Human immunodeficiency virus 1 (HIV-1)–associated dementia complex (HIV dementia) occurs in 10% to 15% of HIV-seropositive individuals with advanced infection and is characterized by cognitive, behavioral, and motor dysfunction. The clinical phenotype of HIV dementia has changed as a result of highly active antiretroviral therapy (HAART) so that mild forms of HIV-associated cognitive impairment predominate, and there is evidence of lower cerebrospinal fluid (CSF) HIV RNA levels and less central nervous system (CNS) immune activation.1 Many surrogate markers from the pre-HAART era are no longer associated with HIV dementia, suggesting an attenuated CNS inflammatory response in HIV-positive individuals receiving HAART. There is an urgent need to identify new surrogate laboratory and neuroimaging markers of HIV-associated cognitive impairment in the era of HAART.