Differences in psychological and somatic symptom cluster score profiles between subjects with Idiopathic environmental intolerance, major depression and schizophrenia.

Idiopathic Environmental Intolerance (IEI) has been associated with psychogenic factors and an increased number of comorbid psychiatric disorders such as depression and anxiety disorder. The purpose of the current study was to examine a possible overlap of psychological and somatic symptoms between subjects with IEI and patients with major depression and schizophrenia as well as to specify characteristic differences. The different symptom clusters included symptoms of chemical intolerance, neurotoxicity and psychological distress as well as measurements of mental health such as anxiety, depression, somatoform symptoms, and schizophrenia-specific disturbances in cognitive domains. IEI patients reported higher overall levels in physical symptoms such as chemical intolerance, neurotoxicity and somatic symptoms not attributable to an organic cause. Schizophrenia patients showed higher overall levels in self-experienced disturbances in several schizophrenia-specific cognitive domains, whereas general psychological distress, anxiety and depression were rated highest by patients with major depression. Importantly, the groups markedly differed in the shapes of profiles of various symptom clusters. Our results provide evidence that IEI patients can be distinguished on the phenomenological level from patients with major depression or schizophrenia, and that distinct domains of psychological and somatic symptoms are particularly problematic in specific diagnostic groups.

[Alcohol induced cognitive deficits]. / Alkohol induzierte kognitive Dysfunktion.

Previous studies could show a complex relationship between alcohol consumption and cognition but also with processes of ageing both social and biological. Acute effects of alcohol during intoxication include clinical signs such as excitation and reduced inhibition, slurred speech, and increased reaction time but also cognitive dysfunction, especially deficits in memory functions. However, these cognitive deficits during alcohol intoxication are reversible while patients with alcohol addiction and chronic alcohol intake show severe impairments of cognitive functions especially deficits in executive functions. Frontal executive impairments in these patients include deficits in problem solving, abstraction, planning, organizing, and working memory.Additionally, gender specific deficits are relevant for the course of the disease and its concomitant health problems with female alcoholics showing a higher vulnerability for cognitive dysfunction and brain atrophy at earlier stages of alcoholism history.

Myeloperoxidase-derived oxidants induce blood-brain barrier dysfunction in vitro and in vivo.

Peripheral leukocytes can exacerbate brain damage by release of cytotoxic mediators that disrupt blood-brain barrier (BBB) function. One of the oxidants released by activated leukocytes is hypochlorous acid (HOCl) formed via the myeloperoxidase (MPO)-H2O2-Cl(-) system. In the present study we examined the role of leukocyte activation, leukocyte-derived MPO and MPO-generated oxidants on BBB function in vitro and in vivo. In a mouse model of lipopolysaccharide (LPS)-induced systemic inflammation, neutrophils that had become adherent released MPO into the cerebrovasculature. In vivo, LPS-induced BBB dysfunction was significantly lower in MPO-deficient mice as compared to wild-type littermates. Both, fMLP-activated leukocytes and the MPO-H2O2-Cl(-) system inflicted barrier dysfunction of primary brain microvascular endothelial cells (BMVEC) that was partially rescued with the MPO inhibitor 4-aminobenzoic acid hydrazide. BMVEC treatment with the MPO-H2O2-Cl(-) system or activated neutrophils resulted in the formation of plasmalogen-derived chlorinated fatty aldehydes. 2-chlorohexadecanal (2-ClHDA) severely compromised BMVEC barrier function and induced morphological alterations in tight and adherens junctions. In situ perfusion of rat brain with 2-ClHDA increased BBB permeability in vivo. 2-ClHDA potently activated the MAPK cascade at physiological concentrations. An ERK1/2 and JNK antagonist (PD098059 and SP600125, respectively) protected against 2-ClHDA-induced barrier dysfunction in vitro. The current data provide evidence that interference with the MPO pathway could protect against BBB dysfunction under (neuro)inflammatory conditions.