Given that microglial-mediated neuroinflammation is a prominent driver of AD pathogenesis and NF-κB, IL-6, and TNF-α levels are found to be elevated in AD patient brains [28], the ability of PE to regulate the expression of these cytokines and enzymes suggests its potential to alleviate AD-related neuroinflammatory damage and mitigate mild cognitive impairment, a prodromal stage of Alzheimer’s disease. Here, TNF is linked to early-onset autosomal dominant Alzheimer disease.