Alzheimer’s disease is a progressive neurodegenerative disease that affects millions of people worldwide. After beta-amyloid peptides are cleaved from their precursor protein, they can form soluble monomers that readily aggregate into larger protein species. This aggregation leads to large insoluble plaques which are neurotoxic and seemingly unable to be cleared by microglia, the brain’s immune cells. Beta-amyloid aggregates interact with microglia which upregulate pro-inflammatory cytokine signaling. One of the earliest cytokines is tumor necrosis factor alpha (TNF-α). TNF-α has been shown to modify phagocytosis and promote the signaling of upstream pro-inflammatory cytokines, which is critical to regain brain homeostasis. Therefore, we propose that TNF-α inhibits beta-amyloid phagocytosis when the proinflammatory cytokine TNF-α is upregulated, TNF-α expression exacerbated as oligomerization increased and phagocytosis is further diminished.