The “”amyloid hypothesis”" postulates that a build-up of A beta p

The “”amyloid hypothesis”" postulates that a build-up of A beta protein is responsible for neuronal loss and the ensuing symptoms of AD. One possible mechanism

of A beta clearance, and hence AD therapy, is phagocytosis of A beta protein by microglial cells. Microglia are the brain’s resident immune cells and phagocytosis is one of their innate functions. We are interested in identifying Selleck Tofacitinib molecules that augment microglial-mediated phagocytosis of A beta protein. We used the rodent BV-2 microglial cell line which readily phagocytose fluorescent latex beads and synthetic A beta(1-42) peptide. BV-2 cells treated with the neuroactive drug valproic acid (VPA) showed greatly enhanced phagocytic activity for both latex beads and A beta. VPA also reduced microglial viability by inducing apoptosis, as previously reported. The relevance of these in vitro results to the treatment of AD is unclear but further investigation into the effects of VPA on the clearance of A beta through enhanced microglial phagocytosis is warranted. (C) 2010 IBRO. Published by Elsevier Ltd. All rights reserved.”
“A central issue in the pathogenesis of tauopathy is the question of how tau protein dysfunction leads Selleckchem PU-H71 to neurodegeneration. We have previously demonstrated that the absence of tau protein is associated with destabilization of microtubules and impaired neurite outgrowth (Dawson et al., 2001; Rapoport et al., 2002). We now hypothesize

that the absence of functional tau protein may render the central nervous system more vulnerable to secondary insults such as the overexpression of mutated beta amyloid precursor protein (APP) and traumatic brain injury. We therefore crossed tau knockout mice (Dawson et al., 2001) to mice overexpressing a mutated human APP (APP(670,671), A(SW)) (Hsiao et al., 1996) and created a mouse model (A(sw)/mTau(-/-)) that provides evidence that the loss of tau function causes degeneration of neuronal processes. The overexpression Methamphetamine of APP(670,671) in tau knockout mice, elicits the extensive formation

of axonal spheroids. While spheroids are only found associated with A beta plaques in mice expressing APP(670,671) on an endogenous mouse tau background (Irizarry et al., 1997), A(sw)/mTau(-/-) mice have spheroids not only surrounding A beta plaques but also in white matter tracks and in the neuropil. Plaque associated and neuropil dystrophic neurites and spheroids are prominent features of Alzheimer’s disease (Masliah et al., 1993; Terry, 1996; Stokin et al., 2005), and our current data suggests that loss of tau function may lead to neurodegeneration. (C) 2010 IBRO. Published by Elsevier Ltd. All rights reserved.”
“Purpose: Nonurothelial malignancies represent a small fraction of bladder malignancies and are less extensively studied, resulting in sparse empirical data on these tumors. We sought insight into tumor characteristics and survival.

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