deletions | additions       diff --git a/Both_CSF_and_imaging_biomarkers__.tex b/Both_CSF_and_imaging_biomarkers__.tex  index 26e9ae1..a1ab516 100644  --- a/Both_CSF_and_imaging_biomarkers__.tex  +++ b/Both_CSF_and_imaging_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, while the most used imaging biomarker is the increased level of Pittsburgh compound Compound-B (PIB) seen  in Positron Emission Tomography (PET) scans of  AD patients. 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 Pittsburgh compound PIB  that binds with A$\beta$ plaques level \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.  A$\beta$ related biomarkers are already in saturation phase for demented patients.  Figure \ref{fig:amyloidImaging} shows the distribution of amyloid image levels in normal, MCI and AD patients.