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Ward RJ1, 3, Hanak C 2, Benoit J 2, Fabry L 2, Verbanck P 2, De Witte P 1, Dexter D 3.
Universite catholique de Louvain, 1348 Louvain-la-Neuve, Belgium
Brugmann Hospital, CHU Brugmann – Paul Brien site, 1030, Brussels, Belgium
Centre for Neuroinflammation & Neurodegeneration, Imperial College London, W12 0NN, UK.
Alcohol-induced neuroinflammation occurs in both chronic and intermittent alcohol abusers. While animal studies have indicated a pro-inflammatory mileau in specific brain regions after intermittent alcohol abuse, (a M1 microglial phenotype) to what extent this is induced in chronic alcohol abuse remains unclear. Some studies have reported increased levels of systemic pro- inflammatory cytokines in the plasma of chronic alcohol abusers but it is unknown whether this reflects glial activation. Such inflammatory mediators together with activated monocytes and lymphocytes can cross the blood brain barrier to trigger glial activation which can alter synaptic plasticity and contribute to cognitive dysfunction and depression.
Therefore alcoholic patients undergoing alcohol detoxification were divided according to Lesch typology and levels of pro-inflammatory cytokines ascertained 24h and 21 days after detoxification, together with an assessment of cognitive function and depression. Lesch typology 1 patients showed higher levels of pro-inflammatory mediators, i.e. ferritin and IL-6, 24h after detoxification compared to the other typologies, 2 and 3, which remained elevated even after 21 days of detoxification. In contrast, both Lesch typology 2 and 3 showed lower levels of pro-inflammatory mediators at these two time points. Furthermore, cognitive testing by Brown-Pederson and Stroop showed greater induction of errors in Lesch typology 1 patients than the other two typologies. Our recent studies indicated that alcohol induced pro-inflammatory microglia, M1 phenotype, induced in the hippocampus of rats administered an intermittent alcohol regime, contributes to spatial memory deficits.1 The assay of raised systemic pro-inflammatory mediators in homogenous groups of alcohol patients based on the patients’ drinking patterns and origin of substance craving, show association with cognitive dysfunction, possibly reflecting glial activation in specific groups of alcohol abusers.
1.Stefanini, C., Colivicchi MA., Della Corte L., Ward RJ., De Witte P., Lallemand F., Hemmings K., Pitard A., Page MI., Nayak K., Dexter D. (2014) Ethane-β-Sultam Modifies the Activation of the Innate Immune System Induced by Intermi.ttent Ethanol Administration in Female Adolescent Rats. Journal of Alcoholism & Drug Dependence ISSN: 2329-648