It was only a decade ago that T cells in the injured brain were shown to play a protective rather than a destructive role. In this article, we explore the role of the immune system in the healthy brain, focusing on the key function that T lymphocytes selleck inhibitor have in the regulation of cognition. We discuss candidate mechanisms underlying T cell-mediated control of cognitive function in human cognitive diseases associated with immune decline, such as age- and HIV-related dementias, ‘chemo-brain’ and others.”
“The mammalian target of rapamycin (mTOR) exerts neuroprotective

effects under hypoxic or ischemic conditions. To explore whether mTOR participates in neuroprotective signaling through regulation of hypoxia-inducible factor-1 alpha (HIF-1 alpha), vascular endothelial growth factor (VEGF) and neuronal apoptosis in developing rat brain with hypoxia-ischemia (HI), we operated on postnatal day 10 rats by ligating the common carotid artery followed by exposure to systemic hypoxia. Brains were collected at various intervals to detect the expression of mTOR, phosphorylated mTOR (p-mTOR), HIF-1 alpha, VEGF and cleaved caspase 3 (CC3), using immunohistochemistry and Western blot analysis. We also used terminal deoxynucleotidyl transferase-mediated dUTP-nick end labeling (TUNEL) to detect neuronal apoptosis. The p-mTOR protein expression increased

click here at 2 h after HI, peaked at

8 h, lasted 24 h, and then dropped to the basal level. Also, the expression of HIF-1 alpha and VEGF was significantly enhanced and peaked at 8 h after HI. Up-regulated expression of CC3 was observed at 2 h, peaked at 24 h, and lasted 72 h after HI. Increased neuronal apoptosis is associated with reduced HIF-1 alpha and VEGF expression. Furthermore, pretreatment with rapamycin, a mTOR specific inhibitor, significantly inhibited HIF-1 alpha and VEGF protein after HI. The expression of CC3 and the number of TUNEL-positive cells were up-regulated at 8 h and down-regulated at 24 h after HI in the rapamycin-treated group. Our findings suggest that mTOR may participate in the regulation of HIF-1 alpha, VEGF and neuronal apoptosis, serving neuroprotective functions after HI in developing rat brain. (C) 2011 Tozasertib solubility dmso Elsevier Ireland Ltd. All rights reserved.”
“Acute traumatic and ischemic events in the central nervous system (CNS) invariably result in activation of microglial cells as local representatives of the immune system. It is still under debate whether activated microglia promote neuronal survival, or whether they exacerbate the original extent of neuronal damage. Protagonists of the view that microglial cells cause secondary damage have proposed that inhibition of microglial activation by immunosuppression is beneficial after acute CNS damage.