Study Results
Results available
Outcome measurements, participant flow, baseline characteristics, and adverse events have been published for this study.
View full resultsBasic Information
Get a concise snapshot of the trial, including recruitment status, study phase, enrollment targets, and key timeline milestones.
Recruitment Status
COMPLETED
Clinical Phase
PHASE1
Total Enrollment
8 participants
Study Classification
INTERVENTIONAL
Study Start Date
2012-09-30
Study Completion Date
2014-12-31
Brief Summary
Review the sponsor-provided synopsis that highlights what the study is about and why it is being conducted.
This study is a Phase 1 clinical trail to determine the safety, tolerability, and efficacy of Tocilizumab (Actemra) as an adjunct to antipsychotic medications in stable outpatients with schizophrenia. Tocilizumab (structural formula C6428H9976N1720O2018S42) is a recombinant humanized anti-human interleukin-6 (IL-6) receptor monoclonal antibody of the immunoglobulin (Ig) gamma-1 subclass. Tocilizumab is formulated as a concentrate for solution for infusion, and will be administered by intravenous infusion.
The investigators propose an 8-week trial to determine the safety, tolerability, and effectiveness of tocilizumab, given in addition to antipsychotic medications, in 10 stable outpatients with schizophrenia. The investigators hypothesize that tocilizumab will be associated with clinically significant improvement in cognition and total psychotic symptoms over the course of the trial. Tocilizumab is administered as an intravenous infusion every 4 weeks. Following a screening evaluation, participants will receive two infusions of tocilizumab, one at baseline and another at week 4 of the study. The investigators will measure changes in cognitive function and symptoms over an 8-week period. Complementing previous positive clinical trials of non-steroidal anti-inflammatory drugs, this would be a "proof-of-concept" study that targeting specific cytokines is a viable treatment for schizophrenia.
Interleukin 6 and its receptor were discovered and cloned at Osaka University, Japan, by Tadamitsu Kishimoto in the 1980s. In 1997, Chugai Pharmaceuticals began the clinical development of tocilizumab for the treatment of rheumatoid arthritis. Clinical studies for Castleman's disease and systemic juvenile idiopathic arthritis started in 2001 and 2002, respectively. Hoffmann-La Roche co-developed the drug due to a license agreement in 2003.
Data presented in 2008 showed the effectiveness of tocilizumab in combination therapy with methotrexate for rheumatoid arthritis treatment. In further studies, it was effective and generally well tolerated when administered either as monotherapy or in combination with conventional disease-modifying antirheumatic drugs in adult patients with moderate to severe rheumatoid arthritis.
The investigators propose an 8-week trial to determine the safety, tolerability, and effectiveness of tocilizumab, given in addition to antipsychotic medications, in 10 stable outpatients with schizophrenia. The investigators hypothesize that tocilizumab will be associated with clinically significant improvement in cognition and total psychotic symptoms over the course of the trial. Tocilizumab is administered as an intravenous infusion every 4 weeks. Following a screening evaluation, participants will receive two infusions of tocilizumab, one at baseline and another at week 4 of the study. The investigators will measure changes in cognitive function and symptoms over an 8-week period. Complementing previous positive clinical trials of non-steroidal anti-inflammatory drugs, this would be a "proof-of-concept" study that targeting specific cytokines is a viable treatment for schizophrenia.
Interleukin 6 and its receptor were discovered and cloned at Osaka University, Japan, by Tadamitsu Kishimoto in the 1980s. In 1997, Chugai Pharmaceuticals began the clinical development of tocilizumab for the treatment of rheumatoid arthritis. Clinical studies for Castleman's disease and systemic juvenile idiopathic arthritis started in 2001 and 2002, respectively. Hoffmann-La Roche co-developed the drug due to a license agreement in 2003.
Data presented in 2008 showed the effectiveness of tocilizumab in combination therapy with methotrexate for rheumatoid arthritis treatment. In further studies, it was effective and generally well tolerated when administered either as monotherapy or in combination with conventional disease-modifying antirheumatic drugs in adult patients with moderate to severe rheumatoid arthritis.
Related Clinical Trials
Explore similar clinical trials based on study characteristics and research focus.
