Furthermore, inhibition of caspase-1, a major component of the NOD-like receptor domain-containing protein 1 (NLRP1) inflammasome, attenuated hyperoxia-induced NLRP1 inflammasome activation, which was associated with reduced cerebral atrophy and cell death as well as increased proliferation in the neurogenic subventricular and subgranular zone [47]. Here, NLRP1 is linked to Cerebral atrophy.