In addition, HO-1 is increased in neurofibrillary tangles, senile plaque neurites, granulovacuolar degeneration and neuropil threads in human AD brains (Smith et al., 1994; Perry et al., 2003), suggesting the redistribution of iron due to release from heme proteins in affected areas of the AD brain. This evidence concerns the gene HMOX1 and Alzheimer disease.