Abstract: Alzheimer’s disease (AD) remains one of the significant causes of death and morbidity in the older population (2021). The cause of AD remains unclear despite there being numerous hypotheses. Perhaps the most widely accepted hypothesis is the amyloid cascade hypothesis which is based on the accumulation of amyloid beta (Aβ) in neurons (Dhakal et al., 2019). Aβ is produced from amyloid precursor protein (APP) after its processing via beta-secretase and gamma-secretase enzymes, while the processing of APP by alpha-secretase instead of β-secretase forms a non-amyloidogenic amyloid-α protein. The increased processing of APP via β-secretase and not by the α-secretase resulting in Aβ formation is an important aspect of AD. Recent studies suggest iron overloading as one of the major contributors of APP processing by β-secretase, proposing it as a major cause (Gleason and Bush, 2021). Insights from genomic studies in Iceland revealed mutations on amyloid precursor protein restricting Aβ formation protect people from AD (Jonsson et al., 2012). It has been reported that people having the Icelandic variant are at least five times less likely to develop AD as compared to the people without it. Considering this evidence, Aβ’s cruciality in AD progression has been undisputed. The Aβ protein comprises two major isoforms: 40 amino acids (Aβ40) and 42 amino acids (Aβ42) (Nair et al., 2014). While Aβ40 is soluble and readily cleared from cells, Aβ42 is toxic and aggregate-prone that can cause proteotoxic stress. In young individuals, the amyloid aggregates are efficiently cleared from neurons. But with aging the ability of the cells to clear these aggregates is reduced and soon develops to become part of the amyloid plaques (Dhakal et al., 2019). Although Aβ42 aggregates to form fibrils and plaques in affected brains, only the soluble oligomeric forms of Aβ42 are reported to cause oxidative damage and mitochondrial dysfunction aiding in the cascade of pathological events ultimately progressing towards AD pathology. Although it is still unclear what causes the initial Aβ accumulation and impairment in cellular defense systems, the combined effect of aging, mitochondrial dysfunction, impairment of mitochondrial turnover, iron overloading, loss of cellular ability to clear aggregated proteins, and accumulation of oxidative damage are some of the most important aspects of AD pathogenesis (Dhakal and Macreadie, 2020).