The decreased level of acetylcholine (ACh) in the CNS is one of the most pronounced characteristics of AD . Other major AD hallmarks, such as extracellular formation and accumulation of amyloid-β (Aβ) and intracellular neurofibrillary tangles (NFT), have an interconnection with cholinergic system malfunction . Furthermore, oxidative stress, neuroinflammation, and biometal dyshomeostasis are also critical contributors to the multifaceted pathogenesis of AD . These mechanisms have become primary targets in developing potential therapeutics. Except for the recentely approved monoclonal antibodies, no effective or curative treatments have been discovered .