Evidence map›Paper›PMID 28967385›Full record

ReviewBiological psychiatry2018

Anti-Amyloid-β Monoclonal Antibodies for Alzheimer's Disease: Pitfalls and Promise.

Christopher H van Dyck

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Biological psychiatry, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 266 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
266citing papers in PubMed, 5 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

266 citing papers in PubMed, 5 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. Pooled it
  6. Trial
  7. Trial
  8. Trial
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  10. Preclinical and clinical biomarker studies of CT1812: A novel approach to Alzheimer's disease modification.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2021
    Trial
  11. Trial
  12. Article
  13. Review
  14. Article
  15. Review
  16. Ex vivo comparison of ACU193 and lecanemab reveals binding differences in mouse brain.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
  17. Review
  18. Article
  19. Article
  20. Article

206 more citing papers are in PubMed but not listed here.

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

1 author.

Christopher H van DyckAlzheimer's Disease Research Unit and Departments of Psychiatry, Neuroscience, and Neurology, Yale University School of Medicine, New Haven, Connecticut. Electronic address: christopher.vandyck@yale.edu.

Funding

Yale Clinical and Translational Science Award (U Component)UL1TR001863 · NCATS · YALE UNIVERSITY · PI John H. Krystal, LUCILA OHNO-MACHADO · 2016 to 2026
$102.9M
Yale University Clinical and Translational Science Award ProgramUL1TR000142 · NCATS · YALE UNIVERSITY · PI SHERWIN, ROBERT S · 2012 to 2015
$31.8M
Yale Alzheimer Disease Research CenterP50AG047270 · NIA · YALE UNIVERSITY · PI MAROTTOLI, RICHARD · 2015 to 2019
$8.3M
PET Imaging of Synaptic Density in Alzheimers DiseaseR01AG052560 · NIA · YALE UNIVERSITY · PI CARSON, RICHARD E., VAN DYCK, CHRISTOPHER H · 2017 to 2020
$3.2M
Fyn Inhibition by AZD0530 for Alzheimers DiseaseUH2TR000967 · NCATS · YALE UNIVERSITY · PI NYGAARD, HAAKON BERGE, STRITTMATTER, STEPHEN M · 2013 to 2013
$2.9M
Guanfacine Treatment for Prefrontal Cognitive Dysfunction in Elderly SubjectsR01AG030457 · NIA · YALE UNIVERSITY · PI VAN DYCK, CHRISTOPHER H · 2008 to 2010
$1.1M
NCATS NIH HHS UH2 TR000967NCATS NIH HHS UL1 TR000142NCATS NIH HHS UL1 TR001863NIA NIH HHS P50 AG047270NIA NIH HHS R01 AG030457NIA NIH HHS R01 AG052560
6 · The paper itself

Abstract

The majority of putative disease-modifying treatments in development for Alzheimer's disease are directed against the amyloid-β (Aβ) peptide. Among the anti-Aβ therapeutic approaches, the most extensively developed is immunotherapy-specifically, passive immunization through administration of exogenous monoclonal antibodies (mAbs). Although testing of mAbs has been fraught with failure and confusing results, the experience gained from these trials has provided important clues for better treatments. This review summarizes the experience to date with anti-Aβ mAbs to enter clinical trials for Alzheimer's disease and examines the evidence for clinical efficacy and the major problems with safety-i.e., amyloid-related imaging abnormalities. As mAbs differ considerably with regard to their epitopes and the conformations of Aβ that they recognize (monomers, oligomers, protofibrils, fibrils), the consequences of targeting different species are also considered. An often-cited explanation for the failure of anti-Aβ mAb trials is that they are set too late in the disease process. New trials are indeed evaluating treatments at prodromal and preclinical stages. We should expect to see additional studies of presymptomatic Alzheimer's disease to join the ongoing prevention trials, for which mAbs continue to serve as the mainstay.

Indexed as

AgedAged, 80 and overAlzheimer DiseaseAmyloid beta-PeptidesAntibodies, MonoclonalHumansImmunotherapyMiddle AgedAmyloid beta-PeptidesAntibodies, MonoclonalAlzheimer’s diseaseAmyloid-related imaging abnormalitiesAmyloid-βAmyloid-β oligomersImmunotherapyMonoclonal antibodies

Identifiers

PMID28967385
PMCPMC5767539

What OpenQuestion holds

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LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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.