Harnessing Neuroimmune Interactions for Disease Modification in Alzheimer’s & Parkinson’s
- Modulating TNF mediated neuroinflammation with dominant negative inhibitors, targeting chronic microglial activation across Alzheimer’s and Parkinson’s models, slowing neurodegeneration by restoring immune homeostasis
- Investigating gut–brain axis dynamics and microbiome-derived metabolites such as butyrate, unveiling epigenetic and immune pathways that differ in PD and Alzheimer’s, enabling novel therapeutic strategies that address both central and peripheral drivers of pathogenesis
- Exploring the roles of microglia, RGS10 signalling, and gene–environment interactions, revealing how immune regulation, stress responses, and genetic context influence neuronal resilience, informing personalized interventions to prevent or slow progression in neurodegenerative diseases