Plasma Aβ42 as Biomarker of Prodromal Alzheimer's Disease Progression in Patients with Amnestic Mild Cognitive Impairment: Evidence from the PharmaCog/E-ADNI Study

Paolo Maria Rossini, Diego Albani, Moira Marizzoni, Clarissa Ferrari, Federica Fusco, Lucia Boeri, Ilaria Raimondi, Jorge Jovicich, Claudio Babiloni, Andrea Soricelli, Roberta Lizio, Samantha Galluzzi, Libera Cavaliere, Mira Didic, Peter Schönknecht, José Luis Molinuevo, Flavio Nobili, Lucilla Parnetti, Pierre Payoux, Luisella BocchioMarco Salvatore, Magda Tsolaki, Pieter Jelle Visser, Jill C. Richardson, Jens Wiltfang, Régis Bordet, Olivier Blin, Gianluigi Forloni, Giovanni B. Frisoni

Risultato della ricerca: Contributo in rivistaArticolo in rivista

11 Citazioni (Scopus)

Abstract

It is an open issue whether blood biomarkers serve to diagnose Alzheimer's disease (AD) or monitor its progression over time from prodromal stages. Here, we addressed this question starting from data of the European FP7 IMI-PharmaCog/E-ADNI longitudinal study in amnesic mild cognitive impairment (aMCI) patients including biological, clinical, neuropsychological (e.g., ADAS-Cog13), neuroimaging, and electroencephalographic measures. PharmaCog/E-ADNI patients were classified as "positive" (i.e., "prodromal AD" n = 76) or "negative" (n = 52) based on a diagnostic cut-off of Aβ42/P-tau in cerebrospinal fluid as well as APOE ε 4 genotype. Blood was sampled at baseline and at two follow-ups (12 and 18 months), when plasma amyloid peptide 42 and 40 (Aβ42, Aβ40) and apolipoprotein J (clusterin, CLU) were assessed. Linear Mixed Models found no significant differences in plasma molecules between the "positive" (i.e., prodromal AD) and "negative" groups at baseline. In contrast, plasma Aβ42 showed a greater reduction over time in the prodromal AD than the "negative" aMCI group (p = 0.048), while CLU and Aβ40 increased, but similarly in the two groups. Furthermore, plasma Aβ42 correlated with the ADAS-Cog13 score both in aMCI patients as a whole and the prodromal AD group alone. Finally, CLU correlated with the ADAS-Cog13 only in the whole aMCI group, and no association with ADAS-Cog13 was found for Aβ40. In conclusion, plasma Aβ42 showed disease progression-related features in aMCI patients with prodromal AD.
Lingua originaleEnglish
pagine (da-a)1-12
Numero di pagine12
RivistaJournal of Alzheimer's Disease
DOI
Stato di pubblicazionePubblicato - 2018

Keywords

  • Amnesic mild cognitive impairment
  • PharmaCog project
  • amyloid-beta peptide
  • biomarkers
  • clinical trial
  • clusterin
  • prodromal Alzheimer’s disease

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