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
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
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
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
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
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
Amyloid plaque deposition [39,42-44]. Indeed, most forms of dementia are accompanied by a widespread degeneration in the cerebral cortex - such as the plaques in AD brain. AD is thus considered a "cortical dementia." HAD is also considered to be a cortical dementia however there is also targeted damage to regions lying under the cortex. Some authors consider HAD to be a subcortical dementia howeve