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
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
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
Ycoprotein that is predominantly expressed by activated T cells, B cells, myeloid cells, and platelets. It has been well established that CD40L upregulates the immune response by leading to increased CD4+ T cell activation; an effect which promotes the replication of HIV in infected lymphocytes and immune cells [104] and also that robust CD40 ligation promotes an inflammatory and neurotoxic enviro
Ycoprotein that is predominantly expressed by activated T cells, B cells, myeloid cells, and platelets. It has been well established that CD40L upregulates the immune response by leading to increased CD4+ T cell activation; an effect which promotes the replication of HIV in infected lymphocytes and immune cells [104] and also that robust CD40 ligation promotes an inflammatory and neurotoxic enviro
Sed tau (a component of the neurofibrillary tangle, a second AD neuropathological hallmark) have been proposed as sensitive and specific markers of AD in several studies [47,48]. It has also been found that changes in CSF Ab and tau are comparable to those observed in AD and HAD patients [49]. The pathogenic significance of these biomarkers is not well established but it has been hypothesized that