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amilial Alzheimer disease mutations can be rescued by mutations in the APP GxxxG motif. J Biol Chem 285: 2163621643. 50. Citron M, Eckman CB, Diehl TS, Corcoran C, Ostaszewski BL, et al. Additive effects of PS1 and APP mutations on secretion of the 42-residue amyloid beta-protein. Neurobiol Dis 5: 107116. 51. Dumanchin C, Tournier I, Martin C, Didic M, Belliard S, et al. Biological effects of four PSEN1 gene mutations causing Alzheimer disease with spastic paraparesis and cotton wool plaques. Hum Mutat 27: 1063. 52. Kumar-Singh S, Theuns J, Van Broeck B, Pirici D, Vennekens K, et al. Mean age-of-onset of familial alzheimer disease caused by presenilin mutations correlates with both increased Abeta42 and decreased Abeta40. Hum Mutat 27: 686695. 53. Steiner H, Romig H, Grim MG, Philipp U, Pesold B, et al. The biological and pathological function of the presenilin-1 Deltaexon 9 mutation is “1659636 independent of its defect to undergo proteolytic processing. J Biol Chem 274: 76157618. 54. Houlden H, Baker M, McGowan E, Lewis P, Hutton M, et al. Variant Alzheimer’s disease with spastic paraparesis and cotton wool plaques is caused by PS-1 mutations that lead to exceptionally high amyloid-beta concentrations. Ann Neurol 48: 806808. 55. Pardossi-Piquard R, Petit A, Kawarai T, Sunyach C, Alves da Costa C, et al. Presenilin-dependent transcriptional control of the Abeta-degrading enzyme neprilysin by intracellular domains of betaAPP and APLP. Neuron 46: 541554. 56. Veeraraghavalu K, Choi SH, Zhang X, Sisodia SS Presenilin 1 mutants impair the self-renewal and differentiation of adult murine subventricular zoneneuronal progenitors via cell-autonomous mechanisms involving notch signaling. J Neurosci 30: 69036915. 57. Saura CA, Choi SY, Beglopoulos V, Malkani S, Zhang D, et al. Loss of presenilin function causes MedChemExpress RS1 impairments of memory and synaptic plasticity followed by age-dependent neurodegeneration. Neuron 42: 2336. 58. Wolfe MS gamma-Secretase inhibitors and modulators for Alzheimer’s disease. Journal of neurochemistry 120 Suppl 1: 8998. 59. Schor NF What the halted phase III gamma-secretase inhibitor trial may be telling us. Annals of neurology 69: ” 237239. 60. Xu X Gamma-secretase catalyzes sequential cleavages of the AbetaPP transmembrane domain. Journal of Alzheimer’s disease: JAD 16: 211224. 61. Salmon P, Trono D Production and titration of lentiviral vectors. Curr Protoc Hum Genet Chapter 12: Unit 12 10. 13 Propofol is a widely used intravenous anesthetic. In addition to its sedation/hypnotic properties, propofol displays neuroprotective effects. As an activator of GABAA receptors, an inhibitor of NMDA receptors and a modulator of calcium influx through slow calcium channels, propofol improves the neurological outcome. In a rat cerebral ischemia model, propofol treatment was shown to decrease the infarct size in the hippocampus. In addition, propofol administration also decreased the apoptotic rate and improved cell viability in hypoxic neuronal cultures. Moreover, propofol has a phenolic hydroxyl group, which is similar to that of vitamin E and demonstrates antioxidant activity by scavenging free radicals. On the organelle and tissue level, the treatment of rat brain oxidative stress injury with propofol confers neuroprotective effects through an inhibition of lipid peroxidation. Although, such pleiotropic mechanisms have been suggested to contribute to propofol-mediated neuroprotection, its capabilities are still not completely understood. Rece

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Author: Cholesterol Absorption Inhibitors