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A$\beta$ is one of the most important biomarkers of AD.  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_2013}.  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}.