In vitro studies showed reduced phosphorylation of synapsin in AD post mortem tissue suggesting that perturbation of synapsin phosphorylation occur early in pathological states such as AD.CSFGAP has also been analysed in neurodegenerative diseases including AD, FTD, and PD patients compared to controls.CSFGAP was only signicantly reduced in PD compared to the other groups, and was not changed in AD, or FTD compared to controls.This could imply that degeneration of presynaptic terminals was limited in all groups.However based on previous ndings using immunoblottingimmunohistochemistry methods this seems unlikely. An other explanation is that the results reect the concomitant degeneration and regeneration of synapses, the sum of which causes only mild changes in the CSFGAP levels.Our previous study on brain tissue levels GAP found both Norfloxacin decreases and increases in different regions in AD, which supports this notion.Using DE analysis and the silver staining technique, large differences in protein patterns in CSF between patients with brain disorders such as AD, schizophrenia, PD and multiple sclerosis were shown, however many of these proteins have not yet been identied.In the proteomic study of CSF proteins in a group of AD patients, the levels of six proteins and their isoforms, including proapolipoprotein, apolipoprotein E, microglobulin, and ubiquitin were significantly altered.The most notable changes were seen among the apolipoproteins, especially proapolipoprotein. Furthermore, the partial CSF proteome of AD patients and controls were compared using microstrips. Comparing the intensity of spots between AD and controls, spots were found to be signicantly up or down regulated. Eight proteins were signicantly reduced in CSF of AD patients and they were identied as kininogen, one isoform of glycoprotein, and two isoforms of apoJ, three isoforms of apoE, two isoforms of apoA, trace, cell cycle progression proteins and RBP.Only one protein, one isoform of antitrypsin, was increased in AD patients compared to controls.Fluoxetine Previously detected protein changes were con rmed including apoE, and apoA.Some new proteins changes were identied like kininogen, glycoprotein, apoJ, trace, cell cycle progression and antitrypsin.The most affected proteins in AD were among the apolipoproteins, especially proapolipoprotein.As constituents of highdensity lipoprotein, apoE and apoA have important roles in controlling the lipid homeostasis in peripheral cells.The biological function of apolipoproteins is less clear, but an involvement of them in transporting cholesterol out and in from neurons are obvious.Interestingly, there is also a growing evidence of a link between a disturbance in the apolipoproteins and cholesterol metabolism in AD. In contrast to our study, no signicant difference in apoA brain expression or in CSF levels have been found between AD patients and controls. The conicting data between our study and other studies might be due to the more sensitive detection of different isoforms of apoA by DE.Kininogen involved in the kallikreinkinin system, has earlier been linked to AD.Increased cleavage of kininogen was found in CSF of AD patients and is thought to interact with A in AD.Several of the altered proteins in the comparison between AD patients and controls are isoforms of glycoproteins such as antitrypsin, trace, glycoprotein, apoJ, and apoE.Therefore, potential changes in the glycosylation patterns of these proteins and their role in AD are important in the etiology of AD.

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