RESEARCH INTERESTS

My research focuses on elucidating the molecular mechanisms underlying microglial activation, neuroinflammation, and neuronal injury in neurodegenerative disorders. I am particularly interested in understanding how HIV viral proteins, and drugs of abuse exacerbate neuroinflammatory signaling and glial dysfunction, and in identifying therapeutic small molecules that can modulate these pathogenic responses. Another aspect of my work is investigating the role of extracellular vesicles as mediators of glia-neuron crosstalk, specifically how pathogenic cargo transferred from glial cells to neurons drives neurodegeneration. Through the study of pathways including lysosomal regulation, autophagy-mitophagy, and ferroptosis, my goal is to develop targeted adjunctive therapeutic strategies to attenuate neuroinflammatory signaling and protect neuronal function in the context of HIV and substance use disorders.

ONGOING PROJECTS

C381 Attenuates HIV Tat/cocaine- induced microglial activation and Neuroinflammation

My current research focuses on evaluating a small molecule, C381, as a potential therapeutic strategy to counteract HIV-1 Tat/cocaine-induced cellular dysfunction in the glial cells. This project examines whether targeting lysosomal and mitochondrial dysfunction can reduce cellular stress and neuroinflammatory responses, with the broader goal of identifying novel approaches to protect glial, and neural cells and mitigate neurodegeneration associated with HIV.

HIV Tat-activated microglial extracellular vesicles trigger neuronal ferroptosis

This project explored how extracellular vesicles released from HIV-Tat-activated microglia contribute to neuronal injury through altered intercellular communication. The study focuses on understanding how pathogenic cargo transferred from microglia to neurons disrupts cellular homeostasis and promotes synaptic damage in the context of NeuroHIV. By examining this glia-neuron signaling axis, the work aimed to identify novel pathways that drive neurodegeneration and inform the development of targeted strategies to mitigate neuroinflammation-associated neuronal dysfunction.