title: Marking the markers of Alzheimer's: too good to diagnose, too bad to use?
abstract: One of the most important neurodegenerative diseases of our time is Alzheimer's disease, which mainly affects the elderly population. The accumulation of β-amyloid and tau protein in the brain tissue is the most characteristic pathomechanical event of the disease, later causing neuronal cell death. Setting up an accurate diagnosis of Alzheimer's disease has essentially changed recently, since besides psychometry, neurochemical and neuroimaging examinations are also gaining greater importance in the clinical routine. Thanks to the widening of diagnostic methods, in the future the disease could be recognised even during the preclinical phase. The most remarkable source of brain-derived compounds is the cerebrospinal fluid. Although obtaining cerebrospinal fluid is greatly unpleasant, it poses a low risk and is frequently used as part of the diagnostic procedure. The assay of cerebrospinal fluid means the identification of the level of β-amyloid(1-42), tau and phospho-tau and their ratio, but to get more specific and sensitive investigations there is intensive research work both on the utility of their combination and on finding even more specific biomarkers. This review gives a summary of the biomarkers that are being used and being researched for the diagnostic tests of both familial and sporadic forms of Alzheimer's disease. Other notable sources of neurochemical compounds are the serum and the plasma, however, the identification of their biomarkers is under preclinical examinations. Unfortunately neither the validation of these markers nor the consistent acceptance of the experimental results is possible due to the wide range of protocols in international research. The importance of biomarkers in the development of potential drug candidates is also discussed.
authors.affiliation: Department of Psychiatry, University of Szeged, Szeged, Hungary. olah.zita.87@gmail.com
authors.forename: Zita
authors.initials: Z
authors.lastname: Olah
authors.forename: Magdolna
authors.initials: M
authors.lastname: Pakaski
authors.forename: Zoltan
authors.initials: Z
authors.lastname: Janka
authors.forename: Janos
authors.initials: J
authors.lastname: Kalman
mesh_terms: D017668:Age of Onset; D000544:Alzheimer Disease / Q000097:blood / Q000134:cerebrospinal fluid / Q000175:diagnosis* / Q000235:genetics / Q000378:metabolism* / Q000517:prevention & control; D016229:Amyloid beta-Peptides / Q000134:cerebrospinal fluid* / Q000378:metabolism; D016564:Amyloid beta-Protein Precursor / Q000235:genetics; D015415:Biomarkers / Q000134:cerebrospinal fluid; D001921:Brain / Q000378:metabolism*; D060825:Cognitive Dysfunction / Q000150:complications / Q000175:diagnosis / Q000378:metabolism; D003937:Diagnosis, Differential; D006801:Humans; D008569:Memory Disorders / Q000209:etiology / Q000517:prevention & control; D009154:Mutation; D059906:Neuroimaging; D010766:Phosphorylation; D053764:Presenilin-1 / Q000235:genetics; D053766:Presenilin-2 / Q000235:genetics; D012680:Sensitivity and Specificity; D016875:tau Proteins / Q000134:cerebrospinal fluid* / Q000378:metabolism
chemical_list: C545487:APP protein, human; D016229:Amyloid beta-Peptides; D016564:Amyloid beta-Protein Precursor; D015415:Biomarkers; C508853:PSEN1 protein, human; C508861:PSEN2 protein, human; D053764:Presenilin-1; D053766:Presenilin-2; D016875:tau Proteins