In triple (3xTgAD) transgenic mice lacking TNFR1, exposure to chronic systemic inflammation did not result in intraneuronal accumulation of amyloid immunoreactivity, suggesting that solTNF/TNFR1 signaling may be an important regulator of APP processing and that pathological elevation of TNF may contribute to pre-plaque pathology and acceleration of cognitive deficits (McAlpine et al., under review). Here, TNFRSF1A is linked to Cognitive impairment.