Research Projects

Amyloid-beta (Abeta1-42) peptides, which form plaques in the brain, are the main hallmark of Alzheimer's disease (AD), causing cell death, hyperactivation of glia, neuroinflammation, synaptic dysfunction, and disruption of neural networks. Efforts have been made to develop compounds to alleviate Abeta1-42 neurotoxicity in the last twenty years, but FDA-approved drug Aducanumab has not been able to halt the disease. The failures may be due to poor understanding of Abeta aggregation with herpes simplex virus type 1 (HsV-1), the interaction mechanism between the neuronal membrane, Abeta oligomers, and HsV-1 glycoprotein, the mechanism of HsV-1 glycoprotein association with Abeta peptides and their complex synaptotoxicity, and the difficulty in replicating the human brain membrane in in-vitro experiments. The research aims to address the HsV1-Abeta1-42 complex toxicity on the realistic brain neuronal membrane composition by conducting rigorous investigations. This includes inspecting the mutual relationship between Abeta1-42 oligomers, HsV-1, and brain tissue membrane composition, generating oligomers structures, and exploring the interactions of the oligomers-HsV1 glycoprotein complex with the neuronal membrane composition. The research aims to address why the Abeta1-42-HsV-1 glycoprotein complex kills neurons, which is a challenging task for anti-AD drug discovery.