Plasma Abeta42 as Biomarker of Prodromal Alzheimer's Disease Progression in Patients with Amnestic Mild Cognitive Impairment: Evidence from the PharmaCog/E-ADNI Study

D. Albani, M. Marizzoni, C. Ferrari, F. Fusco, L. Boeri, I. Raimondi, J. Jovicich, C. Babiloni, A. Soricelli, R. Lizio, S. Galluzzi, L. Cavaliere, M. Didic, P. Schonknecht, J. L. Molinuevo, F. Nobili, L. Parnetti, P. Payoux, L. Bocchio, M. SalvatoreP. M. Rossini, M. Tsolaki, P. J. Visser, J. C. Richardson, J. Wiltfang, R. Bordet, O. Blin, G. Forloni, G. B. Frisoni, P. Consortium

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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 Abeta42/P-tau in cerebrospinal fluid as well as APOE epsilon 4 genotype. Blood was sampled at baseline and at two follow-ups (12 and 18 months), when plasma amyloid peptide 42 and 40 (Abeta42, Abeta40) 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 Abeta42 showed a greater reduction over time in the prodromal AD than the "negative" aMCI group (p = 0.048), while CLU and Abeta40 increased, but similarly in the two groups. Furthermore, plasma Abeta42 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 Abeta40. In conclusion, plasma Abeta42 showed disease progression-related features in aMCI patients with prodromal AD.
Original languageEnglish
JournalJournal of Alzheimer's disease : JAD
DOIs
Publication statusPublished - Aug 20 2018

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Clusterin
Disease Progression
Alzheimer Disease
Biomarkers
Prodromal Symptoms
Amyloid
Neuroimaging
Longitudinal Studies
Cerebrospinal Fluid
Cognitive Dysfunction
Linear Models
Genotype
Peptides

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Plasma Abeta42 as Biomarker of Prodromal Alzheimer's Disease Progression in Patients with Amnestic Mild Cognitive Impairment: Evidence from the PharmaCog/E-ADNI Study. / Albani, D.; Marizzoni, M.; Ferrari, C.; Fusco, F.; Boeri, L.; Raimondi, I.; Jovicich, J.; Babiloni, C.; Soricelli, A.; Lizio, R.; Galluzzi, S.; Cavaliere, L.; Didic, M.; Schonknecht, P.; Molinuevo, J. L.; Nobili, F.; Parnetti, L.; Payoux, P.; Bocchio, L.; Salvatore, M.; Rossini, P. M.; Tsolaki, M.; Visser, P. J.; Richardson, J. C.; Wiltfang, J.; Bordet, R.; Blin, O.; Forloni, G.; Frisoni, G. B.; Consortium, P.

In: Journal of Alzheimer's disease : JAD, 20.08.2018.

