Skip to main content
. Author manuscript; available in PMC: 2010 Jun 1.
Published in final edited form as: J Neuroimmune Pharmacol. 2008 Nov 19;4(2):200–212. doi: 10.1007/s11481-008-9136-0

Figure 2. Proposed mechanisms leading to enhanced intraneuronal and perivascular β-amyloid depositions in HIVE brains.

Figure 2

Activated microglia secreted elevated levels of proinflammatory cytokines (IL1-β, TNF-α, IFN-γ) that can up-regulate BACE1 and APP expression in neurons, resulting in increased Aβ generation. HIV viral protein Tat can be up-taken via LRP into neurons where it can inhibit Neprilysin activity, blocking Aβ degradation. The reduced secretion of anti-inflammatory cytokines (IL-4 and IL-10) also contributes to impaired Aβ degradation. Accelerated perivascular Aβ deposition is a consequence of impaired efflux of Aβ into plasma, and/or inhibition of perivascular Aβ degrading enzymes by viral proteins.