Relative power in 4 different frequency click here bands was calculated. The effect of age on global and regional relative power was examined. Globally, young AD patients showed lower alpha- and higher delta-power than old AD patients. Regional analysis showed that these differences were most pronounced in the parieto-occipital region. Young AD patients had lower beta- and higher theta-power than old patients in all but the temporal regions. In controls, there was no age effect on global relative power in any frequency band. Young AD patients present with more severe slowing of spontaneous oscillatory activity than old AD patients, which is most pronounced in the posterior brain areas. This finding

supports the hypothesis that early onset AD presents with a distinct endophenotype. (C) 2012 Elsevier Inc. All rights reserved.”
“Background: Activation of amoeboid 3 microglial cells (AMC) and its related inflammatory response have been linked to the periventricular white matter damage after hypoxia in neonatal brain. Hypoxia increases free ATP in the brain and then induces various effects through ATP receptors. The present study explored the possible mechanism in ATP induced AMC activation in hypoxia.\n\nResults: We first examined the immunoexpression of P2X4, P2X7 and P2Y12 in the corpus callosum (CC) and subependyma associated with the lateral ventricles where both areas are rich in AMC. Among the three purinergic receptors, P2X4 was most

intensely expressed. By double immunofluorescence, Protein Tyrosine Kinase inhibitor P2X4 was specifically localized in AMC (from P0 to P7) but the immunofluorescence in AMC was progressively diminished with advancing age (P14). It was further shown that P2X4 expression was noticeably enhanced in P0 day rats subjected to hypoxia and killed at 4, 24, 72 h and 7 d versus their matching controls by double labeling and western blotting analysis. P2X4 expression was most intense at 7 d whence the inflammatory response was drastic after hypoxia. We then studied the association of P2X4 with cytokine release in AMC after hypoxic exposure. In primary microglial cells exposed to hypoxia, IL-1 beta and TNF-alpha protein levels were up-regulated.

Blockade of P2X4 receptor with 2′, 3′-0-(2, 4, 6-Trinitrophenyl) adenosine 5′-triphosphate, a selective P2X1-7 blocker Selleckchem BIX 01294 resulted in partial suppression of IL-1 beta (24% vs hypoxic group) and TNF-alpha expression (40% vs hypoxic group). However, pyridoxal phosphate-6-azo (benzene-2, 4-disulfonic acid) tetrasodium salt hydrate, a selective P2X1-3, 5-7 blocker did not exert any significant effect on the cytokine expression.\n\nConclusions: It is concluded that P2X4 which is constitutively expressed by AMC in postnatal rats was enhanced in hypoxia. Hypoxia induced increase in IL-1 beta and TNF-alpha expression was reversed by 2′, 3′-0-(2, 4, 6-Trinitrophenyl) adenosine 5′-triphosphate suggesting that P2X4 mediates ATP induced AMC activation and its production of proinflammatory cytokines.