, they looked for genes at or near the marker. The two closest genes they identified are both involved with immune function and are activated when the body is responding to an infection.

The genes are on the male Y chromosome and the female X chromosome, although the genes don't have a specific sex-linked role, Malhotra said. Some of the markers were seen in as many as 30% of the schizophrenia patients, compared with 10% of healthy controls.

The scientists studied another group of 71 schizophrenia patients, and the markers pointed to the same two genes.

“There are a number of common and rare polymorphisms [varieties] that are overrepresented in patients with schizophrenia,” Malhotra said.

He suspects that cytokinesAny of various protein molecules secreted by cells of the immune system that serve to regulate the immune system., substances produced by the immune system, might play a role as a genetic switch that puts certain people at risk.

“It's interesting work,” said Dr. Robert Yolken, a professor of pediatrics and director of the Stanley Laboratory of Developmental Neurovirology at Johns Hopkins University School of Medicine. “It fits with the prediction that Dr. [E.] Fuller Torrey and I made that genes discovered in schizophrenia will be associated with an immune response.

“It would make sense that some of the genes are determinants of the response to infection.”

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Notes and comments

<DiseaseHierarchy>

Discover Magazine, “The Insanity Virus” http://dl.dropbox.com/u/2014679/Insanity%20Virus.pdf

Leweke, F. M., C. W. Gerth, et al. (2004). “Antibodies to infectious agents in individuals with recent onset schizophrenia.” Eur Arch Psychiatry Clin Neurosci 254(1): 4-8. 14991372

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.

Torrey, E. F., J. Miller, et al. (1997). “Seasonality of births in schizophrenia and bipolar disorder: a review of the literature.” Schizophr Res 28(1): 1-38. 9428062

More than 250 studies, covering 29 Northern and five Southern Hemisphere countries, have been published on the birth seasonality of individuals who develop schizophrenia and/or bipolar disorder. Despite methodological problems, the studies are remarkably consistent in showing a 5-8% winter-spring excess of births for both schizophrenia and mania/bipolar disorder. This seasonal birth excess is also found in schizoaffective disorder (December-March), major depression (March-May), and autism (March) but not in other psychiatric conditions with the possible exceptions of eating disorders and antisocial personality disorder. The seasonal birth pattern also may shift over time. Attempts to correlate the seasonal birth excess with specific features of schizophrenia suggest that winter-spring births are probably related to urban births and to a negative family history. Possible correlations include lesser severity of illness and neurophysiological measures. There appears to be no correlation with gender, social class, race, measurable pregnancy and birth complications, clinical subtypes, or neurological, neuropsychological, or neuroimaging measures. Virtually no correlation studies have been done for bipolar disorder. Regarding the cause of the birth seasonality, statistical artifact and parental procreational habits are unlikely explanations. Seasonal effects of genes, subtle pregnancy and birth complications, light and internal chemistry, toxins, nutrition, temperature/weather, and infectious agents or a combination of these are all viable possibilities.

Schizophr Res. 2010 Aug;121(1-3):46-54. Epub 2010 Jun 9. Structural brain alterations in schizophrenia following fetal exposure to the inflammatory cytokineAny of various protein molecules secreted by cells of the immune system that serve to regulate the immune system. interleukin-8. Ellman LM, Deicken RF, Vinogradov S, Kremen WS, Poole JH, Kern DM, Tsai WY, Schaefer CA, Brown AS. Department of Psychology, Temple University, Philadelphia, PA 19122-6085, United States. ellman@temple.edu Abstract BACKGROUND: Maternal infection during pregnancy has been repeatedly associated with increased risk for schizophrenia. Nevertheless, most viruses do not cross the placenta; therefore, the damaging effects to the fetus appear to be related to maternal antiviral responses to infection (e.g. proinflammatory cytokines). Fetal exposure to the proinflammatory cytokine interleukin-8 (IL-8) has been significantly associated with risk of schizophrenia in offspring. This study sought to determine the association between fetal exposure to IL-8 and structural brain changes among schizophrenia cases and controls. METHODS: Subjects were 17 cases diagnosed with schizophrenia from the Developmental Insult and Brain Anomaly in Schizophrenia (DIBS) study. Psychiatric diagnoses were determined among offspring with semi-structured interviews and medical records review. IL-8 was determined from assays in archived prenatal sera and volumetric analyses of neuroanatomical regions were obtained from T1-weighted magnetic resonance imaging in adulthood. Eight controls were included for exploratory purposes. RESULTS: Among cases, fetal exposure to increases in IL-8 was associated with significant increases in ventricular cerebrospinal fluid, significant decreases in left entorhinal cortex volumes and significant decreases in right posterior cingulate volumes. Decreases that approached significance also were found in volumes of the right caudate, the putamen (bilaterally), and the right superior temporal gyrus. No significant associations were observed among controls. CONCLUSION: Fetal exposure to elevations in maternal IL-8 led to structural neuroanatomic alterations among cases in regions of the brain consistently implicated in schizophrenia research. In utero exposure to elevations in IL-8 may partially account for brain disturbances commonly found in schizophrenia. Copyright 2010 Elsevier B.V. All rights reserved.