Tocilizumab in Schizophrenia
NCT02874573
Schizophrenia
Psychotic Disorders
UNKNOWN
PHASE1
Siltuximab in Schizophrenia
NCT02796859
Schizophrenia
Psychotic Disorders
UNKNOWN
PHASE1/PHASE2
Tocilizumab as Add-On Treatment For Residual Positive, Negative, and Cognitive Symptoms of Schizophrenia
NCT02034474
Schizophrenia
Schizoaffective Disorder
COMPLETED
PHASE4
An Open-Label Study to Evaluate the Efficacy and Tolerability of Xanomeline/Trospium In First Episode/Early Phase Schizophrenia Patients
NCT06923891
Schizophrenia
NOT_YET_RECRUITING
PHASE4
Study Of An FDA-approved Drug As Additional Therapy In Patients With Schizophrenia
NCT00086593
Schizophrenia
COMPLETED
PHASE3
Detailed Description
Dive into the extended narrative that explains the scientific background, objectives, and procedures in greater depth.
Schizophrenia is a chronic, debilitating disorder with life-long consequences on affected individuals and families. Schizophrenia is also associated with impaired cognition or thinking, which persists despite currently available treatments, and is an important determinant of quality of life and overall function. Associations between immune system abnormalities and schizophrenia, in particular increased inflammation, are one of the more enduring findings in the field. Four of six trials found that treatment with non-steroidal anti-inflammatory drugs (NSAIDs) was associated with significant improvement in psychopathology (Muller et al., 2010a; Muller et al., 2010b). Serum cytokine levels predicted response in two studies (Laan et al., 2010; Muller et al., 2004), and another study found a trend for improved cognition (Muller et al., 2005) with adjunctive NSAID treatment. These findings provide important empirical support for a pathophysiological role for inflammation in a subset of patients with schizophrenia.
Cytokines are key regulators of inflammation that exert effects in the periphery and the brain. IL-6 is a cytokine produced by peripheral blood leukocytes, and central nervous system microglia and astrocytes. Serum IL-6 levels are increased in patients with schizophrenia, and two studies reported significant positive correlations between IL-6 and total psychopathology at baseline and following antipsychotic treatment (Miller et al., 2011). Schizophrenia is associated with impaired cognition, which persists despite current treatments, and is an important determinant of quality of life and overall function. In populations outside of schizophrenia, higher serum IL-6 levels are associated with poorer cognition, cognitive decline, and smaller hippocampal gray matter volume (Marsland et al., 2006; Marsland et al., 2008). In a first-episode psychosis sample, IL-6 messenger ribonucleic acid expression was a significant predictor of smaller left hippocampal volume (Mondelli et al., 2011).
Several other lines of evidence provide a theoretical background for targeting IL-6 in schizophrenia. Polymorphisms of the gene for IL-6 (Paul-Samojedny et al., 2010) and its receptor (Sun et al., 2008) have been associated with schizophrenia. In mice, a single maternal injection of IL-6 during pregnancy caused prepulse and latent inhibition deficits in the adult offspring (Smith et al., 2007). Prenatal maternal infections are a replicated risk factor for schizophrenia (Brown and Derkits, 2010). In a rat prenatal immune activation model, adult offspring have increased serum IL-6 levels, at an age with homology to the usual age of onset of schizophrenia, that are significantly decreased following treatment with haloperidol (Romero et al., 2007; Romero et al., 2010). Another animal study found that ketamine-induced neuronal production of IL-6 is responsible for the activation of brain NADPH-oxidase and subsequent dysfunction of fast-spiking parvalbumin-expressing interneurons (Behrens et al., 2008). These findings provide further support for a potential role of IL-6 in the pathophysiology of schizophrenia.
In our Preliminary Study, patients with schizophrenia, age 18-70 and taking non-clozapine antipsychotics, had a fasting blood draw for serum cytokines, and assessment of psychopathology, including cognition. Subjects were not taking NSAIDs, and had no history of immune disorders, illicit drug use in the past month, or antibiotic use in the past 2 weeks. In 39 patients, after controlling for potential confounding effects of age, sex, race, smoking, BMI, socioeconomic status, serum cortisol, psychotropic medications, intelligence quotient, and severity of psychopathology, higher serum IL-6 levels predicted greater cognitive impairment, measured by the Brief Assessment of Cognition in Schizophrenia (BACS) composite score, in a linear regression model (p=0.002, Figure 1). Higher IL-6 levels were also associated with significantly lower scores on the Verbal Memory (r=-0.40, p\<0.01) and Motor Speed (r=-0.42, p\<0.01) subtests of the BACS.
