Evidence map›Paper›PMID 26458742›Full record

ArticleNature communications2015

Neuronal uptake and propagation of a rare phosphorylated high-molecular-weight tau derived from Alzheimer's disease brain.

Shuko Takeda, Susanne Wegmann, Hansang Cho, Sarah L DeVos, Caitlin Commins, Allyson D Roe, Samantha B Nicholls, George A Carlson, Rose Pitstick, Chloe K Nobuhara and 5 more

Abstract read
In one paragraph

Article in Nature communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 222 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
222citing 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

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

  1. Pooled it
  2. Trial
  3. Trial
  4. Article
  5. Article
  6. Article
  7. Review
  8. Elevation in network dynamics amplifies amyloid-dependent tau pathology.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
  9. Article
  10. Cells · 2026
    Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Intercellular propagation of RIPK1/RIPK3 amyloid fibrils.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  20. Article

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

15 authors.

Shuko TakedaDepartment of Neurology, Alzheimer's Disease Research Laboratory, MassGeneral Institute for Neurodegenerative Disease, Massachusetts General Hospital, Harvard Medical School, Charlestown, Massachusetts 02129, USA.
Susanne WegmannDepartment of Neurology, Alzheimer's Disease Research Laboratory, MassGeneral Institute for Neurodegenerative Disease, Massachusetts General Hospital, Harvard Medical School, Charlestown, Massachusetts 02129, USA.
Hansang ChoBioMEMS Resource Center, Massachusetts General Hospital, Harvard Medical School, Charlestown, Massachusetts 02129, USA.
Sarah L DeVosDepartment of Neurology, Alzheimer's Disease Research Laboratory, MassGeneral Institute for Neurodegenerative Disease, Massachusetts General Hospital, Harvard Medical School, Charlestown, Massachusetts 02129, USA.
Caitlin ComminsDepartment of Neurology, Alzheimer's Disease Research Laboratory, MassGeneral Institute for Neurodegenerative Disease, Massachusetts General Hospital, Harvard Medical School, Charlestown, Massachusetts 02129, USA.
Allyson D RoeDepartment of Neurology, Alzheimer's Disease Research Laboratory, MassGeneral Institute for Neurodegenerative Disease, Massachusetts General Hospital, Harvard Medical School, Charlestown, Massachusetts 02129, USA.
Samantha B NichollsDepartment of Neurology, Alzheimer's Disease Research Laboratory, MassGeneral Institute for Neurodegenerative Disease, Massachusetts General Hospital, Harvard Medical School, Charlestown, Massachusetts 02129, USA.
George A CarlsonMcLaughlin Research Institute, Great Falls, Montana 59405, USA.
Rose PitstickMcLaughlin Research Institute, Great Falls, Montana 59405, USA.
Chloe K NobuharaDepartment of Neurology, Alzheimer's Disease Research Laboratory, MassGeneral Institute for Neurodegenerative Disease, Massachusetts General Hospital, Harvard Medical School, Charlestown, Massachusetts 02129, USA.
Isabel CostantinoDepartment of Neurology, Alzheimer's Disease Research Laboratory, MassGeneral Institute for Neurodegenerative Disease, Massachusetts General Hospital, Harvard Medical School, Charlestown, Massachusetts 02129, USA.
Matthew P FroschDepartment of Neurology, Alzheimer's Disease Research Laboratory, MassGeneral Institute for Neurodegenerative Disease, Massachusetts General Hospital, Harvard Medical School, Charlestown, Massachusetts 02129, USA.
Daniel J MüllerDepartment of Biosystems Science and Engineering, Eidgenössische Technische Hochschule Zürich, 4058 Basel, Switzerland.
Daniel IrimiaBioMEMS Resource Center, Massachusetts General Hospital, Harvard Medical School, Charlestown, Massachusetts 02129, USA.
Bradley T HymanDepartment of Neurology, Alzheimer's Disease Research Laboratory, MassGeneral Institute for Neurodegenerative Disease, Massachusetts General Hospital, Harvard Medical School, Charlestown, Massachusetts 02129, USA.

Funding

THE ROLE OF ADVANCED CAA IN ALZHEIMER'S DEMENTIAP50AG005134 · NIA · MASSACHUSETTS GENERAL HOSPITAL · PI SPERLING, REISA A. · 1985 to 2018
$42.1M
Bio-MicroElectroMechanical Systems Resource CenterP41EB002503 · NIBIB · MASSACHUSETTS GENERAL HOSPITAL · PI TONER, MEHMET · 2004 to 2018
$17.4M
Interdepartmental Neuroscience CenterP30NS045776 · NINDS · MASSACHUSETTS GENERAL HOSPITAL · PI BREAKEFIELD, XANDRA OWENS, TANNOUS, BAKHOS A · 2003 to 2018
$11.1M
Neutrophil Decision Making in Confined Environments in Health and DiseaseR01GM092804 · NIGMS · MASSACHUSETTS GENERAL HOSPITAL · PI IRIMIA, DANIEL · 2010 to 2022
$4.3M
Anatomical Changes in Tau Transgenic ModelsR01AG026249 · NIA · MASSACHUSETTS GENERAL HOSPITAL · PI HYMAN, BRADLEY T. · 2004 to 2014
$3.7M
NIA NIH HHS AG026249NIA NIH HHS P50 AG005134NIA NIH HHS P50AG05134NIA NIH HHS R01 AG026249NIBIB NIH HHS P41 EB002503NIGMS NIH HHS GM092804NIGMS NIH HHS R01 GM092804NINDS NIH HHS P30 NS045776
6 · The paper itself

Abstract

Tau pathology is known to spread in a hierarchical pattern in Alzheimer's disease (AD) brain during disease progression, likely by trans-synaptic tau transfer between neurons. However, the tau species involved in inter-neuron propagation remains unclear. To identify tau species responsible for propagation, we examined uptake and propagation properties of different tau species derived from postmortem cortical extracts and brain interstitial fluid of tau-transgenic mice, as well as human AD cortices. Here we show that PBS-soluble phosphorylated high-molecular-weight (HMW) tau, though very low in abundance, is taken up, axonally transported, and passed on to synaptically connected neurons. Our findings suggest that a rare species of soluble phosphorylated HMW tau is the endogenous form of tau involved in propagation and could be a target for therapeutic intervention and biomarker development.

Indexed as

AgedAged, 80 and overAlzheimer DiseaseAnimalsBrainCell SurvivalFemaleHEK293 CellsHumansMaleMice, Inbred C57BLMice, TransgenicMicrofluidic Analytical TechniquesNeuronsPhosphorylationtau Proteinstau Proteins

Identifiers

PMID26458742
PMCPMC4608380

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.