Alzheimer's disease (AD) is a neurodegenerative disorder affecting millions worldwide. One of the leading hypotheses for the underlying cause of AD is a reduction in nicotinic receptor levels in the brain. Among the nicotinic receptors, the alpha-7-nicotinic acetylcholine receptor (α7nAChR) has received particular attention due to its involvement in cognitive function.α7nAChR is a ligand-gated ion channel that is primarily found in the hippocampus and prefrontal cortex, areas of the brain responsible for learning, memory, and attention. Studies have shown that α7nAChR dysfunction is a key contributor to the pathogenesis of AD. The receptor is involved in regulating amyloidbeta (Aβ) production, a hallmark of AD pathology. Many drugs have been investigated as α7nAChR agonists or allosteric modulators to improve cognitive deficits in AD. Clinical studies have shown promising results with α7nAChR agonists, including improved memory and cognitive function. Although several studies have shown the significance of the α7 nAChR in AD, little is known about its function in AD pathogenesis. As a result, in this review, we have outlined the basic information of the α7 nAChR's structure, functions, cellular responses to its activation, and its role in AD's pathogenesis.