Reference #: 2013-052
Currently, there are no therapies available for treating HIV-associated dementia (HAD). HIV envelope glycoprotein, gp120 appears to exhibit cytotoxic activities in the picomolar range by activating apoptotic pathways that lead to neuronal dysfunction and loss. Researchers at Georgetown University’s Department
of Neuroscience found that gp120 accumulates inside neurons and causes neuronal degeneration by interacting with tubulin β-3 (TUBB3), a major component of neuronal microtubules. They identified the binding site of gp120 to TUBB3 and then designed a small peptide (Helix-A) that displaced gp120 from binding to TUBB3. To enhance the intracellular delivery of the peptide, they crosslinked Helix-A to mesoporous silica nanoparticles (Helix-A nano).
Without intervention, gp120 continues to accumulate and predisposes neurons to inflammatory responses, which amplify the progression of the clinical pathology. Thus, this discovery provides new significant data that will help in the design of adjunct therapies against HAD.
- HelixA gp120 as a therapy to prevent HIV-mediated neurodegeneration
Gp120 Helix-A nano prevents gp120-mediated neurite pruning and neuronal loss
Italo Mocchetti, Ph.D.
U.S. Patent no. 9,399,663