(C) 2008 Elsevier Inc All rights reserved “
“Multiple syste

(C) 2008 Elsevier Inc. All rights reserved.”
“Multiple system atrophy is a sporadic, progressive, neurodegenerative disease characterized by an oligodendroglial accumulation of alpha-synuclein (alpha-syn). The mechanisms underlying the oligodendroglial accumulation of alpha-syn in the brains of patients with multiple system atrophy have attracted a great ACP-196 clinical trial deal of interest, given the primarily neuronal role reported for this protein. We examined the interactions between neuronal and oligodendroglial

alpha-syn in the progeny of crosses between parental transgenic (tg) mouse lines that express alpha-syn either under the oligodendroglial-specific myelin-basic protein promoter (MBP1-h alpha-syn tg) or under the neuronal platelet-derived growth factor promoter (PDGF-h alpha-syn tg). Our results demonstrate www.selleckchem.com/products/dabrafenib-gsk2118436.html that progeny from the cross [h alpha-syn double (dbl) tg mice] displayed a robust redistribution of alpha-syn accumulation, with a relocalization from a neuronal or a mixed neuronal/oligodendroglial alpha-syn expression to a more oligodendroglial pattern in both the neocortex and the basal ganglia that closely resembled the parental MBP-h alpha-syn tg line. The h alpha-syn

dbl tg mice also displayed motor deficits, concomitant with reduced levels of tyrosine hydroxylase and augmented neuropathological alterations in the basal ganglia. These results suggest that the central nervous system milieu in the h alpha-syn dbl tg mice favors an oligodendroglial accumulation of alpha-syn. This model represents an important tool to examine the interactions between neuronal

and oligodendrocytic Sucrase alpha-syn in diseases such as multiple system atrophy. NeuroReport 23:259-264 (C) 2012 Wolters Kluwer Health vertical bar Lippincott Williams & Wilkins.”
“A substantial body of evidence has accumulated linking an increased incidence of cardiovascular disease in patients with acute kidney injury (AKI), chronic kidney disease (CKD), and end-stage renal disease (ESRD). A multitude of novel risk factors related to decreased kidney function might interact with the renal and systemic immune systems involved in renal injury and repair to participate in accelerated atherogenesis (Immune inflammation-Renal injuryAtherosclerosis-the IRA Paradigm). In this review, we will discuss several of these novel risk factors and present the potential for the role of the immune-inflammatory system in accelerated atherosclerosis of kidney disease. Kidney International (2011) 80, 453-463; doi:10.1038/ki.2011.178; published online 22 June 2011″
“Cognitive neuroscience research relies, in part, on homologies between the brains of human and non-human primates. A quandary therefore arises when presumed anatomical homologues exhibit different functional properties. Such a situation has recently arisen in the case of the anterior cingulate cortex (ACC). In humans, numerous studies suggest a role for ACC in detecting conflicts in information processing.

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