ABSTRACT

Alzheimer’s disease (AD) is an age-associated neurodegenerative disorder. The major clinical hallmarks of AD are progressive cognitive impairments-primarily in learning and memory-with behavioral abnormalities. The neuropathological hallmarks of AD encompass extracellular senile plaques of β-amyloid (Aβ) deposits and intracellular neurobrillary tangles (NFTs) from the accumulation of hyperphosphorylated microtubule-associated protein tau. This is followed by neuronal and synaptic loss (Duyckaerts et al., 2009).