Fariha Karim

1 Introduction Alzheimer's disease (AD) is a common neurodegenerative disease with aggregated neurofibrillary tangles (NFT) (abbreviated hereafter as “tau”) and amyloid beta (Aβ) plaques as prevalent biomarkers in the brain (Jack et al. 2018). Abnormal tau hyperphosphorylation results from an imbalance between normal tau-associated phosphates and protein kinases, causing aggregation into NFT in AD brains (Köpke et al. 1993; Wang et al. 2013).

1. Introduction Nicotinic acetylcholine α7-subtype receptors (α7 nAChRs) are pentameric ligand-gated ion channels implicated in Alzheimer’s disease (AD) pathology [1,2]. Located in presynaptic and postsynaptic neurons of brain regions including the cerebral cortex and hippocampus (HP) [3], α7 nAChRs are important mediators of intracellular signaling and neurotransmitter release, which are necessary for maintaining normal cognitive function [4,5].

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