In the first year, one clinical trial is planned. We will conduct an 8-week open-label trial to determine the safety, tolerability, and efficacy of tocilizumab as an adjunct to antipsychotic medications in 10 stable outpatients with schizophrenia.
Tocilizumab has not been used before in the treatment of schizophrenia, and using it this way is experimental. The risks that have been found in people with rheumatoid arthritis are known, but there may be unknown risks when used in schizophrenia. Clinically significant adverse drug reactions include anaphylaxis (0.4%), infections (0.1-7.8%), intestinal perforation, neutropenia (7.0%), and cardiac failure. Known side effects of tocilizumab that are common include: increase in hepatic enzymes (AST, ALT), hypertension, headache, neutropenia, infusion-related reactions, upper respiratory tract infections, and nasopharyngitis.
Less common side effects include: peripheral edema, dizziness, rash, increased total cholesterol and LDL, hypothyroidism, diarrhea, abdominal pain, mouth ulcerations, gastric ulcer, stomatitis, weight gain, gastritis, thrombocytopenia, leukopenia, increased bilirubin, conjunctivitis, nephrolithiasis, bronchitis, cough, dyspnea, herpes simplex. Rare side effects include: cellulitis, fungal infections, diverticulitis, gastroenteritis, herpes zoster, hypertriglyceridemia, malignancy (including breast and colon), multiple sclerosis, otitis media, pneumonia, sepsis, tuberculosis, urinary tract infections, and varicella.
Subjects with schizophrenia will be accessed from outpatient psychiatry clinic at Georgia Health Sciences University or other satellite collaborative sites. The study has 5 visits: screening, baseline, and 2, 4, and 8 weeks. At Screening, all subjects will be administered the evaluation to sign consent, informed consent, and the structured clinical interview for Diagnostic and Statistical Manual psychosis and affective disorders modules. We will perform a medical history and physical exam, fasting labs (CBC, Complete Metabolic Panel, lipid panel, urinalysis, and urine drug screen (UDS)), a tuberculin skin test, and a 12-lead electrocardiogram. At Baseline, we will perform the Positive and Negative Syndrome Scale, BACS, and Clinical Global Impressions scale (CGI), and draw blood for IL-6 and high-sensitivity c-reactive protein (hsCRP). All subjects will receive a 4 mg/kg infusion of tocilizumab, the recommended starting dose for adults with rheumatoid arthritis. We will contact the subjects by phone on day 1 and 7 after the infusion to assess for any infusion-related events. At Week 2 and 4, we will perform an interval history, physical exam, Positive and Negative Syndrome Scale, BACS, and CGI. Different versions of the BACS will be used to avoid practice effects. At Week 4, we will obtain fasting labs (CBC, Complete Metabolic Panel, lipid panel, IL-6, hsCRP, and UDS), and subjects will receive a 4 mg/kg infusion of tocilizumab, We will contact the subjects by phone day 1 and 7 after the second infusion to assess for any infusion-related events. At Week 8, we will perform an interval history, physical exam, and administer the Positive and Negative Syndrome Scale, BACS, CGI, and obtain fasting labs (CBC, Complete Metabolic Panel, lipid panel, IL-6, hsCRP, and UDS). Patients will be withdrawn if they meet any exclusion criterion at any time point.
Cytokines are key regulators of inflammation that exert effects in the periphery and the brain. IL-6 is a cytokine produced by peripheral blood leukocytes, and central nervous system microglia and astrocytes. Serum IL-6 levels are increased in patients with schizophrenia, and two studies reported significant positive correlations between IL-6 and total psychopathology at baseline and following antipsychotic treatment (Miller et al., 2011). Schizophrenia is associated with impaired cognition, which persists despite current treatments, and is an important determinant of quality of life and overall function. In populations outside of schizophrenia, higher serum IL-6 levels are associated with poorer cognition, cognitive decline, and smaller hippocampal gray matter volume (Marsland et al., 2006; Marsland et al., 2008). In a first-episode psychosis sample, IL-6 messenger ribonucleic acid expression was a significant predictor of smaller left hippocampal volume (Mondelli et al., 2011).
