Increased prevalence of antibrain antibodies in the sera from schizophrenic patients

Henneberg, A.E.; Horter, Shona; Ruffert, S.

doi:10.1016/0920-9964(94)90004-3

Cited by 80 publications

(39 citation statements)

References 59 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Clozapine treatment did not induce a panel of common autoantibodies in our patients in the course of 6 weeks, in particular it did not induce autoantibodies against thromboplastin, which had been reported in a patient with clozapine-associated coagulopathy (Davis et al 1994). Autoantibodies against gangliosides, CNS tissue, and cell nuclei for which increased prevalences in schizophrenic patients were reported (Chengappa et al 1992;Chengappa et al 1995;Ganguli et al 1992;Henneberg et al 1994;LevySoussan et al 1994;Stevens and Weller 1992) were not present at all, neither at baseline nor after 6 weeks of clozapine treatment. However, because all of our patients were refractory to treatment with classic neuroleptics, our data fit well with the study of Levy-Soussan and colleagues (1994), who reported that the prevalence of autoantibodies is lower in patients who do not respond to classic neuroleptics.…”

Section: Discussionsupporting

confidence: 52%

Effects of Clozapine on In Vitro Immune Parameters A Longitudinal Study in Clozapine-Treated Schizophrenic Patients

Hinze-Selch

Becker

Stein

et al. 1998

Neuropsychopharmacology

View full text Add to dashboard Cite

Section: Discussionsupporting

confidence: 52%

Effects of Clozapine on In Vitro Immune Parameters A Longitudinal Study in Clozapine-Treated Schizophrenic Patients

Hinze-Selch

Becker

Stein

et al. 1998

Neuropsychopharmacology

View full text Add to dashboard Cite

“…The evidence strongly supports distinct roles for both maternal Croen et al, 2008b;Singer et al, 2008;Zimmerman et al, 2007) and patient (Henneberg et al, 1994;Libbey and Fujinami, 2010;Ryberg, 1982) autoantibodies in ASD, including an ability to affect structural brain development (Nordahl et al, 2013;Rossi et al, 2011). Offending antibodies of either origin appear to persist systemically for extended periods of time Piras et al, 2014;Singer et al, 2006;Zimmerman et al, 2007), and although there exists a correlation between the two there does appear to be at least some differences in effect (Piras et al, 2014).…”

Section: Anti-brain Antibodiesmentioning

confidence: 92%

“…Singh (2009) proposed a theoretical autoimmune mechanism for autism, suggesting that an environmental trigger (eg, a virus) could provoke faulty immune regulation that results in autoimmunity to the brain, leading to the observed neuropathology. Autoantibodies, such as those described above, have been found in patients of other autoimmune disorders, including multiple sclerosis (Ryberg, 1982), schizophrenia (Henneberg et al, 1994), and SLE (Libbey and Fujinami, 2010). Evidence for the association has mounted, including a 2015 study that found a more than double risk of ASD in children of mothers with SLE than those of controls (Vinet et al, 2015).…”

Section: Asd As An Autoimmune Disordermentioning

confidence: 97%

“…In addition to the prenatal, maternal autoantibodies previously discussed, numerous studies have reported the presence of circulating anti-brain immunoglobulins in patients with ASD, as well as related conditions such as multiple sclerosis (Ryberg, 1982), schizophrenia (Henneberg et al, 1994), and systemic lupus erythematosus (SLE) (Libbey and Fujinami, 2010;Mackay et al, 2015;Suurmond and Diamond, 2015). Singer et al (2006) found that children with autism were more likely than their non-autistic siblings or controls to have serum that tested positive via western blot to fresh human brain samples (caudate, putamen, and prefrontal cortex).…”

Section: Anti-brain Antibodies In Children With Asdmentioning

confidence: 99%

“…However, while work in this area is currently underway from several lines of investigation and in multiple laboratories, it seems evident that maternal autoantibodies appear to influence, if not define, a specific subset of ASD. Given the existence of autoantibodies associated with other neurological disorders such as schizophrenia (Henneberg et al, 1994) and multiple sclerosis (Ryberg, 1982), there is clearly more to be addressed as to both the genesis and function of these antibodies in neurodevelopmental disorders. It is also critical that this work is validated and replicated by more than one investigator.…”

