ABSTRACT
Introduction............................................................................................................183 Memory Deficits Correlate with Aβ Load ............................................................184 Interventions Improving Memory in APP Transgenic Mice ................................186 Mechanisms of Aβ-Associated Memory Impairment in Transgenic Mice ..........189 Conclusions............................................................................................................191 Acknowledgments..................................................................................................192 References..............................................................................................................192
The identification of the Aβ peptide as a major component of amyloid deposited in brain vessels and subsequently of parenchymal plaques in the brains of Alzheimer’s victims [1] led to a focus on this molecule as a key element in the pathophysiology of Alzheimer’s disease (AD). Subsequent work found that some mutations causing the disease occurred in the amyloid precursor protein (APP) that is processed, in some circumstances, into the Aβ peptide [2]. Ultimately, all mutations causing AD have been demonstrated to result in overproduction of the long variant of the Aβ peptide [3]. Thus the pathology, genetics, and the in vitro neurotoxicity of the Aβ peptide has led to a focus on the aggregation and accumulation of this material as a prime target for therapies designed to treat AD.
