Ain lesions without Ab deposits. They include multiple sclerosis plaques [111] as well as lesions of adrenoleukodystrophy, DRPLA, and ischemic strokes [115]. Ab was also shown to induce CD40 expression by cultured microglia [116,117] and cultured vascular endothelial cells [116,118][118-120]. HIV-1 induces the latter phenomenon as well [121] It may be the mechanism by which CD40 expression is up-r
Vioral complications [66-69]. Microglia, as a major target of HIV-1 infection in the CNS, are typically a viral reservoir [70-72] and are also key in HIV-1 neuroinvasiveness-penetration into the CNS by the virus [72,73]. Most importantly, a discrepancy between the localization of HIV-infected cells and the severity of neurocognitive symptoms has been described [74-76]. Thus, other mechanisms secon
Vioral complications [66-69]. Microglia, as a major target of HIV-1 infection in the CNS, are typically a viral reservoir [70-72] and are also key in HIV-1 neuroinvasiveness-penetration into the CNS by the virus [72,73]. Most importantly, a discrepancy between the localization of HIV-infected cells and the severity of neurocognitive symptoms has been described [74-76]. Thus, other mechanisms secon
The microglia signal transduction pathways mediating the neurotoxic response of Ab demonstrated that mitogen-activated protein-kinase (MAPK) superfamily members ERK1/2 and p38 MAPK act as mediators [95-97]. Furthermore, several lines of evidence indicate the NF-B in microglia is stimulated by b-amyloid [98,99]. Activation of NF-B can stimulate transcription of genes expressing TNF-a, IL-1, IL-6, m