PMID: 20553865

Infections like the flu are common occurrences during pregnancy, and research has shown that children born to mothers who suffered from flu, viruses and other infections during pregnancy have about a 1.5 to 7 times increased risk for schizophrenia. A new study out of Temple University examines what’s behind that link.

In a study published this month in Schizophrenia Research, Temple University psychologist Lauren Ellman found that exposure during pregnancy to certain immune proteins, such as those produced in response to the flu, leads to increased risk for brain abnormalities associated with schizophrenia in offspring.

The good news, says Ellman, is that not all of the women in the study who showed an increase in immune proteins gave birth to offspring who developed brain alterations. “This tells us that some other factor — perhaps a genetic vulnerability or something from the environment — must also be present for the increased immune protein levels to lead to the brain alterations we identified,” she said.

Previous studies, including one by Ellman, have already established a link between maternal exposure to flu and increased risk for schizophrenia in offspring, but it was not clear why the link existed, because most infections do not cross the placenta. Researchers then began to look at maternal immune responses to infection as the possible cause for the increased risk.

Of particular interest to the researchers were proteins termed proinflammatory cytokines, which are produced by the body in response to infection.

“Now, it appears that the damaging effects to the fetus are related to these maternal responses to infection during pregnancy rather than to the infections themselves,” Ellman said.

Ellman's study was conducted on archived blood samples drawn during the 1950s and 1960s from a group of approximately 12,000 pregnant women during each trimester of their pregnancies. The women and their offspring were followed after delivery, so those whose children had developed schizophrenia could be easily identified.

Her study showed a direct correlation between structural brain changes among offspring diagnosed with schizophrenia and increases in maternal levels of interleukin-8 (IL-8), one of the proinflammatory cytokines produced when fighting infection during pregnancy.

“The brain abnormalities we found are ones consistently linked with schizophrenia, suggesting that an elevated immune response during pregnancy might contribute to some of the brain abnormalities associated with the disorder,” Ellman said.

Maternal IL-8 levels were not related to any brain changes among a control group of offspring, indicating that vulnerability to schizophrenia needed to be present for the fetal brain to be affected, she said.

“Our findings underscore the potential importance of prenatal contributions to schizophrenia, with implications for prevention, early intervention, and treatment strategies,” said Ellman.

Ellman is uniquely positioned to answer questions related to pregnancy and fetal development. An assistant professor of psychology in Temple's College of Liberal Arts, she examines how maternal stress and immune functioning during pregnancy impact fetal brain development.

“I set out to study the impact of stress during pregnancy, and it became clear pretty quickly that you couldn't study the impact of stress without looking at the immune system,” she said. “The two are completely intertwined.”

According to Ellman, one of the main ways pregnancy makes women susceptible to infections is that changes in the immune system during pregnancy reduce some of the body's key defenses. In addition, maternal emotional states, like stress, can alter immune functioning. This increased vulnerability to infection comes at a time when the fetal brain is experiencing enormous growth.

“In light of our study, which calls attention to a pregnant woman's increased susceptibility to infection and the potential risks to her developing fetus, it is easy to see why the medical community routinely recommends that women who are pregnant or planning to become pregnant take special precautions to prevent infection, such as getting vaccinated,” she said.

http://www.temple.edu/newsroom/2010_2011/08/stories/Immune_responses.htm

Arch Gen Psychiatry. 2010 Sep;67(9):889-894.

Neonatal Vitamin D Status and Risk of Schizophrenia: A Population-Based Case-Control Study.

McGrath JJ, Eyles DW, Pedersen CB, Anderson C, Ko P, Burne TH, Norgaard-Pedersen B, Hougaard DM, Mortensen PB.

D National Centre for Register-based Research, Taasingegade 1, University of Aarhus 8000, Aarhus C, Denmark. pbm@ncrr.dk.

Abstract

CONTEXT: Clues from the epidemiology of schizophrenia suggest that low levels of developmental vitamin D may be associated with increased risk of schizophrenia.

OBJECTIVE: To directly examine the association between neonatal vitamin D status and risk of schizophrenia.

DESIGN: Individually matched case-control study drawn from a population-based cohort.

SETTING: Danish national health registers and neonatal biobank.

