To clarify the causes and underlying mechanisms of Alzheimer's disease, a typical disorder in cognitively-impaired elderly people, and develop safe and effective prevention/treatment methods. Explores the molecular mechanisms of the mutation of amyloid b protein (Aβ) (Note 1) into polymers toxic to nerve cells with a focus on Aβ's binding to nerve cell membrane lipid. Develops new methods to prevent/treat Alzheimer's disease by regulating cholesterol metabolism in the brain, since it is suggested that the onset of Alzheimer's disease is significantly affected by changes in cholesterol metabolism. Explores the Aβ production-controlling mechanisms of presenilin (PS) genes, the causative genes of familial Alzheimer's disease, in terms of the pathology of PS gene mutation to establish methods to inhibit Aβ production. Identifies Aβ oligomer (Note 2), considered to be the key molecular form to Aβ's neurotoxicity, and clarifies its formation, molecular structure, and development of toxicity to develop new methods to diagnose, prevent, and treat Alzheimer's disease. Note1： Small protein that constitutes senile plaques, the lesions of Alzheimer's disease. Note2： A compound composed of several to 10-plus Aβ molecules back to index