Pectively, correspond to the type ii or iii microglial states described in the preceding paragraph. Further, the factors which cause polarization to M1 or M2, reinforce the maintenance of that phenotype in a cycle-like manner [8,9] (Figure 1). Increased M1 polarization is consistent with increased TNF-a observed in plasma and brain specimens in HAD and AD, and may play a role in the pathophysiolog
Pectively, correspond to the type ii or iii microglial states described in the preceding paragraph. Further, the factors which cause polarization to M1 or M2, reinforce the maintenance of that phenotype in a cycle-like manner [8,9] (Figure 1). Increased M1 polarization is consistent with increased TNF-a observed in plasma and brain specimens in HAD and AD, and may play a role in the pathophysiolog
Owed a direct correlation between microglial activation/infection and cognitive decline [19]. Studies have found microglial HIV infection as central in exacerbating HIV dementia [20,21]. Importantly, neuronal dysfunction and death in HIV infection results from cytokine stimulation, but especially several cytokine-mediated apoptotic mechanisms emanating from microglia. Thus microglial cytokine prod
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
Milar to that of AD. b-amyloid is a potent and direct neurotoxic agent [77-79], much like the HIV-1 proteins gp120 and Tat, and it induces a cascade of cellular mechanisms including activation of microglia [80], which leads to neuronal damage [81]. Indeed, reactive microglia are closely associated with neuritic and b-amyloid plaques, just as they are with HIV1 Tat protein [82-89]. Using electron m
Milar to that of AD. b-amyloid is a potent and direct neurotoxic agent [77-79], much like the HIV-1 proteins gp120 and Tat, and it induces a cascade of cellular mechanisms including activation of microglia [80], which leads to neuronal damage [81]. Indeed, reactive microglia are closely associated with neuritic and b-amyloid plaques, just as they are with HIV1 Tat protein [82-89]. Using electron m
Ignificantly longer lives. While HAART has been increasing the lifespan of those infected with HIV, it has also led to an increased prevalence of HAD [32-38]. As the pathology of HAD, like Alzheimer's Disease (AD), is commonly characterized by an increase in the amount of amyloid-beta (Ab) peptide in the brain [39], evidence suggesting microglia modulate the clearance of potentially neurotoxic Ab
Ignificantly longer lives. While HAART has been increasing the lifespan of those infected with HIV, it has also led to an increased prevalence of HAD [32-38]. As the pathology of HAD, like Alzheimer's Disease (AD), is commonly characterized by an increase in the amount of amyloid-beta (Ab) peptide in the brain [39], evidence suggesting microglia modulate the clearance of potentially neurotoxic Ab