Addressing referee critiques. JS, AC, SR, and JJ were responsible for the initial literature search and first draft one of the review. DO contributed to the generation of Figure 1. JT provided review material for incorporation into the paper regarding the role of CD45 in neurodegeneration in the context of AD. FF provided clinical background regarding HIV and Alzheimer's-type dementias. All author
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
Y and also visibly damaged subcortical areas [45,46]. Amyloid plaques in AD result from the deposition of amyloid beta (Ab) which is a putative pathogenic molecule in AD. Ab is the cleavage product of the amyloid precursor protein (APP) and APP mutations are associated with inherited forms of AD. The clinical implication or pathogenic consequences of brain amyloid deposition are still controversia