TY - JOUR
T1 - Plasma amyloid-β as a biomarker in alzheimer's disease
T2 - The AIBL study of aging
AU - Lui, James K.
AU - Laws, Simon M.
AU - Li, Qiao Xin
AU - Villemagne, Victor L.
AU - Ames, David
AU - Brown, Belinda
AU - Bush, Ashley I.
AU - De Ruyck, Karl
AU - Dromey, Jasmin
AU - Ellis, Kathryn A.
AU - Faux, Noel G.
AU - Foster, Jonathan
AU - Fowler, Christopher
AU - Gupta, Veer
AU - Hudson, Peter
AU - Laughton, Katrina
AU - Masters, Colin L.
AU - Pertile, Kelly
AU - Rembach, Alan
AU - Rimajova, Mira
AU - Rodrigues, Mark
AU - Rowe, Christopher C.
AU - Rumble, Rebecca
AU - Szoeke, Cassandra
AU - Taddei, Kevin
AU - Taddei, Tania
AU - Trounson, Brett
AU - Ward, Vanessa
AU - Martins, Ralph N.
AU - for the Australian Imaging, Biomarkers and Lifestyle (AIBL) Research Group
PY - 2010
Y1 - 2010
N2 - Amyloid-β (Aβ) plays a central role in the pathogenesis of Alzheimer's disease (AD) and has been postulated as a potential biomarker for AD. However, there is a lack of consensus as to its suitability as an AD biomarker. The objective of this study was to determine the significance of plasma Aβ as an AD biomarker and its relationship with Aβ load and to determine the effect of different assay methods on the interpretation of Aβ levels. Plasma Aβ1-40, Aβ1-42, and N-terminal cleaved fragments were measured using both a commercial multiplex assay and a well-documented ELISA in 1032 individuals drawn from the well-characterized Australian Imaging, Biomarkers and Lifestyle (AIBL) study of aging. Further, Aβ levels were compared to Aβ load derived from positron-emission tomography (PET) with the Pittsburgh compound B (PiB). Lower Aβ1-42 and Aβ1-42/1-40 ratio were observed in patients with AD and inversely correlated with PiB-PET derived Aβ load. However, assay methodology significantly impacted the interpretation of data. The cross-sectional analysis of plasma Aβ isoforms suggests that they may not be sufficient per se to diagnose AD. The value of their measurement in prognosis and monitoring of AD interventions needs further study, in addition to future longitudinal comparisons together with other predictors, which will determine whether plasma Aβ has diagnostic value in a panel of biomarkers.
AB - Amyloid-β (Aβ) plays a central role in the pathogenesis of Alzheimer's disease (AD) and has been postulated as a potential biomarker for AD. However, there is a lack of consensus as to its suitability as an AD biomarker. The objective of this study was to determine the significance of plasma Aβ as an AD biomarker and its relationship with Aβ load and to determine the effect of different assay methods on the interpretation of Aβ levels. Plasma Aβ1-40, Aβ1-42, and N-terminal cleaved fragments were measured using both a commercial multiplex assay and a well-documented ELISA in 1032 individuals drawn from the well-characterized Australian Imaging, Biomarkers and Lifestyle (AIBL) study of aging. Further, Aβ levels were compared to Aβ load derived from positron-emission tomography (PET) with the Pittsburgh compound B (PiB). Lower Aβ1-42 and Aβ1-42/1-40 ratio were observed in patients with AD and inversely correlated with PiB-PET derived Aβ load. However, assay methodology significantly impacted the interpretation of data. The cross-sectional analysis of plasma Aβ isoforms suggests that they may not be sufficient per se to diagnose AD. The value of their measurement in prognosis and monitoring of AD interventions needs further study, in addition to future longitudinal comparisons together with other predictors, which will determine whether plasma Aβ has diagnostic value in a panel of biomarkers.
KW - Alzheimer's disease
KW - amyloid-β
KW - biomarkers
KW - diagnosis
KW - Pittsburgh Compound B
KW - positron-emission topography
UR - http://www.scopus.com/inward/record.url?scp=77954560978&partnerID=8YFLogxK
U2 - 10.3233/JAD-2010-090249
DO - 10.3233/JAD-2010-090249
M3 - Article
C2 - 20413897
AN - SCOPUS:77954560978
SN - 1387-2877
VL - 20
SP - 1233
EP - 1242
JO - Journal of Alzheimer's Disease
JF - Journal of Alzheimer's Disease
IS - 4
ER -
