A lack of TNC enhances the detrimental effects of the overexpression of the mutated amyloid precursor protein, increases the number of microglial cells in the hippocampus and adjacent brain areas, convert the neuroinflammatory response from a pro-inflammatory to an anti-inflammatory state, attenuates cerebral β-amyloid deposition, and protects the neurons of AD mice, resulting in the beneficial modulation of the pathogenesis of AD [64]. Here, APP is linked to Alzheimer disease.