PARTICIPANTS: A total of 424 individuals with schizophrenia and 424 controls matched for sex and date of birth.

MAIN OUTCOME MEASURES: The concentration of 25 hydroxyvitamin D(3) (25[OH]D3) was assessed from neonatal dried blood samples using a highly sensitive liquid chromatography tandem mass spectroscopy method. Relative risks were calculated for the matched pairs when examined for quintiles of 25(OH)D3.

RESULTS: Compared with neonates in the fourth quintile (with 25[OH]D3 concentrations between 40.5 and 50.9 nmol/L), those in each of the lower 3 quintiles had a significantly increased risk of schizophrenia (2-fold elevated risk). Unexpectedly, those in the highest quintile also had a significantly increased risk of schizophrenia. Based on this analysis, the population-attributable fraction associated with neonatal vitamin D status was 44%. The relationship was not explained by a wide range of potential confounding or interacting variables.

CONCLUSIONS: Both low and high concentrations of neonatal vitamin D are associated with increased risk of schizophrenia, and it is feasible that this exposure could contribute to a sizeable proportion of cases in Denmark. In light of the substantial public health implications of this finding, there is an urgent need to further explore the effect of vitamin D status on brain development and later mental health.

PMID: 20819982 [PubMed - as supplied by publisher]

http://healthland.time.com/2010/05/28/cold-sores-may-contribute-to-schizophrenia-symptoms/

Cold sores may contribute to schizophrenia symptoms10)

Schizophr Res. 2010 May;118(1-3):224-31. Epub 2010 Feb 13. Neuroanatomic and cognitive abnormalities related to herpes simplex virus type 1 in schizophrenia. Schretlen DJ, Vannorsdall TD, Winicki JM, Mushtaq Y, Hikida T, Sawa A, Yolken RH, Dickerson FB, Cascella NG. Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States. dschret@jhmi.edu Abstract Herpes simplex virus 1 (HSV-1) tends to replicate in the temporal cortex and can damage the limbic system. The presence of serum antibodies to HSV-1 is associated with cognitive impairment in adults with schizophrenia, suggesting that cerebral gray matter abnormalities might distinguish patient subgroups defined by HSV-1 exposure. We assessed 43 adult outpatients with schizophrenia. The assessment included clinical interviews, neurocognitive testing, anatomic brain magnetic resonance imaging and measures of serum IgG antibodies specific to herpes simplex viruses 1 and 2. We then compared 25 patients who tested positive for antibodies to HSV-1 with 15 who were seronegative for both HSV-1 and HSV-2. The seropositive patients performed significantly worse than the seronegative patients on four neuropsychological measures of psychomotor speed, executive functioning, and explicit verbal memory. Voxel-based morphometric analyses revealed that the same patients showed reduced gray matter volume in the anterior cingulate and areas of the cerebellum. Finally, performance on the test of psychomotor speed and executive functioning that showed the largest between- group effect size correlated with reduced gray matter volume in some of the same brain regions (cingulate and cerebellum) that distinguished the two HSV-1 subgroups. In these outpatients with schizophrenia, HSV-1 seropositivity and performance on a cognitive test that is highly sensitive to it co-localize to closely overlapping brain regions. Copyright © 2010 Elsevier B.V. All rights reserved. PMID: 20153952

Neuroinflammation in Schizophrenia-Related Psychosis: A Pet Study11)

the Abstract: Doorduin J, de Vries EF, Willemsen AT, de Groot JC, Dierckx RA, Klein HC. Department of Nuclear Medicine and Molecular Imaging, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands. j.doorduin@ngmb.umcg.nl AbstractSchizophrenia is a chronic and disabling brain disease characterized by psychotic episodes with unknown etiology. It is suggested that neuroinflammation plays a role in the pathophysiology of schizophrenia. Neuroinflammation is characterized by the activation of microglia cells, which show an increase in the expression of the peripheral benzodiazepine receptor. The isoquinoline (R)-N-(11)C-methyl-N-(1-methylpropyl)-1-(2-chlorophenyl)isoquinoline-3-carboxamide ((11)C-(R)-PK11195) is a peripheral benzodiazepine receptor ligand that can be used for the imaging of activated microglia cells, and thus neuroinflammation, with PET. We hypothesized that neuroinflammation would be more profound in schizophrenic patients during psychosis, and it was therefore investigated whether neuroinflammation was present in patients within the schizophrenia spectrum who were in a psychotic phase. METHODS: Seven patients within the schizophrenia spectrum who were recovering from psychosis were included. Recovering psychosis was defined by a score of 5 or more on 1 item of the positive scale of the positive and negative symptoms scale (PANSS) or a score of 4 on 2 items. The patients were compared with 8 age-matched healthy volunteers. Dynamic 60-min PET scans were acquired after the injection of (11)C-(R)-PK11195. All subjects underwent T1- and T2-weighted MRI, and the scans were visually examined for abnormalities and used for anatomic coregistration in data analysis. The PET data were analyzed with a 2-tissue-compartment model to calculate the binding potential, using the metabolite-corrected plasma curve as input. RESULTS: A significantly higher binding potential of (11)C-(R)-PK11195, indicative of neuroinflammation, was found in the hippocampus of schizophrenic patients than in healthy volunteers (2.07 +/- 0.42 vs. 1.37 +/- 0.30; P = 0.004). A nonsignificant 30% higher (11)C-(R)-PK11195 binding potential was found in the whole-brain gray matter of schizophrenic patients. The MR images did not reveal any visual abnormalities. CONCLUSION: The present study suggests that focal neuroinflammation may play an important role in schizophrenia during psychosis. PMID: 19837763 [PubMed - indexed for MEDLINE]

