Elucidating Neuroinflammatory Mechanisms Involved in Alzheimer’s Disease

Alzheimer`s disease (AD) is an irreversible neurodegenerative illness, and the exact etiology of the disease remains unknown. Multifaceted evidence supports the hypothesis that inflammatory-immune mechanisms contribute to Alzheimer`s disease (AD) neuropathology. The ability of innate immune cells, particularly microglia, to mediate neuroinflammation in AD has been implicated as a significant contributor to disease pathogenesis.
The differentiation of human-induced pluripotent stem cells (iPSCs) into microglia-like cells (MGL) in vitro presents unprecedented opportunities to model AD in patient-specific disease-associated inflammatory mechanisms. However, this model lacks the neuronal component and the microenvironment and thus cannot fully model significant contributions of neuron-immune interactions that underlie disease pathogenesis. We are using in vitro co-culture model using iPS-derived MGL and brain organoids to investigate the neuroinflammatory and cellular interaction mechanisms underlying AD pathogenesis ,we will present our recent findings in this project.