A variety of depletion methods for speci c removal of high abundant proteins from body uids have also been developed.However, additional depletion methodologies have recently become available therefore ve commercially available depletion columns have been comprehensively evaluated and compared regarding their efciency, specicity and reproducibility for removal of high abundant proteins in biological uids. D LC is timeconsuming and this technique is not yet suitable for clinical testing.A strategy employing LPIEF in the rst dimension, D gels in combination with gel elution in the second dimension and MSMS analysis has been used for discovery and Flurbiprofen identication of proteins from human CSF and brain tissue. Characterization of tau protein from CSF by the combination of LPIEF and immunoblotting showed that both phosphorylated and unphosphorylated tau isoforms are present in CSF, and the tau protein appeared both in truncated and as full length forms in CSF. Using monoclonal antibodies that detect all isoforms of tau independent of phosphorylation, ELISA methods have been developed that measure total CSF tau level. An Endurobol increase in CSF tau in AD patients has been found in a numerous of studies.The sensitivity to identify AD patients varies between reports, but has been around, while its specicity in differenting AD from normal aging has been in the range of. However, other studies have found that high tau levels also are found in other neurodegenerative diseases as for example in frontal lobe dementia. To further elucidate the involvement of total tau and phosphorylated tau in various dementia disorders, the CSF concentration of tau and phosphotau in probable and possible AD, FTD, and, PD have been determined. The results suggests that the CSF concentrations of tau and phosphotau are increased in about two thirds of probable AD, and in half of those with possible AD, but are normal in FTD, PD, and controls.The soluble forms of APP are present in brain and CSF. Studies on CSF from sporadic forms of AD patients compared to healthy controls have not discriminated between these two forms using sandwich enzyme linked immunosorbent assay methods. Most studies have been focused on quantication of the two A peptides, A and A in CSF.Using different assays specic for A, a marked increase in A in CSFAD has been found in a numerous of studies.However, one study found an increase in A in AD, which may be due to methodological differences or differences in patient and control groups.The sensitivity to identify AD patients has been approximately, while its speci city in differencing AD from normal aging has been in the range of. In contrast, the level of CSF A is unchanged in AD patients compared to healthy controls. The reduction of CSFA is reecting the deposition of the A peptide in senile plaques, with lower levels secreted to the CSF.An A SELDI immunoassay was rst developed to analyze different A peptides found in cell culture medium.The pattern of A peptides found in human CSF and in brain homogenate from AD patients have been investigated using the same method. This peptide was only observed in CSF of AD patients.