Abstract: The current Alzheimer's disease model mouse, developed by manipulating the expression of a gene directly related to distinctive pathology that is specific to the disease, such as acceleration of amyloid plaque deposition, is a model of a preclinical state, or of a pathology that is fundamentally different from human Alzheimer's disease. In view of the current state described above, the present invention addresses the problem of developing a non-human transgenic animal in which Alzheimer's pathology is more accurately reflected, and thereby elucidating a disease mechanism or contributing to drug discovery. In the present invention, by heterozygous knockout of the drebrin gene of a non-human Alzheimer's disease model animal used as a base, senescence risk can be imparted to the conventional non-human Alzheimer's disease model animal. Alzheimer's pathology is more accurately reflected in this non-human Alzheimer's disease model animal.

Abstract: Provided is a cardiotoxicity assessment method which comprises: seeding cardiomyocytes in a culture container together with a culture medium; adding a drug to the culture medium in the culture container to bring the drug into contact with the cardiomyocytes; and measuring a heart disease biomarker secreted from the cardiomyocytes to assess cardiotoxicity of the drug, wherein at least a culture surface of the culture container is composed of an alicyclic structure-containing polymer, and the culture surface has a surface free energy of 30 to 37 mN/m.