Failure to Detect Immunologic Stigmata in Schizophrenia

Ehrnst, Anneka; Wiesel, Frits‐Axel; Bjerkenstedt, Lars; Tribukait, B.; Jönsson, Jakob

doi:10.1159/000117895

Cited by 15 publications

(3 citation statements)

References 4 publications

(7 reference statements)

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“…The first steps to understanding how antigen-antibody pathology might play in mental illness has been established by animal research (Williams and Schupf, 1977), which is questionably relevant to human pathophysiology. In clinical research, while some found serum antibrain antibodies in 28-95% of studied schizophrenics (Kuznetoza and Semenov, 1961;Fessel, 1962;DeLisi et al, 1985;Henneberg et al, 1994), others were unable to reproduce these findings (Rubin, 1965;Logan and Deodhar, 1970;Ehrnst et al, 1982).…”

Section: Limitations and Future Workmentioning

confidence: 97%

A multi-etiology model of systemic degeneration in schizophrenia

Rǎdulescu

2009

Journal of Theoretical Biology

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Section: Limitations and Future Workmentioning

confidence: 97%

A multi-etiology model of systemic degeneration in schizophrenia

Rǎdulescu

2009

Journal of Theoretical Biology

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“…The first steps to understanding how antigen-antibody pathology might play in mental illness has been established by animal research [69], which is debatably relevant to human pathophysiology. In clinical research, while some found serum antibrain antibodies in 28-95% of studied schizophrenics [32] [18] [12] [25], others were unable to reproduce these findings [52] [37] [16].…”

Section: The Limits and Advantages Of Modelingmentioning

confidence: 99%

A multi-etiology model of systemic degeneration in schizophrenia

Radulescu

2008

Preprint

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We discuss the possibility of multiple underlying etiologies of the condition currently labeled as schizophrenia. We support this hypothesis with a theoretical model of the prefrontal-limbic system. We show how the dynamical behavior of this model depends on an entire set of physiological parameters, representing synaptic strengths, vulnerability to stress-induced cortisol, dopamine regulation and rates of autoantibody production. Malfunction of different such parameters produces similar outward dysregulation of the system, which may readily lead to diagnosis difficulties in a clinician's office. We further place this paradigm within the contexts of pathophysiology and of antipsychotic pharmacology. We finally propose brain profiling as the future quantitative diagnostic toolbox that agrees with a multiple etiologies hypothesis of schizophrenia.

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“…Eine erniedrigte Aktivität der Killerzellen, die als Streßphänomen interpretiert wurde (DeLisi u. Wyatt, 1982; Glaser et al, 1986;Sasaki et al, 1994), findet sich ebenso wie eine Aktivität im Normalbereich (Schindler et a1., 1986;Resch et al, 1988). Auch die Untersuchung der Immunglobuline führte zu unterschiedlichen Ergebnissen: Während einige Autoren keinen Unterschied zwischen schizophren Erkrankten und Gesunden fanden (DeLisi, 1986;Ehrnst et al, 1982), ließen sich auch erhöhte (Reichelt u. Landmark, 1995) und erniedrigte Immunglobulinspiegel darstellen (Sasaki et al, 1994).…”

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Zur Häufigkeit immunologischer Auffälligkeiten bei akuten Schizophrenien

Fabisch¹,

Fabisch²,

Langs³

et al. 1999

Fortschr Neurol Psychiatr

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Immunological examinations in schizophrenic patients have shown that there are many alterations in both arms of the immune system, i.e. cellular and humoral activities. The results are quite heterogeneous, as not even all schizophrenics show these pathological changes. Immunological findings are assumed to be etiopathogenetically related to the disease process or to be an epiphenomenon. The present study supposes that immunological alterations as they can be found during the course of schizophrenia may be an indicator for somatic vulnerability or an epiphenomenon. 60 male inpatients, fulfilling DSM-IV criteria of schizophrenia where examined during their acute phases of psychosis and during their phases of clinical improvement, by means of a serological profile including cellular and humoral parameters. The control group consisted of 42 healthy male volunteers. It was the aim of this study to find out if there were (a) overall differences in the immune profiles between patients and control group and (b) differences between different categories of schizophrenic disorder. During the acute phase nearly half of the schizophrenic patients showed pathologic immunological parameters, whereas none of the controls did. During the phase of clinical improvement the number of patients with normal immunological findings predominated. Furthermore there was a difference between the Paranoid and the Disorganized Subtype, the latter showing more immunological abnormalities. The results of this study give further support to the hypothesis that immunological aberrations should not be seen as closely etiopathogenetically related to schizophrenic disorders, but rather as an epiphenomenon (e.g. as a stress marker) and/or as indicators for somatic vulnerability.

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Failure to Detect Immunologic Stigmata in Schizophrenia

Cited by 15 publications

References 4 publications

A multi-etiology model of systemic degeneration in schizophrenia

A multi-etiology model of systemic degeneration in schizophrenia

A multi-etiology model of systemic degeneration in schizophrenia

Zur Häufigkeit immunologischer Auffälligkeiten bei akuten Schizophrenien

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