Several other lines of evidence provide a theoretical background for targeting IL-6 in schizophrenia. Polymorphisms of the gene for IL-6 (Paul-Samojedny et al., 2010) and its receptor (Sun et al., 2008) have been associated with schizophrenia. In mice, a single maternal injection of IL-6 during pregnancy caused prepulse and latent inhibition deficits in the adult offspring (Smith et al., 2007). Prenatal maternal infections are a replicated risk factor for schizophrenia (Brown and Derkits, 2010). In a rat prenatal immune activation model, adult offspring have increased serum IL-6 levels, at an age with homology to the usual age of onset of schizophrenia, that are significantly decreased following treatment with haloperidol (Romero et al., 2007; Romero et al., 2010). Another animal study found that ketamine-induced neuronal production of IL-6 is responsible for the activation of brain NADPH-oxidase and subsequent dysfunction of fast-spiking parvalbumin-expressing interneurons (Behrens et al., 2008). These findings provide further support for a potential role of IL-6 in the pathophysiology of schizophrenia.
In our Preliminary Study, patients with schizophrenia, age 18-70 and taking non-clozapine antipsychotics, had a fasting blood draw for serum cytokines, and assessment of psychopathology, including cognition. Subjects were not taking NSAIDs, and had no history of immune disorders, illicit drug use in the past month, or antibiotic use in the past 2 weeks. In 39 patients, after controlling for potential confounding effects of age, sex, race, smoking, BMI, socioeconomic status, serum cortisol, psychotropic medications, intelligence quotient, and severity of psychopathology, higher serum IL-6 levels predicted greater cognitive impairment, measured by the Brief Assessment of Cognition in Schizophrenia (BACS) composite score, in a linear regression model (p=0.002, Figure 1). Higher IL-6 levels were also associated with significantly lower scores on the Verbal Memory (r=-0.40, p\<0.01) and Motor Speed (r=-0.42, p\<0.01) subtests of the BACS.
In the first year, one clinical trial is planned. We will conduct an 8-week open-label trial to determine the safety, tolerability, and efficacy of tocilizumab as an adjunct to antipsychotic medications in 10 stable outpatients with schizophrenia.
Tocilizumab has not been used before in the treatment of schizophrenia, and using it this way is experimental. The risks that have been found in people with rheumatoid arthritis are known, but there may be unknown risks when used in schizophrenia. Clinically significant adverse drug reactions include anaphylaxis (0.4%), infections (0.1-7.8%), intestinal perforation, neutropenia (7.0%), and cardiac failure. Known side effects of tocilizumab that are common include: increase in hepatic enzymes (AST, ALT), hypertension, headache, neutropenia, infusion-related reactions, upper respiratory tract infections, and nasopharyngitis.
Less common side effects include: peripheral edema, dizziness, rash, increased total cholesterol and LDL, hypothyroidism, diarrhea, abdominal pain, mouth ulcerations, gastric ulcer, stomatitis, weight gain, gastritis, thrombocytopenia, leukopenia, increased bilirubin, conjunctivitis, nephrolithiasis, bronchitis, cough, dyspnea, herpes simplex. Rare side effects include: cellulitis, fungal infections, diverticulitis, gastroenteritis, herpes zoster, hypertriglyceridemia, malignancy (including breast and colon), multiple sclerosis, otitis media, pneumonia, sepsis, tuberculosis, urinary tract infections, and varicella.
