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Editorial

Editorial

, MD (Chief Editor)
Page 477 | Published online: 11 Sep 2013

Dear colleagues,

I am excited to introduce our seventh issue of 2013 that opens with up to date original articles on biological markers in schizophrenia and autism and concludes with newest research results on biological treatment of alcoholism.

By investigating post-mortem pituitaries of schizophrenia patients and controls using liquid chromatography tandem mass spectrometry and other techniques, Krishnamurthy and colleagues set out to identify a molecular profile for schizophrenia. The authors found several differently expressed molecules in schizophrenia patients as compared to controls, including hypothalamic-pituitary-adrenal axis associated constituents and molecules associated with lipid transport and metabolism.

Von Wilmsdorff and colleagues examined the influence of the neuroregulin-1 (NRG1) risk genotype and effects of antipsychotics on the expression of excitatory amino acid transporters (EAATs). They compared post-mortem brain samples from schizophrenia and control subjects and investigated several gene expressions by in situ hybridization. Results indicated that increased SLC1A3 expression in schizophrenia facilitates transport and may result in reduced glutamate neurotransmission, whereas decreased SLC1A6 expression in the NRG1 risk variant may be an adaptive effect to restore glutamate signalling.

Possible contributions of variations in the oxytocin gene and the oxytocin receptor gene to schizophrenia susceptibility were investigated by Montag and colleagues using a case–control design. The authors found significant associations of several SNPs in both the oxytocin gene and the oxytocin receptor gene with a diagnosis of schizophrenia. Moreover, significant associations of SNPs in the oxytocin receptor gene with general psychopathology and negative symptom scores in schizophrenic patients were reported.

Okusaga and colleagues set out to replicate previous findings on elevated gliadin antibody levels in schizophrenia in a larger sample and in a different geographical location. Even after adjusting for potential confounders, the authors detected elevated gliadin antibodies in a sample of 950 adults with schizophrenia when compared to 1000 healthy controls.

Introducing the second subtopic of this issue, Toma and colleagues report their findings on biomarkers in autism. By conducting a case–control association study with 326 autistic patients and 350 healthy controls that focused on 37 candidate genes of the dopaminergic and serotonergic system as well as of neurotrophic factors, they found significant associations between the DDC gene and autism.

Cytokine profiles in amniotic fluid were investigated by Abdallah and colleagues in children developing autism spectrum disorders and healthy controls. For this purpose the authors retrieved clinical data of a historic birth cohort from nationwide registers. Although it was not possible to determine to which extent the disclosed cytokine patterns were unique to autism, results revealed elevated levels of various cytokines in amniotic fluid samples of autism spectrum disorders.

Concluding with a brief report on biological treatment of alcohol dependence, Lieb and colleagues present results on the effects of acute blocking of the endogenous opioid system in 20 alcohol-dependent patients who were treated with naloxone. Results included expected biological effects, i.e. cortisol increase, of opioid receptor blockade by naloxone treatment, but excluded psychological effects, i.e. reduced craving, in alcohol-dependent subjects.

Yours sincerely,

Siegfried Kasper, MD

Chief Editor

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