Evidence map›Paper›PMID 28424326›Full record

ArticleScience translational medicine2017

Anti-tau antibody administration increases plasma tau in transgenic mice and patients with tauopathy.

Kiran Yanamandra, Tirth K Patel, Hong Jiang, Suzanne Schindler, Jason D Ulrich, Adam L Boxer, Bruce L Miller, Diana R Kerwin, Gilbert Gallardo, Floy Stewart and 12 more

Abstract read
In one paragraph

Article in Science translational medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed, 1 pooled it
8.1field-weighted citation impact, top 2% of its field
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

60 citing papers in PubMed, 1 synthesis or guideline pooled it, 99 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Trial
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Observational
  11. Review
  12. CD8 + T cell-based molecular subtypes with heterogeneous immune landscapes and clinical significance in acute myeloid leukemia.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024
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  13. Role of sleep in neurodegeneration: the consensus report of the 5th Think Tank World Sleep Forum.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2024
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  15. Review
  16. Review
  17. Article
  18. Article
  19. The Adult Neurogenesis Theory of Alzheimer's Disease.Journal of Alzheimer's disease : JAD · 2023
    Article
  20. 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

22 authors at 5 institutions in 1 country.

Kiran YanamandraHope Center for Neurological Disorders and Knight Alzheimer's Disease Research Center, Department of Neurology, Washington University, St. Louis, MO 63110,USA.
Tirth K PatelHope Center for Neurological Disorders and Knight Alzheimer's Disease Research Center, Department of Neurology, Washington University, St. Louis, MO 63110,USA.
Hong JiangHope Center for Neurological Disorders and Knight Alzheimer's Disease Research Center, Department of Neurology, Washington University, St. Louis, MO 63110,USA.
Suzanne SchindlerHope Center for Neurological Disorders and Knight Alzheimer's Disease Research Center, Department of Neurology, Washington University, St. Louis, MO 63110,USA.
Jason D UlrichHope Center for Neurological Disorders and Knight Alzheimer's Disease Research Center, Department of Neurology, Washington University, St. Louis, MO 63110,USA.
Adam L BoxerClinical Trials Program, Memory and Aging Center, Department of Neurology, University of California, San Francisco, San Francisco, CA 94143, USA.
Bruce L MillerClinical Trials Program, Memory and Aging Center, Department of Neurology, University of California, San Francisco, San Francisco, CA 94143, USA.
Diana R KerwinTexas Alzheimer's and Memory Disorders, Texas Health Presbyterian Hospital Dallas, Dallas, TX 75231, USA.
Gilbert GallardoHope Center for Neurological Disorders and Knight Alzheimer's Disease Research Center, Department of Neurology, Washington University, St. Louis, MO 63110,USA.
Floy StewartHope Center for Neurological Disorders and Knight Alzheimer's Disease Research Center, Department of Neurology, Washington University, St. Louis, MO 63110,USA.
Mary Beth FinnHope Center for Neurological Disorders and Knight Alzheimer's Disease Research Center, Department of Neurology, Washington University, St. Louis, MO 63110,USA.
Nigel J CairnsHope Center for Neurological Disorders and Knight Alzheimer's Disease Research Center, Department of Neurology, Washington University, St. Louis, MO 63110,USA.
Philip B VergheseC2N Diagnostics, Center for Emerging Technologies, 4041 Forest Park Avenue, St. Louis, MO 63108, USA.
Ilana FogelmanC2N Diagnostics, Center for Emerging Technologies, 4041 Forest Park Avenue, St. Louis, MO 63108, USA.
Tim WestC2N Diagnostics, Center for Emerging Technologies, 4041 Forest Park Avenue, St. Louis, MO 63108, USA.
Joel BraunsteinC2N Diagnostics, Center for Emerging Technologies, 4041 Forest Park Avenue, St. Louis, MO 63108, USA.
Grace RobinsonHope Center for Neurological Disorders and Knight Alzheimer's Disease Research Center, Department of Neurology, Washington University, St. Louis, MO 63110,USA.
Jennifer KeyserHope Center for Neurological Disorders and Knight Alzheimer's Disease Research Center, Department of Neurology, Washington University, St. Louis, MO 63110,USA.
Joseph RohHope Center for Neurological Disorders and Knight Alzheimer's Disease Research Center, Department of Neurology, Washington University, St. Louis, MO 63110,USA.
Stephanie S KnapikC2N Diagnostics, Center for Emerging Technologies, 4041 Forest Park Avenue, St. Louis, MO 63108, USA.
Yan HuC2N Diagnostics, Center for Emerging Technologies, 4041 Forest Park Avenue, St. Louis, MO 63108, USA.
David M HoltzmanHope Center for Neurological Disorders and Knight Alzheimer's Disease Research Center, Department of Neurology, Washington University, St. Louis, MO 63110,USA. holtzman@neuro.wustl.edu.
Hope Center for Neurological Disorders · USC2N Diagnostics (United States) · USUniversity Memory and Aging Center · USAbbVie (United States) · USTexas Health Dallas · US