Subjects with schizophrenia will be accessed from outpatient psychiatry clinic at Georgia Health Sciences University or other satellite collaborative sites. The study has 5 visits: screening, baseline, and 2, 4, and 8 weeks. At Screening, all subjects will be administered the evaluation to sign consent, informed consent, and the structured clinical interview for Diagnostic and Statistical Manual psychosis and affective disorders modules. We will perform a medical history and physical exam, fasting labs (CBC, Complete Metabolic Panel, lipid panel, urinalysis, and urine drug screen (UDS)), a tuberculin skin test, and a 12-lead electrocardiogram. At Baseline, we will perform the Positive and Negative Syndrome Scale, BACS, and Clinical Global Impressions scale (CGI), and draw blood for IL-6 and high-sensitivity c-reactive protein (hsCRP). All subjects will receive a 4 mg/kg infusion of tocilizumab, the recommended starting dose for adults with rheumatoid arthritis. We will contact the subjects by phone on day 1 and 7 after the infusion to assess for any infusion-related events. At Week 2 and 4, we will perform an interval history, physical exam, Positive and Negative Syndrome Scale, BACS, and CGI. Different versions of the BACS will be used to avoid practice effects. At Week 4, we will obtain fasting labs (CBC, Complete Metabolic Panel, lipid panel, IL-6, hsCRP, and UDS), and subjects will receive a 4 mg/kg infusion of tocilizumab, We will contact the subjects by phone day 1 and 7 after the second infusion to assess for any infusion-related events. At Week 8, we will perform an interval history, physical exam, and administer the Positive and Negative Syndrome Scale, BACS, CGI, and obtain fasting labs (CBC, Complete Metabolic Panel, lipid panel, IL-6, hsCRP, and UDS). Patients will be withdrawn if they meet any exclusion criterion at any time point.
Conditions
See the medical conditions and disease areas that this research is targeting or investigating.
Schizophrenia
Study Design
Understand how the trial is structured, including allocation methods, masking strategies, primary purpose, and other design elements.
Allocation Method
NA
Intervention Model
SINGLE_GROUP
Primary Study Purpose
TREATMENT
Blinding Strategy
NONE
Study Groups
Review each arm or cohort in the study, along with the interventions and objectives associated with them.
Tocilizumab
Following a screening evaluation, participants will receive two infusions of tocilizumab, one at baseline and another at week 4 of the study. All subjects will receive a 4 mg/kg infusion of tocilizumab, the recommended starting dose for adults with rheumatoid arthritis.
Group Type
EXPERIMENTAL
Tocilizumab
Intervention Type
DRUG
Therapeutic/Pharmacologic Class of Drug:
Tocilizumab is a recombinant humanized anti-human interleukin-6 (IL-6) receptor monoclonal antibody of the immunoglobulin (Ig) gamma-1 subclass.
Type of Dosage Form:
Concentrate for solution for infusion.
Route of Administration:
Intravenous (i.v.) infusion.
Interventions
Learn about the drugs, procedures, or behavioral strategies being tested and how they are applied within this trial.
Tocilizumab
Therapeutic/Pharmacologic Class of Drug:
Tocilizumab is a recombinant humanized anti-human interleukin-6 (IL-6) receptor monoclonal antibody of the immunoglobulin (Ig) gamma-1 subclass.
Type of Dosage Form:
Concentrate for solution for infusion.
Route of Administration:
Intravenous (i.v.) infusion.
Intervention Type
DRUG
Other Intervention Names
Discover alternative or legacy names that may be used to describe the listed interventions across different sources.
Brand Name: Actemra
NDA/Serial Number: STN 125276/S022 (Cross ref: IND 11972)
Eligibility Criteria
Check the participation requirements, including inclusion and exclusion rules, age limits, and whether healthy volunteers are accepted.
