Increased levels of HO-1 were observed in association with neurofibrillary tangles (NFTs) and senile plaques (Takeda et al., 2000) and in hippocampal neurons of AD patients, together with increases of serine phosphorylation, tyrosine nitration and 4-HNE modification of HO-1, as though adaptive increases in HO-1 expression and activation were counteracting the structural and functional impairment of HO-1, via tyrosine nitration and HNE-HO-1 adduct formation. Here, HMOX1 is linked to Alzheimer disease.