If you listen to the seminar at Kings College London ( http://www.youtube.com/watch?v=uha9lyVoEf0) you will hear at 54:22 the audience say “we never thought about that” when I was pointing out that antibodies were a result of innate immune system failure, rather than adaptive immune failure.

The key thing is that top scientists are indeed thinking about inflammationThe complex biological response of vascular tissues to harmful stimuli such as pathogens or damaged cells. It is a protective attempt by the organism to remove the injurious stimuli as well as initiate the healing process for the tissue. behind psychiatric and neurological disease, and we must try and guide those thought processes so that they start looking for the correct cause of the inflammation

..Trevor..

Schizophr Res. 2011 Jul;129(2-3):191-5. Epub 2011 May 5.

Increased prevalence of Chlamydophila DNA in post-mortem brain frontal cortex from patients with schizophrenia.

Fellerhoff B, Wank R.

Source

Institute of Immunology, University of Munich, Goethestrasse 31, D-80336 Munich, Germany; Immunotherapy Research Center, Immunis e.V., Pettenkoferstrasse 8, D-80336 Munich, Germany.

Abstract

Infection can initiate symptoms of mental illness. It has been shown previously that Chlamydophila DNA is present six times more often in the blood of patients with schizophrenia than in the blood of control individuals. Monocytes, the main targets of Chlamydiaceae infection, are microglia precursors. We identified Chlamydiaceae infection using blinded brain DNA samples derived from the frontal cortex. Using PCR and sequence analysis, we found Chlamydophila DNA to be four times greater in patients with schizophrenia than in controls (schizophrenia: N=34, microbial DNA frequency 23.5%; controls: N=35, microbial DNA frequency 5.7%; P=0.045, OR=5.08). Persistent Chlamydophila-infected microglia or neuronal cells may impair neuronal circuits and thus be a mechanism for causing psychiatric illness in these patients.

Copyright © 2011 Elsevier B.V. All rights reserved. PMID: 21546214

Mayo Clinic management strategies

Schizophrenia is a severe mental disorder that can result in hallucinations, delusions, and extremely disordered thinking and behavior.

References

1) , 5)
Viruses and schizophrenia: a focus on herpes simplex virus.
Yolken R
Herpes11 Suppl 2p83A-88A(2004 Jun)
2)
3)
Borna disease virus and psychiatry.
Taieb O, Baleyte JM, Mazet P, Fillet AM
Eur Psychiatry16p3-10(2001 Feb)
4)
Helicobacter pylori: a role in schizophrenia?
Yilmaz Y, Gul CB, Arabul M, Eren MA
Med Sci Monit14pHY13-6(2008 Jul)
6)
Retroviruses and the pathogenesis of schizophrenia.
Lewis DA
Proc Natl Acad Sci U S A98p4293-4(2001 Apr 10)
7)
Prenatal infection as a risk factor for schizophrenia.
Brown AS
Schizophr Bull32p200-2(2006 Apr)
8)
Association between prenatal exposure to bacterial infection and risk of schizophrenia.
Sørensen HJ, Mortensen EL, Reinisch JM, Mednick SA
Schizophr Bull35p631-7(2009 May)
9)
Bacterial persistence and expression of disease.
Domingue GJ Sr, Woody HB
Clin Microbiol Rev10p320-44(1997 Apr)
10)
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11)
Neuroinflammation in schizophrenia-related psychosis: a PET study.
Doorduin J, de Vries EF, Willemsen AT, de Groot JC, Dierckx RA, Klein HC
J Nucl Med50p1801-7(2009 Nov)
home/diseases/schizophrenia.txt · Last modified: 07.03.2017 by sallieq
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