The possibility to identify new proteins in human CSF is important for the development of new neuronal markers for different types of neurodegenerative diseases.The combination of D LCLC and MSMS has been used for identication of proteins in ventricular CSF from ten subjects. They found proteins and of them were unique to individuals, whereas only of the identied proteins were found in all subjects.CSF biomarkers for neurodegenerative diseases are of great value as diagnostic aids, especially early in the course of the disease, when the clinical symptoms are vague and diagnosis are difcult, but when therapeutic compounds have the greatest potential of being effective.Reliable CSF biomarkers will be even more necessary when new therapeutic compounds reach the clinical phase.Much effort has focused on nding one single neurochemical biomarker for AD, one for FTD etc.First, this may be elusive unless the biomarker is related to a pathogenic step that is unique for AD or FTD etc.For example neurodegeneration or synaptic pathology is not only found in AD, or in FTD.Biomarkers for neurodegenerative disorders should reect all the pathogenic processes of that disease.Proteomic technology provide to analyse several biomarkers in a single CSF sample, which might discover new better instruments for clinical diagnosis of neurodegenerative diseases.By using a protein pattern, like in D gels, or from SELDI analysis or from multiparametric immunoassays, we are not limited by the sensitivity and specicity of any single biomarker.Detection of new biomarkers will further strengthen diagnosis and provide useful information in drug trials.The combination of immunoassays and proteomic methods show that AD, FTD, and PD patients express differential proteins patterns, which reect divergent underlying pathophysiological mechanisms and neuropathological changes in these diseases.Submit your manuscr ipts at http:www.hindawi.com The results from the individualdata sets were combined in a genomewide inversevarianceweighted metaana lysis.; the G allele of rs was most strongly associated with af fected status. This SNP is located kb downst ream of and in linkage disequilibrium with rs.In the VEGAS analyses in which linkage disequilibrium between the markers was taken into account, the TREM gene was signif icant ly associated with A lzheimers disease. A lso, in these analyses, the strongest singlemarker association was observed for rs. To further assess the ef fect size of the T allele at rs, we genot yped Lorlatinib samples.These threedimensional regression coefficient maps show dif ferences in brain volume in the temporal lobe associated with the TREM risk allele.The riskallele carriers had signif icantly accelerated brain atrophy; they lost brain tissue at a rate that was signif icantly faster than that in noncarriers. Statistical tests were per formed with the use of permutation tests, which are QNZ robust in the presence of outliers and small sample sizes. The TREM risk variant may af fect signaling by TREM receptors expressed on microglial cells in the brain, perhaps interfering with the ant iinf lammatoryfunct ions of these cells and their removal of apoptot ictissue.This research was also supported by NIH grants P AG and K AG.TREM is expressed mainly on microglia in the central ner vous system and appears to mediate the phagocytosis of apoptot ic neurons.