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Decreased CSF amyloid beta (1-40) levels in frontotemporal lobar degeneration
  1. YAL Pijnenburg (y.pijnenburg{at}vumc.nl)
  1. VUMC, Netherlands
    1. SNM Schoonenboom (niki.schoonenboom{at}vumc.nl)
    1. VUMC, Netherlands
      1. PD Mehta
      1. Institute for basic reasearch in developmental disabilities, United States
        1. SP Mehta
        1. Institute for basic reasearch in developmental disorders, United States
          1. C Mulder (c.mulder{at}vumc.nl)
          1. Clinical Chemistry, VUMC, Netherlands
            1. R Veerhuis (r.veerhuis{at}vumc.nl)
            1. Vrije Universiteit medical center, Netherlands
              1. MA Blankenstein (ma.blankenstein{at}vumc.nl)
              1. VU Medisch Centrum, Netherlands
                1. P Scheltens (p.scheltens{at}vumc.nl)
                1. VU medical Center, Netherlands

                  Abstract

                  The role of amyloid metabolism in the pathophysiology of FTLD remains to be elucidated. We compared CSF levels of amyloid beta 1-40 (Aβ40) and amyloid beta 1-42 (Aβ42) in patients with frontotemporal lobar degeneration (FTLD, n=21) versus patients with Alzheimer’s disease (AD, n=39) and control subjects (n=30). While in AD cases Aβ42 levels were lower and CSF Aβ40 levels equal to those in controls, a significant decrease in Aβ40 and increase in CSF Aβ42/Aβ40 ratio was observed in FTLD compared AD and control subjects. These findings favour a differential involvement of amyloid β peptides in FTLD compared to AD.

                  • Alzheimer's disease
                  • Cerebrospinal fluid
                  • amyloid beta
                  • biomarker
                  • frontotemporal lobar degeneration

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