Inclusion Criteria
* male and female
* age 18-50
* capable of giving informed consent
* diagnosis of schizophrenia
* stable based on clinical judgement, no psychiatric hospitalizations in past 3 months, and on the same psychotropic medications for \>4 weeks
* taking a non-clozapine antipsychotic
* age 18-50
* capable of giving informed consent
* diagnosis of schizophrenia
* stable based on clinical judgement, no psychiatric hospitalizations in past 3 months, and on the same psychotropic medications for \>4 weeks
* taking a non-clozapine antipsychotic
Exclusion Criteria
* imminent danger to self/others
* antibiotic use in the past 2 weeks
* current scheduled use of immunomodulatory agents
* history of an immune disorder
* illicit drug use in the past 30 days
* any unstable or untreated medical condition
* history of gastrointestinal ulcers, diverticulitis, malignancy, central nervous system demyelinating disorder, seizure disorder, or tuberculosis
* low absolute neutrophil (\<2000) or platelet (\<100,000) count
* abnormal hepatic (AST or ALT \>1.5 times the upper limit of normal) or renal (BUN or creatinine\>1.5 times the upper limit of normal) function
* any abnormal lab test result judged to be clinically significant
* active, chronic or recurrent infections
* pregnancy
* breastfeeding
* female and of child-bearing potential who is not using any contraception
* antibiotic use in the past 2 weeks
* current scheduled use of immunomodulatory agents
* history of an immune disorder
* illicit drug use in the past 30 days
* any unstable or untreated medical condition
* history of gastrointestinal ulcers, diverticulitis, malignancy, central nervous system demyelinating disorder, seizure disorder, or tuberculosis
* low absolute neutrophil (\<2000) or platelet (\<100,000) count
* abnormal hepatic (AST or ALT \>1.5 times the upper limit of normal) or renal (BUN or creatinine\>1.5 times the upper limit of normal) function
* any abnormal lab test result judged to be clinically significant
* active, chronic or recurrent infections
* pregnancy
* breastfeeding
* female and of child-bearing potential who is not using any contraception
Minimum Eligible Age
18 Years
Maximum Eligible Age
50 Years
Eligible Sex
ALL
Accepts Healthy Volunteers
No
Sponsors
Meet the organizations funding or collaborating on the study and learn about their roles.
Brian Miller
OTHER
Sponsor Role
lead
Responsible Party
Identify the individual or organization who holds primary responsibility for the study information submitted to regulators.
Brian Miller
Assistant Professor
Responsibility Role
SPONSOR_INVESTIGATOR
Principal Investigators
Learn about the lead researchers overseeing the trial and their institutional affiliations.
Brian Miller, MD, PhD, MPH
Role: PRINCIPAL_INVESTIGATOR
Augusta University - Department of Psychiatry and Health Behavior
Locations
Explore where the study is taking place and check the recruitment status at each participating site.
Georgia Health Sciences University
Augusta, Georgia, United States
Site Status
Countries
Review the countries where the study has at least one active or historical site.
United States
References
Explore related publications, articles, or registry entries linked to this study.
Muller N. COX-2 inhibitors as antidepressants and antipsychotics: clinical evidence. Curr Opin Investig Drugs. 2010 Jan;11(1):31-42.
Reference Type
BACKGROUND
Muller N, Krause D, Dehning S, Musil R, Schennach-Wolff R, Obermeier M, Moller HJ, Klauss V, Schwarz MJ, Riedel M. Celecoxib treatment in an early stage of schizophrenia: results of a randomized, double-blind, placebo-controlled trial of celecoxib augmentation of amisulpride treatment. Schizophr Res. 2010 Aug;121(1-3):118-24. doi: 10.1016/j.schres.2010.04.015. Epub 2010 May 31.
Reference Type
BACKGROUND
Muller N, Ulmschneider M, Scheppach C, Schwarz MJ, Ackenheil M, Moller HJ, Gruber R, Riedel M. COX-2 inhibition as a treatment approach in schizophrenia: immunological considerations and clinical effects of celecoxib add-on therapy. Eur Arch Psychiatry Clin Neurosci. 2004 Feb;254(1):14-22. doi: 10.1007/s00406-004-0478-1.
Reference Type
BACKGROUND
Laan W, Grobbee DE, Selten JP, Heijnen CJ, Kahn RS, Burger H. Adjuvant aspirin therapy reduces symptoms of schizophrenia spectrum disorders: results from a randomized, double-blind, placebo-controlled trial. J Clin Psychiatry. 2010 May;71(5):520-7. doi: 10.4088/JCP.09m05117yel.
Reference Type
BACKGROUND
Muller N, Riedel M, Schwarz MJ, Engel RR. Clinical effects of COX-2 inhibitors on cognition in schizophrenia. Eur Arch Psychiatry Clin Neurosci. 2005 Apr;255(2):149-51. doi: 10.1007/s00406-004-0548-4. Epub 2004 Nov 19.
