One major school of thought in AD links the cause of AD to A\(\beta\) pathophysiology supporting the amyloid cascade hypothesis proposed by Hardy et al. \cite{Hardy_1992}. The main idea of this hypothesis is that the deposition of A\(\beta\), a peptide fragment of a membrane protein called amyloid precursor protein (APP), is the root cause of AD with the NFTs, neuronal deaths, vascular damage, and dementia occurring as a direct result of this deposition. A\(\beta\) peptides aggregate to form oligomers (put footnote about what oligomers are) that subsequently produce depositions of extracellular macroscopic A\(\beta\) plaques (also known as senile plaques). There are only three genes known to lead to the early onset in familial form of AD (fAD): APP, PSEN1 and PSEN2 \cite{Bird_2008}. Due to the role of these three genes in the sequence of senile plaques formation from the A\(\beta\) peptides, the amyloid cascade hypothesis has received stronger support \cite{Herrup_2015}. Although lots of studies have been based on this hypothesis, it is important to note that there are also studies disagreeing with it \cite{Herrup_2015}. The existing debate is in whether A\(\beta\) is the primary cause of AD or not. However, the growing body of evidence from several studies have made it universally accepted that A\(\beta\) is strongly correlated to AD and it will remain as an important component in AD research.