Deficiency of TN-C could ameliorate the detrimental effects of mutated amyloid precursor protein overexpression, increase the number of microglia in the hippocampus and the adjacent cerebrum, shift neuroinflammation from a pro- to an anti-inflammatory pattern, reduce the cerebral amyloid β-protein (Aβ) plaque load, and protect neurons in AD mice, thus exerting beneficial effects on AD pathogenesis (Figure 5). Here, APP is linked to Alzheimer disease.