By revealing a direct link between BMAA-induced mitochondrial dysfunction and neurodegeneration, including the development of AD features, such as Aβ peptides oligomerization and Tau hyperphosphorylation, along with the demonstration that cortical neurons are indeed capable of activating the NLRP3 inflammasome and of producing mature IL-1β, we here define a novel plausible pathway to sporadic AD. The gene discussed is IL1B; the disease is Alzheimer disease.