MAPT and Alzheimer disease: These proinflammatory substrates have been known to exacerbate AD pathology by promoting Aβ plaque and tau NFT formations, and similarly, these AD pathological hallmarks have been additionally responsible for upregulating the proinflammatory cascade, resulting in a positive-feedback-loop-like response promoting more inflammation, degeneration, and atrophy [49,50,51,52].