Conversely, IL-33 deficiency caused neurodegeneration and deposition of abnormal tau protein, including hyper-phosphorylated, paired helical fragment, and insoluble tau in the cerebral cortex and hippocampus of aging IL-33−/− mice, which was accompanied by the early onset of aging-related AD-like impairment of cognition and memory [95]. The gene discussed is IL33; the disease is Alzheimer disease.