Evidence map›Paper›PMID 38159140›Full record

ArticleActa neuropathologica2023

Optimal blood tau species for the detection of Alzheimer's disease neuropathology: an immunoprecipitation mass spectrometry and autopsy study.

Laia Montoliu-Gaya, Michael L Alosco, Eukyung Yhang, Yorghos Tripodis, Daniel Sconzo, Madeline Ally, Lana Grötschel, Nicholas J Ashton, Juan Lantero-Rodriguez, Mathias Sauer and 26 more

Abstract read
In one paragraph

Article in Acta neuropathologica, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 1 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

36 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Article
  4. Observational
  5. Article
  6. Prognostic value of plasma %p-tau217 in cognitively unimpaired older adults.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
  7. Article
  8. Analytical and clinical validation of the Lumipulse G plasma p-tau217 assay for clinical implementation.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
  9. Article
  10. Association of [Neurology · 2026
    Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Observational
  18. Article
  19. Article
  20. Plasma tau biomarkers are distinctly associated with tau tangles and decreased with Lewy body pathology.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

36 authors.

Laia Montoliu-Gaya *Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden. laia.montoliu.gaya@gu.se.ORCID 0000-0001-7684-6318
Michael L Alosco *Boston University Alzheimer's Disease Research Center and CTE Center, Boston University, Chobanian and Avedisian School of Medicine, Boston, MA, 02118, USA.
Eukyung YhangDepartment of Biostatistics, Boston University School of Public Health, Boston, MA, 02118, USA.
Yorghos TripodisDepartment of Biostatistics, Boston University School of Public Health, Boston, MA, 02118, USA.
Daniel SconzoBoston University Alzheimer's Disease Research Center and CTE Center, Boston University, Chobanian and Avedisian School of Medicine, Boston, MA, 02118, USA.
Madeline AllyUniversity of Arizona, Tucson, AZ, USA.
Lana GrötschelDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Nicholas J AshtonDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Juan Lantero-RodriguezDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Mathias SauerDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Bárbara GomesDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Johanna NilssonDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Gunnar BrinkmalmDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Michael A SugarmanDepartment of Neurology, Medical University of South Carolina, Charleston, SC, 29425, USA.
Hugo J AparicioBoston University Alzheimer's Disease Research Center and CTE Center, Boston University, Chobanian and Avedisian School of Medicine, Boston, MA, 02118, USA.
Brett MartinBiostatistics and Epidemiology Data Analytics Center, Boston University School of Public Health, Boston, MA, 02118, USA.
Joseph N PalmisanoBiostatistics and Epidemiology Data Analytics Center, Boston University School of Public Health, Boston, MA, 02118, USA.
Eric G SteinbergBoston University Alzheimer's Disease Research Center and CTE Center, Boston University, Chobanian and Avedisian School of Medicine, Boston, MA, 02118, USA.
Irene SimkinDepartment of Medicine, Boston University, Chobanian and Avedisian School of Medicine, Boston, MA, 02118, USA.
Katherine W TurkBoston University Alzheimer's Disease Research Center and CTE Center, Boston University, Chobanian and Avedisian School of Medicine, Boston, MA, 02118, USA.
Andrew E BudsonBoston University Alzheimer's Disease Research Center and CTE Center, Boston University, Chobanian and Avedisian School of Medicine, Boston, MA, 02118, USA.
Rhoda AuBoston University Alzheimer's Disease Research Center and CTE Center, Boston University, Chobanian and Avedisian School of Medicine, Boston, MA, 02118, USA.
Lindsay FarrerBoston University Alzheimer's Disease Research Center and CTE Center, Boston University, Chobanian and Avedisian School of Medicine, Boston, MA, 02118, USA.
Gyungah R JunBoston University Alzheimer's Disease Research Center and CTE Center, Boston University, Chobanian and Avedisian School of Medicine, Boston, MA, 02118, USA.
Neil W KowallBoston University Alzheimer's Disease Research Center and CTE Center, Boston University, Chobanian and Avedisian School of Medicine, Boston, MA, 02118, USA.
Robert A SternBoston University Alzheimer's Disease Research Center and CTE Center, Boston University, Chobanian and Avedisian School of Medicine, Boston, MA, 02118, USA.
Lee E GoldsteinBoston University Alzheimer's Disease Research Center and CTE Center, Boston University, Chobanian and Avedisian School of Medicine, Boston, MA, 02118, USA.
Wei Qiao QiuBoston University Alzheimer's Disease Research Center and CTE Center, Boston University, Chobanian and Avedisian School of Medicine, Boston, MA, 02118, USA.
Jesse MezBoston University Alzheimer's Disease Research Center and CTE Center, Boston University, Chobanian and Avedisian School of Medicine, Boston, MA, 02118, USA.
Bertrand Russell HuberBoston University Alzheimer's Disease Research Center and CTE Center, Boston University, Chobanian and Avedisian School of Medicine, Boston, MA, 02118, USA.
Victor E AlvarezBoston University Alzheimer's Disease Research Center and CTE Center, Boston University, Chobanian and Avedisian School of Medicine, Boston, MA, 02118, USA.
Ann C McKeeBoston University Alzheimer's Disease Research Center and CTE Center, Boston University, Chobanian and Avedisian School of Medicine, Boston, MA, 02118, USA.
Henrik ZetterbergDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Johan GobomDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Thor D Stein *Boston University Alzheimer's Disease Research Center and CTE Center, Boston University, Chobanian and Avedisian School of Medicine, Boston, MA, 02118, USA.
Kaj Blennow *Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.

