Evidence map›Paper›PMID 25810517›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2015

Tau immunotherapy modulates both pathological tau and upstream amyloid pathology in an Alzheimer's disease mouse model.

Diana L Castillo-Carranza, Marcos J Guerrero-Muñoz, Urmi Sengupta, Caterina Hernandez, Alan D T Barrett, Kelly Dineley, Rakez Kayed

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
80citing papers in PubMed, 1 pooled it
11.9field-weighted citation impact, top 1% 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

80 citing papers in PubMed, 1 synthesis or guideline pooled it, 145 citations in OpenAlex.

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

Diana L Castillo-CarranzaMitchell Center for Neurodegenerative Diseases, Departments of Neurology, Neuroscience and Cell Biology, and.
Marcos J Guerrero-MuñozMitchell Center for Neurodegenerative Diseases, Departments of Neurology, Neuroscience and Cell Biology, and.
Urmi SenguptaMitchell Center for Neurodegenerative Diseases, Departments of Neurology, Neuroscience and Cell Biology, and.
Caterina HernandezMitchell Center for Neurodegenerative Diseases, Departments of Neurology, Neuroscience and Cell Biology, and.
Alan D T BarrettSealy Center for Vaccine Development, University of Texas Medical Branch, Galveston, Texas 77555.
Kelly DineleyMitchell Center for Neurodegenerative Diseases, Departments of Neurology, Neuroscience and Cell Biology, and.
Rakez KayedMitchell Center for Neurodegenerative Diseases, Departments of Neurology, Neuroscience and Cell Biology, and Sealy Center for Vaccine Development, University of Texas Medical Branch, Galveston, Texas 77555 rakayed@utmb.edu.
The University of Texas Medical Branch at Galveston · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In Alzheimer's disease (AD), the pathological accumulation of tau appears to be a downstream effect of amyloid β protein (Aβ). However, the relationship between these two proteins and memory loss is unclear. In this study, we evaluated the specific removal of pathological tau oligomers in aged Tg2576 mice by passive immunotherapy using tau oligomer-specific monoclonal antibody. Removal of tau oligomers reversed memory deficits and accelerated plaque deposition in the brain. Surprisingly, Aβ*56 levels decreased, suggesting a link between tau and Aβ oligomers in the promotion of cognitive decline. The results suggest that tau oligomerization is not only a consequence of Aβ pathology but also a critical mediator of the toxic effects observed afterward in AD. Overall, these findings support the potential of tau oligomers as a therapeutic target for AD.

Indexed as

AgingAlzheimer DiseaseAmyloid beta-PeptidesAnimalsAntibodies, MonoclonalBrainDisease Models, AnimalMaleMemory DisordersMiceMice, TransgenicPeptide FragmentsPlaque, Amyloidtau ProteinsAmyloid beta-PeptidesAntibodies, MonoclonalPeptide Fragmentstau ProteinsAlzheimer's diseaseAβ*56immunotherapyTau oligomersTg2576

Identifiers

PMID25810517
PMCPMC6705372
OpenAlexW2065413916

What OpenQuestion holds

Textmetadata
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.