In recent years, we face an increase in the aging of the HIV-1-infected population, which is not only due to effective antiretroviral therapy but also to new infections among older people. Even with the use of the antiretroviral therapy, HIV-associated neurocognitive disorders represent an increasing problem as the HIV-1-infected population ages. Increased amyloid beta (Aβ) deposition is characteristic of HIV-1-infected brains, and it has been hypothesized that brain vascular dysfunction contributes to this phenomenon, with a critical role suggested for the blood-brain barrier in brain Aβ homeostasis. This review will describe the mechanisms by which the blood-brain barrier may contribute to brain Aβ accumulation, and our findings in the context of HIV-1 infection will be discussed.
Copyright © 2012 International Union of Biochemistry and Molecular Biology, Inc.