Funding

WASHINGTON UNIVERSITY ALZHEIMERS DISEASE RESEARCH CENTERP50AG005681 · NIA · WASHINGTON UNIVERSITY · PI MORRIS, JOHN · 1985 to 2019
$52.1M
The Four Repeat Tauopathy Neuroimaging InitiativeR01AG038791 · NIA · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI BOXER, ADAM L. · 2010 to 2020
$18.1M
DEVELOPMENT OF NOVEL THERAPEUTIC ANTI-TAU ANTIBODIESR01AG048678 · NIA · UT SOUTHWESTERN MEDICAL CENTER · PI DIAMOND, MARC I, HOLTZMAN, DAVID M. · 2015 to 2019
$3.3M
Advancing Antibody Technology for tau Immunotherapies and for Investigating tau PathogenesisK01NS096719 · NINDS · WASHINGTON UNIVERSITY · PI GALLARDO, GILBERT · 2016 to 2018
$656k
NIA NIH HHS P50 AG005681NIA NIH HHS R01 AG038791NIA NIH HHS R01 AG048678NINDS NIH HHS K01 NS096719
6 · The paper itself

Abstract

Tauopathies are a group of disorders in which the cytosolic protein tau aggregates and accumulates in cells within the brain, resulting in neurodegeneration. A promising treatment being explored for tauopathies is passive immunization with anti-tau antibodies. We previously found that administration of an anti-tau antibody to human tau transgenic mice increased the concentration of plasma tau. We further explored the effects of administering an anti-tau antibody on plasma tau. After peripheral administration of an anti-tau antibody to human patients with tauopathy and to mice expressing human tau in the central nervous system, there was a dose-dependent increase in plasma tau. In mouse plasma, we found that tau had a short half-life of 8 min that increased to more than 3 hours after administration of anti-tau antibody. As tau transgenic mice accumulated insoluble tau in the brain, brain soluble and interstitial fluid tau decreased. Administration of anti-tau antibody to tau transgenic mice that had decreased brain soluble tau and interstitial fluid tau resulted in an increase in plasma tau, but this increase was less than that observed in tau transgenic mice without these brain changes. Tau transgenic mice subjected to acute neuronal injury using 3-nitropropionic acid showed increased interstitial fluid tau and plasma tau. These data suggest that peripheral administration of an anti-tau antibody results in increased plasma tau, which correlates with the concentration of extracellular and soluble tau in the brain.

Indexed as

AnimalsAntibodiesBrainDisease Models, AnimalDose-Response Relationship, DrugHumansMiceMice, TransgenicNitro CompoundsPropionatesTauopathiestau Proteins3-nitropropionic acidAntibodiesNitro CompoundsPropionatestau Proteins

Identifiers

PMID28424326
PMCPMC5727571
OpenAlexW2605473592

What OpenQuestion holds

Textmetadata
LicenceTDM
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.