Abstract
Introduction: We explored what combination of blood-based biomarkers (amyloid beta [Aβ]1-42/1-40, phosphorylated tau [p-tau]181, neurofilament light [NfL], glial fibrillary acidic protein [GFAP]) differentiates Alzheimer's disease (AD) dementia, frontotemporal dementia (FTD), and dementia with Lewy bodies (DLB). Methods: We measured the biomarkers with Simoa in two separate cohorts (n = 160 and n = 152). In one cohort, Aβ1-42/1-40 was also measured with mass spectrometry (MS). We assessed the differential diagnostic value of the markers, by logistic regression with Wald's backward selection. Results: MS and Simoa Aβ1-42/1-40 similarly differentiated AD from controls. The Simoa panel that optimally differentiated AD from FTD consisted of NfL and p-tau181 (area under the curve [AUC] = 0.94; cohort 1) or NfL, GFAP, and p-tau181 (AUC = 0.90; cohort 2). For AD from DLB, the panel consisted of NfL, p-tau181, and GFAP (AUC = 0.88; cohort 1), and only p-tau181 (AUC = 0.81; cohort 2). Discussion: A combination of plasma p-tau181, NfL, and GFAP, but not Aβ1-42/1-40, might be useful to discriminate AD, FTD, and DLB.
| Original language | English |
|---|---|
| Article number | e12285 |
| Journal | Alzheimer's & Dementia: Diagnosis, Assessment & Disease Monitoring |
| Volume | 14 |
| Issue number | 1 |
| DOIs | |
| Publication status | Published - 2022 |
Keywords
- amyloid beta
- blood biomarker
- glial fibrillary acidic protein
- neurofilament light
- phosphorylated tau
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In: Alzheimer's & Dementia: Diagnosis, Assessment & Disease Monitoring, Vol. 14, No. 1, e12285, 2022.
Research output: Contribution to journal › Article › Academic › peer-review
TY - JOUR
T1 - Differential diagnostic performance of a panel of plasma biomarkers for different types of dementia
AU - Thijssen, Elisabeth H.
AU - Verberk, Inge M. W.
AU - Kindermans, Jana
AU - Abramian, Adlin
AU - Vanbrabant, Jeroen
AU - Ball, Andrew J.
AU - Pijnenburg, Yolande
AU - Lemstra, Afina W.
AU - van der Flier, Wiesje M.
AU - Stoops, Erik
AU - Hirtz, Christophe
AU - Teunissen, Charlotte E.
N1 - Funding Information: ET, IV, JK, AA, and YP report no conflicts of interest. JV is an employee of ADx NeuroSciences. AB was an employee of Quanterix Corporation when the study was performed and holds shares in Quanterix. AL has received funding from stichting Dioraphte, Alzheimer Nederland, and ZonMW Memorabel (project #733050509). AL has performed contract research with Axovant, EIP Pharma, and Combinostics. All funding is paid to her institution. WF has performed contract research for Biogen MA Inc, and Boehringer Ingelheim. All funding is paid to her institution. WF has been an invited speaker at Boehringer Ingelheim, Biogen MA Inc, Danone, Eisai, WebMD Neurology (Medscape), Springer Healthcare. All funding is paid to her institution. WF is consultant to Oxford Health Policy Forum CIC, Roche, and Biogen MA Inc. All funding is paid to her institution. WF participated in advisory boards of Biogen MA Inc and Roche. All funding is paid to her institution. WF was associate editor of in 2020/2021. WF is associate editor at . All funding is paid to her institution. ES is an employee and shareholder of ADx NeuroSciences, Gent, Belgium. CH has a collaboration contract with Shimadzu European Innovation Center including a PhD thesis. CT has a collaboration contract with ADx NeuroSciences and Quanterix, performed contract research for or received grants from AC‐Immune, Axon Neurosciences, Biogen, Brainstorm Therapeutics, Celgene, EIP Pharma, Eisai, PeopleBio, Roche, Toyama, Vivoryon. CT serves on editorial boards of /Springer, , and is editor of a Neuromethods book for Springer. All funding is paid to her institution. Alzheimer, Research & Therapy Brain Medidact Neurologi Alzheimer Research and Therapy, Neurology: Neuroimmunology & Neuroinflammation Funding Information: IV is appointed on a research grant by Alzheimer Nederland (NL‐17004). JK and CH received funding from France Alzheimer (PI : Pr A. Gabelle). Research of CT is supported by the European Commission (Marie Curie International Training Network, grant agreement No 860197 [MIRIADE], and JPND), Health Holland, the Dutch Research Council (ZonMW), Alzheimer Drug Discovery Foundation, The Selfridges Group Foundation, Alzheimer Netherlands, Alzheimer Association. CT is a recipient of ABOARD, which is a public–private partnership receiving funding from ZonMW (#73305095007) and Health∼Holland, Topsector Life Sciences & Health (PPP‐allowance; #LSHM20106). Research programs of Wiesje van der Flier have been funded by ZonMW, NWO, EU‐FP7, EU‐JPND, Alzheimer Nederland, CardioVascular Onderzoek Nederland, Health∼Holland, Topsector Life Sciences & Health, stichting