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
Molecules including major histocompatibility complex (MHC) II and CD40 [15]. Microglia expressing MHC II induce CD4+ T cells to generate IFN-g and TNF-a [16]. In the case of both HAD and AD, this response is considered harmful to the brain and in both diseases TNFa is elevated to neurotoxic levels while only in HAD is IFN-g is prominently elevated [14]. In HIV associated dementia (HAD; also known
Molecules including major histocompatibility complex (MHC) II and CD40 [15]. Microglia expressing MHC II induce CD4+ T cells to generate IFN-g and TNF-a [16]. In the case of both HAD and AD, this response is considered harmful to the brain and in both diseases TNFa is elevated to neurotoxic levels while only in HAD is IFN-g is prominently elevated [14]. In HIV associated dementia (HAD; also known
Molecules including major histocompatibility complex (MHC) II and CD40 [15]. Microglia expressing MHC II induce CD4+ T cells to generate IFN-g and TNF-a [16]. In the case of both HAD and AD, this response is considered harmful to the brain and in both diseases TNFa is elevated to neurotoxic levels while only in HAD is IFN-g is prominently elevated [14]. In HIV associated dementia (HAD; also known
Molecules including major histocompatibility complex (MHC) II and CD40 [15]. Microglia expressing MHC II induce CD4+ T cells to generate IFN-g and TNF-a [16]. In the case of both HAD and AD, this response is considered harmful to the brain and in both diseases TNFa is elevated to neurotoxic levels while only in HAD is IFN-g is prominently elevated [14]. In HIV associated dementia (HAD; also known
Ctedwomen who used NVP-based highly active ART with CD4 counts higher than 350 cells/ .19 ART interruption exposes the HIV patient to risk of developing drug resistance. Proper use of antiretroviral therapy in HIV-1 infection enhances treatment outcomes and immunological recovery.LimitationsThe small sample size of pharmacies which were stocking ARVs is a limitation of this study. The study was co
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
Tes [26,27]. Once infected or activated by HIV- proteins such as gp120 or Tat, microglia begin to excrete endogenous pro-inflammatory cytokines of the M1 subtype [28]. Histopathologically, activated microglia represent a highly accurate correlate to neuronal death and damage in CNS [29]. Severity of dementia in persons with HAD is strongly correlated with the number of activated macrophages and mi