Performance of plasma amyloid, tau, and astrocyte biomarkers to identify cerebral AD pathophysiology
Ferreira, P. C. L.; Tissot, C.; Ferrari-Souza, J. P.; Brum, W.; Bellaver, B.; Leffa, D. T.; Therriault, J.; Benedet, A. L.; Lussier, F.; Chamoun, M.; Bezgin, G.; Servaes, S.; Stevenson, J.; Rahmouni, N.; Pallen, V.; Kang, M. S.; Poltronetti, N. M.; Tudorascu, D. L.; Klunk, W. E.; Villemagne, V.; Cohen, A.; Gauthier, S.; Zimmer, E. R.; Ashton, N. J.; Zetterberg, H. J.; Blennow, K.; Karikari, T. K.; Rosa-Neto, P.; Pascoal, T. A.
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IntroductionPlasma amyloid-{beta} (A{beta}), phosphorylated tau (p-tau), and glial fibrillar acid protein (GFAP) can identify Alzheimers disease (AD) pathophysiology with high accuracy. However, comparing their performance in the same individuals remains under-explored. MethodsWe compared the predictive performance of plasma A{beta}42/40, p-tau(at threonine 181 and 231), neurofilament light (NfL), and GFAP to identify A{beta}- and tau-PET positivity in 138 cognitive unimpaired (CU) and 87 cognitive impaired (CI) individuals. ResultsIn CU, plasma p-tau231 had the best performance to identify both A{beta}- and tau-PET positivity. In CI, plasma GFAP showed the best predictive accuracy to identify both A{beta} and tau-PET positivity. DiscussionOur results support plasma p-tau231 as a marker of early AD pathology and, that GFAP best identifies both PET A{beta} and tau abnormalities in the brain of CI individuals. These findings highlight that the performance of blood-based protein biomarkers to identify the presence of AD pathophysiology is disease-stage dependent.
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