Reference Type
BACKGROUND
Miller BJ, Buckley P, Seabolt W, Mellor A, Kirkpatrick B. Meta-analysis of cytokine alterations in schizophrenia: clinical status and antipsychotic effects. Biol Psychiatry. 2011 Oct 1;70(7):663-71. doi: 10.1016/j.biopsych.2011.04.013. Epub 2011 Jun 8.
Reference Type
BACKGROUND
Marsland AL, Petersen KL, Sathanoori R, Muldoon MF, Neumann SA, Ryan C, Flory JD, Manuck SB. Interleukin-6 covaries inversely with cognitive performance among middle-aged community volunteers. Psychosom Med. 2006 Nov-Dec;68(6):895-903. doi: 10.1097/01.psy.0000238451.22174.92.
Reference Type
BACKGROUND
Marsland AL, Gianaros PJ, Abramowitch SM, Manuck SB, Hariri AR. Interleukin-6 covaries inversely with hippocampal grey matter volume in middle-aged adults. Biol Psychiatry. 2008 Sep 15;64(6):484-90. doi: 10.1016/j.biopsych.2008.04.016. Epub 2008 Jun 2.
Reference Type
BACKGROUND
Mondelli V, Cattaneo A, Murri MB, Di Forti M, Handley R, Hepgul N, Miorelli A, Navari S, Papadopoulos AS, Aitchison KJ, Morgan C, Murray RM, Dazzan P, Pariante CM. Stress and inflammation reduce brain-derived neurotrophic factor expression in first-episode psychosis: a pathway to smaller hippocampal volume. J Clin Psychiatry. 2011 Dec;72(12):1677-1684. doi: 10.4088/JCP.10m06745. Epub 2011 May 18.
Reference Type
BACKGROUND
Paul-Samojedny M, Kowalczyk M, Suchanek R, Owczarek A, Fila-Danilow A, Szczygiel A, Kowalski J. Functional polymorphism in the interleukin-6 and interleukin-10 genes in patients with paranoid schizophrenia--a case-control study. J Mol Neurosci. 2010 Sep;42(1):112-9. doi: 10.1007/s12031-010-9365-6.
Reference Type
BACKGROUND
Sun S, Wang F, Wei J, Cao LY, Qi LY, Xiu MH, Chen S, Li XH, Kosten TA, Kosten TR, Zhang XY. Association between interleukin-6 receptor polymorphism and patients with schizophrenia. Schizophr Res. 2008 Jul;102(1-3):346-7. doi: 10.1016/j.schres.2008.04.018. Epub 2008 May 27. No abstract available.
Reference Type
BACKGROUND
Smith SE, Li J, Garbett K, Mirnics K, Patterson PH. Maternal immune activation alters fetal brain development through interleukin-6. J Neurosci. 2007 Oct 3;27(40):10695-702. doi: 10.1523/JNEUROSCI.2178-07.2007.
Reference Type
BACKGROUND
Brown AS, Derkits EJ. Prenatal infection and schizophrenia: a review of epidemiologic and translational studies. Am J Psychiatry. 2010 Mar;167(3):261-80. doi: 10.1176/appi.ajp.2009.09030361. Epub 2010 Feb 1.
Reference Type
BACKGROUND
Romero E, Ali C, Molina-Holgado E, Castellano B, Guaza C, Borrell J. Neurobehavioral and immunological consequences of prenatal immune activation in rats. Influence of antipsychotics. Neuropsychopharmacology. 2007 Aug;32(8):1791-804. doi: 10.1038/sj.npp.1301292. Epub 2006 Dec 20.
Reference Type
BACKGROUND
Romero E, Guaza C, Castellano B, Borrell J. Ontogeny of sensorimotor gating and immune impairment induced by prenatal immune challenge in rats: implications for the etiopathology of schizophrenia. Mol Psychiatry. 2010 Apr;15(4):372-83. doi: 10.1038/mp.2008.44. Epub 2008 Apr 15.
Reference Type
BACKGROUND
Behrens MM, Ali SS, Dugan LL. Interleukin-6 mediates the increase in NADPH-oxidase in the ketamine model of schizophrenia. J Neurosci. 2008 Dec 17;28(51):13957-66. doi: 10.1523/JNEUROSCI.4457-08.2008.