Funding

Project-005UL1TR001430 · NCATS · BOSTON UNIVERSITY MEDICAL CAMPUS · PI BAIR-MERRITT, MEGAN H, CENTER, DAVID M. · 2015 to 2024
$52.3M
TBDU19AG068753 · NIA · BOSTON UNIVERSITY MEDICAL CAMPUS · PI Rhoda Au · 2020 to 2026
$42.4M
RL5: Research Education CoreP30AG072978 · NIA · BOSTON UNIVERSITY MEDICAL CAMPUS · PI Lindsay A. Farrer · 2021 to 2026
$25.6M
PRECURSORS OF STROKE INCIDENCE AND PROGNOSISR01NS017950 · NINDS · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI Hugo Javier Aparicio, Jose Rafael Romero · 1985 to 2026
$22.9M
Traumatic Brain Injury and Repetitive Head Impacts: Contributions to AD/ADRD and CTE Neuropathology and Resulting Clinical SyndromesU54NS115266 · NINDS · BOSTON UNIVERSITY MEDICAL CAMPUS · PI MCKEE, ANN C. · 2019 to 2023
$10.3M
Multidimensional Assessment of Brain Health as A Marker of Dementia Risk and ResilienceR01AG066524 · NIA · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI KASHANI, AMIR H, RAMACHANDRAN, VASAN S · 2020 to 2024
$9.7M
The effects of iron on oxidative stress and Alzheimer's biomarkers in amyloid-positive and negative elderly normalR01AG068398 · NIA · WEILL MEDICAL COLL OF CORNELL UNIV · PI CHIANG, GLORIA CHIA-YI · 2020 to 2024
$2.8M
DANA; A Tool to Detect Cognitive Changes in Pre-clinical and MCI Patients (Admin Supplement)R44AG063635 · NIA · ANTHROTRONIX, INC. · PI LATHAN, CORINNA E · 2019 to 2020
$2.6M
Identification and characterization of the CD31-ApoE-mCRP pathway for Alzheimer's disease in humans.RF1AG075832 · NIA · BOSTON UNIVERSITY MEDICAL CAMPUS · PI EMILI, ANDREW, QIU, WEI QIAO WENDY · 2023 to 2023
$2.4M
Blood Biomarker Development and Validation in Chronic Traumatic Encephalopathy and Alzheimer's Disease and Alzheimer's Disease Related DementiasRF1NS132290 · NINDS · BOSTON UNIVERSITY MEDICAL CAMPUS · PI ALOSCO, MICHAEL, STEIN, THOR · 2023 to 2023
$1.9M
Repetitive Head Impact Exposure and Later-Life White Matter Signal Abnormalities: An Investigation in Former NFL Players, Subjects with Alzheimer's Disease, and Cognitively Normal ControlsK23NS102399 · NINDS · BOSTON UNIVERSITY MEDICAL CAMPUS · PI ALOSCO, MICHAEL · 2018 to 2022
$793k
Cognitive heterogeneity in those with high Alzheimer's Disease RiskR56AG062109 · NIA · BOSTON UNIVERSITY MEDICAL CAMPUS · PI AU, RHODA · 2018 to 2018
$517k
BLRD VA I01 BX005933CSRD VA IK2 CX002065NIA NIH HHS P30 AG072978NIA NIH HHS R01 AG066524NIA NIH HHS R01 AG068398NIA NIH HHS R44 AG063635NIA NIH HHS R56 AG062109NIA NIH HHS RF1 AG075832NIA NIH HHS U19 AG068753NINDS NIH HHS K23 NS102399NINDS NIH HHS L30 NS093634NINDS NIH HHS R01 NS017950NINDS NIH HHS RF1 NS132290NINDS NIH HHS U54 NS115266
6 · The paper itself

Abstract

Plasma-to-autopsy studies are essential for validation of blood biomarkers and understanding their relation to Alzheimer's disease (AD) pathology. Few such studies have been done on phosphorylated tau (p-tau) and those that exist have made limited or no comparison of the different p-tau variants. This study is the first to use immunoprecipitation mass spectrometry (IP-MS) to compare the accuracy of eight different plasma tau species in predicting autopsy-confirmed AD. The sample included 123 participants (AD = 69, non-AD = 54) from the Boston University Alzheimer's disease Research Center who had an available ante-mortem plasma sample and donated their brain. Plasma samples proximate to death were analyzed by targeted IP-MS for six different tryptic phosphorylated (p-tau-181, 199, 202, 205, 217, 231), and two non-phosphorylated tau (195-205, 212-221) peptides. NIA-Reagan Institute criteria were used for the neuropathological diagnosis of AD. Binary logistic regressions tested the association between each plasma peptide and autopsy-confirmed AD status. Area under the receiver operating curve (AUC) statistics were generated using predicted probabilities from the logistic regression models. Odds Ratio (OR) was used to study associations between the different plasma tau species and CERAD and Braak classifications. All tau species were increased in AD compared to non-AD, but p-tau217, p-tau205 and p-tau231 showed the highest fold-changes. Plasma p-tau217 (AUC = 89.8), p-tau231 (AUC = 83.4), and p-tau205 (AUC = 81.3) all had excellent accuracy in discriminating AD from non-AD brain donors, even among those with CDR < 1). Furthermore, p-tau217, p-tau205 and p-tau231 showed the highest ORs with both CERAD (OR

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAutopsyBiomarkersHumanstau ProteinsAmyloid beta-PeptidesBiomarkerstau ProteinsAlzheimer’s diseaseAutopsyBiomarkersBloodMass spectrometryPhosphorylated tau

Identifiers

PMID38159140
PMCPMC10757700

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.