The contribution of the immune system to homeostatic brain function is a growing field that is still not well understood; however, neuroinflammation is increasingly associated with neurocognitive disorders including Alzheimer’s disease (AD) and post-infectious West Nile virus (WNV) encephalitis, illustrating a need for better understanding of these interactions. My current research investigates the innate immune response of neurons and the impact of microglia in recovery from WNV neurotropic infection. Cognitive dysfunction is a well-documented correlate of viral encephalitis; however the underlying molecular mechanisms are unclear, in part due to lack of murine recovery models.
To study the mechanisms of recovery from viral encephalitis, I use a murine model of intracranial infection with an attenuated strain of West Nile virus (WNV). My overarching hypothesis is that viral encephalitis incites inflammation that accelerates processes of CNS aging, contributing to the development of AD pathology and neurodegeneration. Research in my laboratory uses the WNV encephalitis model to investigate I) how neuroinflammation alters genetic and synaptic programs, which affect and denote aging processes, II) how aging affects microglial response to inflammatory events, altering neuroinflammatory signatures, and III) how neuroinflammatory events affect pathological Tau accumulation, a well-studied correlate of neurodegeneration.