Cognitive Characteristics of TgAPP CRND8 Mice Immunised with Beta Amyloid Peptide

摘要

The progressive cognitive dysfunction of Alzheimer's disease (AD) is accompanied by a series of neuropathological changes, including deposition of amyloid (3 peptide in the parenchyma and blood vessels (A beta) of the human brain. Many lines of evidence indicate that abnormal processing of A beta (a proteolytic derivative of the beta-amyloid precursor protein - betaAPP) plays a central role in initiating the pathogenesis of AD (reviewed in Steineret al. 1999). There are also data indicating a positive correlation between beta-amyloid plaques and cognitive impairment in AD patients (Cummings et al.1996; Haroutunian et al. 1998; Kanne et al.1998). However, there are gaps in our knowledge of the pathogenesis of even the "simple" genetic forms of AD. Thus there has been a need for an animal model that develops some or all aspects of this uniquely human disease in a reproducible fashion to decipher and stratify crucial pathogenic events. Such animal models would also, of course, be useful for testing therapies.