ABSTRACT

Abstract..............................................................................................................121 6.1 Introduction..............................................................................................122 6.2 Amyloid-β................................................................................................122 6.3 Tau............................................................................................................124 6.4 Summary ..................................................................................................125 Acknowledgments .............................................................................................125 References .........................................................................................................126

For nearly a century, the pathological hallmarks of Alzheimer’s disease (AD), namely, senile plaques and neurofibrillary tangles (NFT), have provided a reasonable basis to conclude that their major components, amyloid-β and tau, respectively, are central mediators of disease pathogenesis. Therefore, not surprisingly, efforts to