Elizabeth Pizzi

Research/Areas of Interest

Microglia, the brain’s resident immune cells, have been shown to play critical roles in brain development, various immunological functions, and have emerged as crucial players in neurodegenerative diseases. Recently, advanced single-cell technologies have uncovered diverse microglial populations, revealing distinct activated states which hold significant implications for disease progression. Specific microglial states have been linked to hallmark pathological features of Alzheimer’s Disease (AD). In AD, microglia exert both beneficial (neuroprotective) and detrimental (neurotoxic) functions. They can act positively through phagocytosing amyloid beta plaques, yet they can also become neurotoxic through excessive cytokine production. Activated microglia also contribute to synaptic pruning, a process strongly associated with synapse loss and subsequent cognitive decline in AD. Evidence indicates that microglia-mediated synaptic pruning involves the complement system, a crucial component of the innate immune response. For my project, I aim to investigate the mechanisms underlying complement-mediated synapse loss in AD in a functional, spatial and microglia state-specific manner. By elucidating these mechanisms, I seek to contribute to a deeper understanding of microglial involvement in AD pathology and uncover novel therapeutic targets.