Background: In the past 10 years, significant progress has been made in understanding the pathogenic chain of events that causes Alzheimer’s disease (AD). According to the most widely accepted concept, the production and aggregation of \beta-amyloid (A\beta) peptides play a critical role in AD. As a result, therapeutic intervention with these processes is the focus of intense research. The A\beta peptide is cleaved by the \alpha-secretase, \beta-secretase, and \gamma-secretase enzymes in a region near the pathogenic amyloid precursor protein (APP) and mutations occurring site. Methods: In the current review, a complete picture of the risk factors behind AD has been investigated. Mutations involved in AD progression have also been screened in various studies. Results: Most of the mutations in the amyloid precursor protein (APP) can lead to the accumulation of APP oligomers in the brain, leading to AD. Several point mutations in APP can cause familial AD (FAD), including the Swedish mutation (K>M670/671N>L) and the A673>V mutation. The pathogenic A673>V mutation and Swedish mutation (M670>K/N671>L) are present in the same region of amyloid precursor protein (APP). However, the A673>T mutation has been shown to confer protection against AD. Conclusion: More investigations are needed from geographically distinct regions on mutations associated with AD development and applications of nanomedicines for better management of the disease burden in the future. Nanotechnology-produced metal nanoparticles (NPs) have gotten much attention because of their wide range of uses in the medicinal and agricultural industries. Nanomedicine containing potential phytochemicals, including GX-50 and curcumin conjugated with NPs, maybe a potential candidate for treating AD.