In synthesis, TRAIL efficiently sets into motion and sustain neurodegeneration-related neuroinflammation, as its neutralization implies significant attenuation of inflammatory processes [19], corroborating the hypothesis that is represents an important molecular clue to Aβ-dependent neurodegenerative processes, and may thus well be envisioned as a potential candidate target for innovative immunotherapeutic strategies in AD. Here, TNFSF10 is linked to Alzheimer disease.