HIV-1 and amyloid beta interactions at the blood-brain barrier

NIH RePORTER · NIH · R01 · $472,672 · view on reporter.nih.gov ↗

Abstract

ABSTRACT The most significant development in HIV epidemiology is the increasing age in the infected population. Among HIV-associated comorbidities that have been related to aging, neurocognitive dysfunction and vascular disorders are particularly striking. The current proposal links both conditions together by focusing on the blood-brain barrier (BBB) and neurogenesis of neural progenitor cells (NPC). HIV infected brains are characterized by increased deposition of amyloid beta (Aβ), and we demonstrated in the previous funding cycle that the BBB (formed primarily by the endothelium of brain capillaries) actively participates in this process. The current proposal will explore the role of the brain endothelium-derived extracellular vesicles (ECV) in Aβ transfer to neural progenitor cells (NPC) and their impaired neurogenesis in HIV-infected brains. The proposed research is built on the notion that enhanced accumulation of Aβ, toxicity of anti-retroviral therapeutics, and residual viral replication in HIV-infected brain are driving the brain pathology resulting in neurocognitive decline. The central hypothesis of the proposal is that Aβ carried by ECV derived from the brain endothelium enhances HIV infection of NPC and impairs their differentiation into the neuronal lineage, resulting in neurocognitive decline. Specific mechanisms evaluated in this application include the impact of Aβ carried by the brain endothelium-derived ECV on HIV infection and the impaired neurogenesis of NPC (Aim 1), alterations of gap junction-mediated intercellular communication between infected and non-infected NPC (Aim 2), and (Aim 3) the contribution of anti-retroviral drugs to amyloid deposition and impaired neurogenesis of NPC in HIV-infected brain. Overall, the proposal offers a unique perspective on the interactions between the BBB and Aβ deposits in a HIV-infected brain, resulting in impaired NPC neurogenesis. We expect that the project will provide proof-of-principle for the involvement of Aβ in the development of cognitive dysfunction in HIV.

Key facts

NIH application ID
9917817
Project number
5R01MH072567-13
Recipient
UNIVERSITY OF MIAMI SCHOOL OF MEDICINE
Principal Investigator
Michal Toborek
Activity code
R01
Funding institute
NIH
Fiscal year
2020
Award amount
$472,672
Award type
5
Project period
2005-09-20 → 2022-04-30