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Inverse relation between in vivo amyloid imaging load and cerebrospinal fluid Aβ <sub>42</sub> in humans
Annals of Neurology · 2005 · Vol. 59(3) · pp. 512–519
Anne M. Fagan✉(Washington University in St. Louis)Mark A. Mintun(Washington University in St. Louis)Robert H. Mach(Washington University in St. Louis)Sang‐Yoon Lee(Washington University in St. Louis)Carmen S. Dence(Washington University in St. Louis)Aarti R. Shah(Washington University in St. Louis)Gina LaRossa(Washington University in St. Louis)Michael Spinner(Washington University in St. Louis)William E. Klunk(University of Pittsburgh)Chester A. Mathis(University of Pittsburgh)Steven T. DeKosky(University of Pittsburgh)John C. Morris(Washington University in St. Louis)David M. Holtzman(Hope Center for Neurological Disorders)
Abstract
These observations suggest that brain amyloid deposition results in low CSF Abeta(42), and that amyloid imaging and CSF Abeta(42) may potentially serve as antecedent biomarkers of (preclinical) AD.
Dementia and Cognitive Impairment ResearchAlzheimer's disease research and treatmentsAdvanced Neuroimaging Techniques and ApplicationsCerebrospinal fluidPittsburgh compound BAmyloid (mycology)PathologyIn vivoPathogenesisMedicineDementiaAlzheimer's diseaseInternal medicine
MeSH terms
AgedAged, 80 and overAlzheimer DiseaseAmyloidDiagnostic ImagingFemaleHumansImage Processing, Computer-AssistedMaleMemoryMiddle AgedNeuropsychological TestsPeptide FragmentsTissue DistributionAmyloid beta-Peptides
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