Dioraphte, Gieskes‐Strijbis fonds, stichting Equilibrio, Pasman stichting, stichting Alzheimer & Neuropsychiatrie Foundation, Biogen MA Inc, Boehringer Ingelheim, Life‐MI, AVID, Roche BV, Fujifilm, Combinostics. WF holds the Pasman chair. WF is a recipient of ABOARD, which is a public–private partnership receiving funding from ZonMW (#73305095007) and Health∼Holland, Topsector Life Sciences & Health (PPP‐allowance; #LSHM20106). All funding is paid to her institution. Funding Information: IV is appointed on a research grant by Alzheimer Nederland (NL-17004). JK and CH received funding from France Alzheimer (PI : Pr A. Gabelle). Research of CT is supported by the European Commission (Marie Curie International Training Network, grant agreement No 860197 [MIRIADE], and JPND), Health Holland, the Dutch Research Council (ZonMW), Alzheimer Drug Discovery Foundation, The Selfridges Group Foundation, Alzheimer Netherlands, Alzheimer Association. CT is a recipient of ABOARD, which is a public–private partnership receiving funding from ZonMW (#73305095007) and Health∼Holland, Topsector Life Sciences & Health (PPP-allowance; #LSHM20106). Research programs of Wiesje van der Flier have been funded by ZonMW, NWO, EU-FP7, EU-JPND, Alzheimer Nederland, CardioVascular Onderzoek Nederland, Health∼Holland, Topsector Life Sciences & Health, stichting Dioraphte, Gieskes-Strijbis fonds, stichting Equilibrio, Pasman stichting, stichting Alzheimer & Neuropsychiatrie Foundation, Biogen MA Inc, Boehringer Ingelheim, Life-MI, AVID, Roche BV, Fujifilm, Combinostics. WF holds the Pasman chair. WF is a recipient of ABOARD, which is a public–private partnership receiving funding from ZonMW (#73305095007) and Health∼Holland, Topsector Life Sciences & Health (PPP-allowance; #LSHM20106). All funding is paid to her institution. Publisher Copyright: © 2022 The Authors. Alzheimer's & Dementia: Diagnosis, Assessment & Disease Monitoring published by Wiley Periodicals, LLC on behalf of Alzheimer's Association.
PY - 2022
Y1 - 2022
N2 - Introduction: We explored what combination of blood-based biomarkers (amyloid beta [Aβ]1-42/1-40, phosphorylated tau [p-tau]181, neurofilament light [NfL], glial fibrillary acidic protein [GFAP]) differentiates Alzheimer's disease (AD) dementia, frontotemporal dementia (FTD), and dementia with Lewy bodies (DLB). Methods: We measured the biomarkers with Simoa in two separate cohorts (n = 160 and n = 152). In one cohort, Aβ1-42/1-40 was also measured with mass spectrometry (MS). We assessed the differential diagnostic value of the markers, by logistic regression with Wald's backward selection. Results: MS and Simoa Aβ1-42/1-40 similarly differentiated AD from controls. The Simoa panel that optimally differentiated AD from FTD consisted of NfL and p-tau181 (area under the curve [AUC] = 0.94; cohort 1) or NfL, GFAP, and p-tau181 (AUC = 0.90; cohort 2). For AD from DLB, the panel consisted of NfL, p-tau181, and GFAP (AUC = 0.88; cohort 1), and only p-tau181 (AUC = 0.81; cohort 2). Discussion: A combination of plasma p-tau181, NfL, and GFAP, but not Aβ1-42/1-40, might be useful to discriminate AD, FTD, and DLB.
AB - Introduction: We explored what combination of blood-based biomarkers (amyloid beta [Aβ]1-42/1-40, phosphorylated tau [p-tau]181, neurofilament light [NfL], glial fibrillary acidic protein [GFAP]) differentiates Alzheimer's disease (AD) dementia, frontotemporal dementia (FTD), and dementia with Lewy bodies (DLB). Methods: We measured the biomarkers with Simoa in two separate cohorts (n = 160 and n = 152). In one cohort, Aβ1-42/1-40 was also measured with mass spectrometry (MS). We assessed the differential diagnostic value of the markers, by logistic regression with Wald's backward selection. Results: MS and Simoa Aβ1-42/1-40 similarly differentiated AD from controls. The Simoa panel that optimally differentiated AD from FTD consisted of NfL and p-tau181 (area under the curve [AUC] = 0.94; cohort 1) or NfL, GFAP, and p-tau181 (AUC = 0.90; cohort 2). For AD from DLB, the panel consisted of NfL, p-tau181, and GFAP (AUC = 0.88; cohort 1), and only p-tau181 (AUC = 0.81; cohort 2). Discussion: A combination of plasma p-tau181, NfL, and GFAP, but not Aβ1-42/1-40, might be useful to discriminate AD, FTD, and DLB.
KW - amyloid beta
KW - blood biomarker
KW - glial fibrillary acidic protein
KW - neurofilament light
KW - phosphorylated tau
UR - http://www.scopus.com/inward/record.url?scp=85134999475&partnerID=8YFLogxK
U2 - https://doi.org/10.1002/dad2.12285
DO - https://doi.org/10.1002/dad2.12285
M3 - Article
C2 - 35603139
SN - 2352-8729
VL - 14
JO - Alzheimer's & Dementia: Diagnosis, Assessment & Disease Monitoring
JF - Alzheimer's & Dementia: Diagnosis, Assessment & Disease Monitoring
IS - 1
M1 - e12285
ER -