In contrast to wild type, these mice do not exhibit alpha 7 nAChR agonist induced phosphorylation, thus suggesting that H-3-antagonist-mediated signaling is not dependent on ACh-stimulated GO nAChR activation. In summary, results of these studies suggest that ABT-239 leads to biochemical signaling that promotes cognitive performance Selleckchem CH5424802 as well as attenuation of tau hyperphosphorylation, raising the intriguing possibility that H-3 antagonists have potential for both symptomatic

and disease modifying benefit in the treatment of AD. (C) 2010 Elsevier Ltd. All rights reserved.”
“Viral infections spread based on the ability of viruses to overcome multiple barriers and move from cell to cell, tissue to tissue, and person to person and even across species. While there are fundamental differences between these types of transmissions, it has emerged that the ability of viruses to utilize and manipulate cell-cell contact contributes to the success of viral infections. Central to the excitement in the field of virus cell-to-cell transmission is the idea that cell-to-cell spread is more than the sum of the processes of virus ACY-738 release and entry. This implies that virus release and entry are efficiently

coordinated to sites of cell-cell contact, resulting in a process that is distinct from its individual components. In this review, we will present support for this model, illustrate the ability of viruses to utilize and manipulate cell adhesion molecules, and discuss the mechanism and driving forces of pheromone directional spreading. An understanding of viral cell-to-cell spreading will enhance our ability to intervene in the efficient

spreading of viral infections.”
“The brain-derived neurotrophic factor (BDNF), a member of the neurotrophin family, is involved in nerve growth and survival. Especially, a single nucleotide polymorphism (SNP) in the BDNF gene, Val66Met, has gained a lot of attention, because of its effect on activity-dependent BDNF secretion and its link to impaired memory processes. We hypothesize that the BDNF Val66Met polymorphism may have modulatory effects on the visual sensory (iconic) memory performance. Two hundred and eleven healthy German students (106 female and 105 male) were included in the data analysis. Since BDNF is also discussed to be involved in the pathogenesis of depression, we additionally tested for possible interactions with depressive mood. The BDNF Val66Met polymorphism significantly influenced iconic-memory performance, with the combined Val/Met-Met/Met genotype group revealing less time stability of information stored in iconic memory than the Val/Val group. Furthermore, this stability was positively correlated with depressive mood exclusively in the Val/Val genotype group. Thus, these results show that the BDNF Val66Met polymorphism has an effect on pre-attentive visual sensory memory processes. (C) 2010 Elsevier Ltd. All rights reserved.