We noticed that although immunoblot analysis showed no difference in APOA-I levels in the frontal lobe between AD patients and control subjects, immunohistochemical staining revealed APOA-I-positive immunoreactivity in occasional senile plaques within the AD cortex, similar to APOE [89], suggesting that although the detected APOA-I levels were not reduced, the APOA-I bound to senile plaques lost its normal physiological function and became incorporated into the AD pathology. The gene discussed is APOA1; the disease is Alzheimer disease.