Intermittent hypoxia, a consequence of OSA, has been implicated as the one of themain environmental factors involved in the emergence of AD, by promoting theexpression of genes related to inflammation and cellular aptosis.40 Intermittent hypoxia promotes theactivation of BACE1 (β-site amyloid precursor protein cleavingenzyme),41 responsible forcleavage of the amyloid precursor protein (APP) in β amyloid species(Aβ) accelerating the accumulation of the substance in the CNS. The gene discussed is BACE1; the disease is obstructive sleep apnea syndrome.