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@ARTICLE{Funke:4525,
      author       = {Funke, S. A. and Birkmann, E. and Willbold, D.},
      title        = {{D}etection of {A}myloid-ß aggregates in body fluids: {A}
                      suitable method for early diagnosis of {A}lzheimer's
                      disease?},
      journal      = {Current Alzheimer research},
      volume       = {6},
      issn         = {1567-2050},
      address      = {Hilversum},
      publisher    = {Bentham Science Publishers Ltd.},
      reportid     = {PreJuSER-4525},
      pages        = {285 - 289},
      year         = {2009},
      note         = {Record converted from VDB: 12.11.2012},
      abstract     = {Today, the most reliable diagnosis for Alzheimer's disease
                      (AD) is the post mortem identification of amyloid plaques,
                      consisting of the Amyloid-beta (A beta) peptide, (and
                      neurofibrillary tangles) in the brain of the patient. Great
                      efforts are being made to identify reliable biomarkers for
                      AD that are suitable for minimal invasive early diagnosis
                      and prognosis of AD. During the past years, body fluids of
                      AD patients were assayed for their content of total or
                      soluble A beta (1-40) or A beta (1-42) concentrations using
                      classical (ELISA) or non-classical (with additional signal
                      amplification) read-out. Cerebrospinal fluid (CSF)
                      concentrations of soluble A beta (1-42) are reduced by 40 to
                      50 $\%$ in AD patients compared to age-matched healthy
                      controls as confirmed in more than 30 studies, with both
                      sensitivity and specificity exceeding 80 $\%$ in most of the
                      studies. Thus, it was suggested that low levels of CSF A
                      beta (1-42) might be useful for preclinical diagnosis.
                      Because the current average sensitivity of AD biomarker
                      detection in the CSF is approximately 85 $\%,$ these assays
                      do not offer a considerable increase in predictive value
                      over existing algorithms based on neuropsychological and
                      imaging modalities. Regarding the amyloid cascade
                      hypothesis, A beta oligomers and aggregates are directly
                      involved in the pathogenic process. Therefore, presence of A
                      beta aggregates seem to be the most direct disease biomarker
                      for AD and increasing effort is being made into the
                      development of methods suitable for the detection of
                      different A beta aggregates in body fluids like CSF and
                      plasma. We therefore give an overview of the current state
                      of A beta aggregate specific detection.},
      keywords     = {J (WoSType)},
      cin          = {ISB-3},
      ddc          = {610},
      cid          = {I:(DE-Juel1)VDB942},
      pnm          = {Funktion und Dysfunktion des Nervensystems},
      pid          = {G:(DE-Juel1)FUEK409},
      shelfmark    = {Clinical Neurology / Neurosciences},
      typ          = {PUB:(DE-HGF)16},
      UT           = {WOS:000266522800011},
      url          = {https://juser.fz-juelich.de/record/4525},
}