HIV-1 Tat promotes premature brain aging

Background It is estimated that by 2015, about half of all HIV-positive individuals will be older than 50 due to the introduction of the HAART. Yet those over 50 progress to AIDS faster than adults in their 20s or 30s, and those in the younger age bracket still exhibit illnesses and clinical conditions commonly associated with older people, such as HIVassociated neurocognitive disorders (HAND), certain cancers, liver and bones diseases. For the most part, the reasons for this have remained a mystery. In support of the eradication failure, studies showed the persistence of HIV-1 in brain cells as well as the presence of viral proteins in CSF. This notion was supported by the compelling neuropathological data suggesting that the loss of Synaptic Plasticity occurs with the ongoing presence of virus and despite HAART. Clinically, these neuropathological data manifest by a gradual loss of working memory and learning disability that may manifest by symptoms similar to the ones observed in aged brain. Anatomically, working memory and learning ability functions are assured by neurons of the hippocampus, a brain area known-to-be affected by HIV-1 proteins such as gp120.