Reference Type
BACKGROUND
Other Identifiers
Review additional registry numbers or institutional identifiers associated with this trial.
Pro00000405
Identifier Type: -
Identifier Source: org_study_id
More Related Trials
Additional clinical trials that may be relevant based on similarity analysis.
Treating Cognition in Schizophrenia With Atomoxetine and Cognitive Remediation
NCT00628394
COMPLETED
PHASE4
A Study to Assess the Efficacy and Safety of ML-007C-MA for the Treatment of Inpatient Adults With Schizophrenia
NCT07038876
RECRUITING
PHASE2
Study of SPG302 in Adults With Schizophrenia
NCT06442462
RECRUITING
PHASE2
Safety and Efficacy Study for Cognitive Deficits in Adult Subjects With Schizophrenia
NCT01095562
COMPLETED
PHASE2
A Study of the Safety, PK, and Exploratory Efficacy of SP-624 in Acutely Psychotic Adult Subjects With Schizophrenia
NCT04510298
COMPLETED
PHASE1
A Randomized Controlled Trial With Rituximab for Psychotic Disorder in Adults
NCT05622201
RECRUITING
PHASE2
A Prospective, Open-label, Single-arm, Multicenter Study Evaluating the Efficacy of One Year Treatment With Xanomeline/Trospium on Cognitive Impairment in Clinically Stable Adult Participants With Schizophrenia.
NCT07084831
NOT_YET_RECRUITING
PHASE3
NBI-1117568-SCZ3029: Evaluation of NBI-1117568 in Inpatient Adults With Schizophrenia
NCT06963034
RECRUITING
PHASE3
NBI-1117568-SCZ3030: Evaluation of NBI-1117568 in Inpatient Adults With Schizophrenia
NCT07105098
RECRUITING
PHASE3
A Phase 2 Efficacy and Safety Study of TAK-063 in Participants With an Acute Exacerbation of Schizophrenia
NCT02477020
COMPLETED
PHASE2
In-Patient Study In Schizophrenic Patients
NCT00197093
COMPLETED
PHASE1
Safety and Efficacy of Study Drug Versus Placebo for Negative Symptoms of Schizophrenia
NCT00063297
COMPLETED
PHASE2
Ocrelizumab for Psychosis by Autoimmunity
NCT03971487
RECRUITING
PHASE1/PHASE2
An Exploratory, Double-arm, 8-week Study to Explore the Feasibility and Acceptability of Abbreviated Treatment with CT-156 in People with Schizophrenia.
NCT06486948
COMPLETED
NA
Safety and Tolerability of BI 409306 in Patients With Schizophrenia
NCT01892384
COMPLETED
PHASE1
Long-term Safety and Efficacy of ABT-126 in Subjects With Schizophrenia: An Extension Study for Subjects Completing Study M10-855 (NCT01655680)
NCT01834638
TERMINATED
PHASE2
A Study to Evaluate the Overall Effects of Treatment With Abbreviated CT-156 in People With Schizophrenia
NCT06136936
COMPLETED
NA
Proof of Concept Study of Cognitive Improvement in Patients With Schizophrenia
NCT00528905
COMPLETED
PHASE2
A Study of LY2140023 in Schizophrenia Patients With Prominent Negative Symptoms
NCT01052103
COMPLETED
PHASE2
An Extension Study of Safety and Tolerability of SEP-363856 in Adult Subjects With Schizophrenia
NCT02970929
COMPLETED
PHASE2
Biomarker Strategies for Medication-Enhanced Cognitive Training in Schizophrenia
NCT01555697
COMPLETED
PHASE1/PHASE2
Efficacy, Safety, Tolerability, and Pharmacokinetics of NBI-1117568 in Adults With Schizophrenia
NCT05545111
COMPLETED
PHASE2
Minocycline for Schizophrenia
NCT01809158
COMPLETED
PHASE4
Pilot Study of Atomoxetine To Enhance COgnition In Patients With Schizophrenia
NCT00488163
COMPLETED
PHASE4
Study of the Safety, Tolerability, and Pharmacokinetics of Once Weekly Zicronapine in Patients With Schizophrenia
NCT01377233
COMPLETED
PHASE2