Research output: Contribution to journalArticle

Albani, D, Marizzoni, M, Ferrari, C, Fusco, F, Boeri, L, Raimondi, I, Jovicich, J, Babiloni, C, Soricelli, A, Lizio, R, Galluzzi, S, Cavaliere, L, Didic, M, Schonknecht, P, Molinuevo, JL, Nobili, F, Parnetti, L, Payoux, P, Bocchio, L, Salvatore, M, Rossini, PM, Tsolaki, M, Visser, PJ, Richardson, JC, Wiltfang, J, Bordet, R, Blin, O, Forloni, G, Frisoni, GB & Consortium, P 2018, 'Plasma Abeta42 as Biomarker of Prodromal Alzheimer's Disease Progression in Patients with Amnestic Mild Cognitive Impairment: Evidence from the PharmaCog/E-ADNI Study', Journal of Alzheimer's disease : JAD. https://doi.org/10.3233/JAD-180321 [doi]
Albani, D. ; Marizzoni, M. ; Ferrari, C. ; Fusco, F. ; Boeri, L. ; Raimondi, I. ; Jovicich, J. ; Babiloni, C. ; Soricelli, A. ; Lizio, R. ; Galluzzi, S. ; Cavaliere, L. ; Didic, M. ; Schonknecht, P. ; Molinuevo, J. L. ; Nobili, F. ; Parnetti, L. ; Payoux, P. ; Bocchio, L. ; Salvatore, M. ; Rossini, P. M. ; Tsolaki, M. ; Visser, P. J. ; Richardson, J. C. ; Wiltfang, J. ; Bordet, R. ; Blin, O. ; Forloni, G. ; Frisoni, G. B. ; Consortium, P. / Plasma Abeta42 as Biomarker of Prodromal Alzheimer's Disease Progression in Patients with Amnestic Mild Cognitive Impairment: Evidence from the PharmaCog/E-ADNI Study. In: Journal of Alzheimer's disease : JAD. 2018.
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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 Abeta42/P-tau in cerebrospinal fluid as well as APOE epsilon 4 genotype. Blood was sampled at baseline and at two follow-ups (12 and 18 months), when plasma amyloid peptide 42 and 40 (Abeta42, Abeta40) 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 Abeta42 showed a greater reduction over time in the prodromal AD than the {"}negative{"} aMCI group (p = 0.048), while CLU and Abeta40 increased, but similarly in the two groups. Furthermore, plasma Abeta42 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 Abeta40. In conclusion, plasma Abeta42 showed disease progression-related features in aMCI patients with prodromal AD.",
author = "D. Albani and M. Marizzoni and C. Ferrari and F. Fusco and L. Boeri and I. Raimondi and J. Jovicich and C. Babiloni and A. Soricelli and R. Lizio and S. Galluzzi and L. Cavaliere and M. Didic and P. Schonknecht and Molinuevo, {J. L.} and F. Nobili and L. Parnetti and P. Payoux and L. Bocchio and M. Salvatore and Rossini, {P. M.} and M. Tsolaki and Visser, {P. J.} and Richardson, {J. C.} and J. Wiltfang and R. Bordet and O. Blin and G. Forloni and Frisoni, {G. B.} and P. Consortium",
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T1 - Plasma Abeta42 as Biomarker of Prodromal Alzheimer's Disease Progression in Patients with Amnestic Mild Cognitive Impairment: Evidence from the PharmaCog/E-ADNI Study

AU - Albani, D.

AU - Marizzoni, M.

AU - Ferrari, C.

AU - Fusco, F.

AU - Boeri, L.

AU - Raimondi, I.

AU - Jovicich, J.

AU - Babiloni, C.

AU - Soricelli, A.

AU - Lizio, R.

AU - Galluzzi, S.

AU - Cavaliere, L.

AU - Didic, M.

AU - Schonknecht, P.

AU - Molinuevo, J. L.

AU - Nobili, F.

AU - Parnetti, L.

AU - Payoux, P.

AU - Bocchio, L.

AU - Salvatore, M.

AU - Rossini, P. M.

AU - Tsolaki, M.

AU - Visser, P. J.

AU - Richardson, J. C.

AU - Wiltfang, J.

AU - Bordet, R.

AU - Blin, O.

AU - Forloni, G.

AU - Frisoni, G. B.

AU - Consortium, P.

N1 - LR: 20180828; JID: 9814863; OTO: NOTNLM; 2018/08/29 06:00 [entrez]; 2018/08/29 06:00 [pubmed]; 2018/08/29 06:00 [medline]; aheadofprint

PY - 2018/8/20

Y1 - 2018/8/20

N2 - 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 Abeta42/P-tau in cerebrospinal fluid as well as APOE epsilon 4 genotype. Blood was sampled at baseline and at two follow-ups (12 and 18 months), when plasma amyloid peptide 42 and 40 (Abeta42, Abeta40) 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 Abeta42 showed a greater reduction over time in the prodromal AD than the "negative" aMCI group (p = 0.048), while CLU and Abeta40 increased, but similarly in the two groups. Furthermore, plasma Abeta42 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 Abeta40. In conclusion, plasma Abeta42 showed disease progression-related features in aMCI patients with prodromal AD.

AB - 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 Abeta42/P-tau in cerebrospinal fluid as well as APOE epsilon 4 genotype. Blood was sampled at baseline and at two follow-ups (12 and 18 months), when plasma amyloid peptide 42 and 40 (Abeta42, Abeta40) 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 Abeta42 showed a greater reduction over time in the prodromal AD than the "negative" aMCI group (p = 0.048), while CLU and Abeta40 increased, but similarly in the two groups. Furthermore, plasma Abeta42 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 Abeta40. In conclusion, plasma Abeta42 showed disease progression-related features in aMCI patients with prodromal AD.

U2 - 10.3233/JAD-180321 [doi]

DO - 10.3233/JAD-180321 [doi]

M3 - Article

JO - Journal of Alzheimer's Disease

JF - Journal of Alzheimer's Disease

SN - 1387-2877

ER -