deletions | additions       diff --git a/amyloidBeta_targeting_biomarkers.tex b/amyloidBeta_targeting_biomarkers.tex  index c927574..3b095c0 100644  --- a/amyloidBeta_targeting_biomarkers.tex  +++ b/amyloidBeta_targeting_biomarkers.tex 
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Both CSF and imaging biomarkers targeting A$\beta$ pathophysiology are available and have been widely used in AD research.  The established CSF biomarker is the decreased level of amyloid-$\beta_{1-42}$ (A$\beta42$) in AD \cite{Anoop_2010}, while the most used imaging biomarker is the increased level of Pittsburgh Compound-B (PiB) seen in Positron Emission Tomography (PET) scans of AD patients \cite{Johnson_2012}.  Show A$\beta$ figure 4 from \cite{Johnson_2012} here.  A$\beta_{42}$ is 42-amino-acid soluble form of A$\beta$ and is believed to be lowered when it gets converted to the insoluble A$\beta$ plaques.  This view is consistent to the findings of inverse relationship between CSF A$\beta42$ levels, and PIB levels which binds with A$\beta$ plaques \cite{Fagan_2006}.  Figure \ref{fig:hypotheticalModelJack_2013} shows the dynamics of these biomarkers where we see that biomarkers targeting $A\beta$ pathophysiology are sensitive well before the cognitive impairment begins.