deletions | additions       diff --git a/Both_CSF_and_imaging_biomarkers__.tex b/Both_CSF_and_imaging_biomarkers__.tex  index 67106da..c927574 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 \cite{Anoop_2010}, while the most used imaging biomarker is the increased level of Pittsburgh Compound-B (PiB) seen in PET Positron Emission Tomography (PET)  scans of AD patients \cite{Johnson_2012}. Show A$\beta$ figure 4 from \cite{Johnson_2012} here.  A$\beta42$ 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.  A$\beta$ related biomarkers are already in saturation phase for demented patients.  Figure \ref{fig:senilePlaquesImaging_Johnson2012} \ref{fig:amyloidImaging}  shows the distribution of amyloid beta plaque image  levelsusing PiB PET imaging  in normal control (NC), mild cognitively impaired (MCI) normal, MCI  and AD patients.The biggest advantage of amyloid imaging could be in identifying the high risk NC and MCI patients who are most likely to benefit from potential disease modifying drugs.