Section: Animal Models Strongly Support the Maternal Autoantibody Modelmentioning

confidence: 99%

See 2 more Smart Citations

The Role of the Immune System in Autism Spectrum Disorder

Meltzer

Water

2016

Neuropsychopharmacol

387

293

View full text Add to dashboard Cite

Autism is a neurodevelopmental disorder characterized by deficits in communication and social skills as well as repetitive and stereotypical behaviors. While much effort has focused on the identification of genes associated with autism, research emerging within the past two decades suggests that immune dysfunction is a viable risk factor contributing to the neurodevelopmental deficits observed in autism spectrum disorders (ASD). Further, it is the heterogeneity within this disorder that has brought to light much of the current thinking regarding the subphenotypes within ASD and how the immune system is associated with these distinctions. This review will focus on the two main axes of immune involvement in ASD, namely dysfunction in the prenatal and postnatal periods. During gestation, prenatal insults including maternal infection and subsequent immunological activation may increase the risk of autism in the child. Similarly, the presence of maternally derived anti-brain autoantibodies found in~20% of mothers whose children are at risk for developing autism has defined an additional subphenotype of ASD. The postnatal environment, on the other hand, is characterized by related but distinct profiles of immune dysregulation, inflammation, and endogenous autoantibodies that all persist within the affected individual. Further definition of the role of immune dysregulation in ASD thus necessitates a deeper understanding of the interaction between both maternal and child immune systems, and the role they have in diagnosis and treatment.

show abstract

Increased Prevalence of Diverse N -Methyl-D-Aspartate Glutamate Receptor Antibodies in Patients With an Initial Diagnosis of Schizophrenia

Steiner¹,

Walter²,

Glanz³

et al. 2013

JAMA Psychiatry

331

174

View full text Add to dashboard Cite

Evidence for symptomatic convergence of schizophrenia and N-methyl-D-aspartate glutamate receptor (NMDA-R) encephalitis highlights the need for an assessment of antibody prevalence and specificity for distinct disease mechanisms in patients with a diagnosis of schizophrenia among glutamatergic pathophysiologic abnormalities in psychiatric disorders. Objectives: To compare the specificity and prevalence of NMDA-R antibodies in schizophrenia (DSM-IV criteria) with those of other psychiatric diagnoses and to determine whether antibody subtypes characterize overlap with and distinction from those in NMDA-R encephalitis. Design: Serum from 459 patients admitted with acute schizophrenia, major depression (MD), and borderline personality disorder (BLPD) or individuals serving as matched controls was obtained from our scientific blood bank. To explore epitope specificity and antibody subtype, IgA/IgG/IgM NMDA-R (NR1a or NR1a/NR2b) and ␣-amino-3-hydroxyl-5-methyl-4-isoxazole-propionate receptors (AMPA-R) (GluR1/GluR2) serum antibodies were determined. Participants: Two hundred thirty matched healthy controls were compared with patients (unmedicated for at least 6 weeks) with schizophrenia (n=121), MD (n=70), or BLPD (n=38). Main Outcome Measures: The primary outcome was the overall number of seropositive cases for NMDA-R and AMPA-R antibodies; the secondary outcome was disease specificity of IgA/IgG/IgM antibodies and epitope specificity for clinical subgroups. Results: Diverse NMDA-R antibodies were identified in 15 subjects, primarily those with an initial schizophrenia diagnosis (9.9%), opposed to MD (2.8%), BLPD (0), and controls (0.4%). Retrospectively, 2 patients initially classified as having catatonic or disorganized schizophrenia were reclassified as having misdiagnosed NMDA-R encephalitis (presence of specific serum and cerebrospinal fluid IgG NR1a antibodies). In all other seropositive cases, the antibodies consisted of classes IgA and/or IgM or were directed against NR1a/NR2b (not against NR1a alone). None of the patients or controls had antibodies against AMPA-R. Conclusions: Acutely ill patients with an initial schizophrenia diagnosis show an increased prevalence of NMDA-R antibodies. The repertoire of antibody subtypes in schizophrenia and MD is different from that with NMDA-R encephalitis. The latter disorder should be considered as a differential diagnosis, particularly in young females with acute disorganized behavior or catatonia.

show abstract

Increased prevalence of antibrain antibodies in the sera from schizophrenic patients

Cited by 80 publications

References 59 publications

Effects of Clozapine on In Vitro Immune Parameters A Longitudinal Study in Clozapine-Treated Schizophrenic Patients

Effects of Clozapine on In Vitro Immune Parameters A Longitudinal Study in Clozapine-Treated Schizophrenic Patients

The Role of the Immune System in Autism Spectrum Disorder

Increased Prevalence of Diverse N -Methyl-D-Aspartate Glutamate Receptor Antibodies in Patients With an Initial Diagnosis of Schizophrenia

Contact Info

Product

Resources

About