Experimental neuropathology of Alzheimer’s disease: animals models
The presence of deposits of b-amyloid dereivatives of an amyloid protein precursor (PPA) have been found in a great variety of elderly animals. However, very few developed neurofibrillary tangles or other lesions usually seen in the human brain with Alzheimer’s disease (AD) (such as Hirano bodies). Transgenic (tg) and ‘knock-out’ (ko) mice models are not perfect, but are a considerable advance in the study of AD and other neurodegenerative disorders. Some tg mice models may develop considerable deposits of amyloid material at the age of 8 months, and these deposits may increase as the animal ages. When PPA mutant gene mice are crossed with those with a presenile mutant, these crossed mice develop amyloid deposits faster than either of the individual mutants. These mice are the beginning of a line of research which may lead to major advances in the treatment of AD
