Evidence map›Paper›PMID 39592224›Full record

ArticleeNeuro2024

Tau Accumulation Induces Microglial State Alterations in Alzheimer's Disease Model Mice.

Kenichi Nagata, Shoko Hashimoto, Daisuke Joho, Ryo Fujioka, Yukio Matsuba, Misaki Sekiguchi, Naomi Mihira, Daisuke Motooka, Yu-Chen Liu, Daisuke Okuzaki and 5 more

Abstract read
In one paragraph

Article in eNeuro, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
–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

8 citing papers in PubMed.

  1. Article
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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

15 authors.

Kenichi NagataDepartment of Functional Anatomy and Neuroscience, Nagoya University, Graduate School of Medicine, Aichi 466-8550, Japan knagata@med.nagoya-u.ac.jp hiroki.sasaguri@riken.jp.ORCID 0000-0001-8377-7197
Shoko HashimotoLaboratory for Proteolytic Neuroscience, RIKEN Center for Brain Science, Saitama 351-0198, Japan.
Daisuke JohoDementia Pathophysiology Collaboration Unit, RIKEN Center for Brain Science, Saitama 351-0198, Japan.ORCID 0009-0008-5623-0266
Ryo FujiokaLaboratory for Proteolytic Neuroscience, RIKEN Center for Brain Science, Saitama 351-0198, Japan.
Yukio MatsubaLaboratory for Proteolytic Neuroscience, RIKEN Center for Brain Science, Saitama 351-0198, Japan.
Misaki SekiguchiLaboratory for Proteolytic Neuroscience, RIKEN Center for Brain Science, Saitama 351-0198, Japan.
Naomi MihiraLaboratory for Proteolytic Neuroscience, RIKEN Center for Brain Science, Saitama 351-0198, Japan.
Daisuke MotookaGenome Information Research Center, Research Institute for Microbial Diseases, Osaka University, Osaka 565-0871, Japan.
Yu-Chen LiuIntegrated Frontier Research for Medical Science Division, Institute for Open and Transdisciplinary Research Initiatives, Osaka University, Osaka 565-0871, Japan.
Daisuke OkuzakiIntegrated Frontier Research for Medical Science Division, Institute for Open and Transdisciplinary Research Initiatives, Osaka University, Osaka 565-0871, Japan.
Masataka KikuchiDepartment of Computational Biology and Medical Sciences, Graduate School of Frontier Science, The University of Tokyo, Chiba 277-0882, Japan.
Shigeo MurayamaDepartment of Neuropathology, Tokyo Metropolitan Institute of Gerontology, Tokyo 173-0015, Japan.
Takaomi C SaidoLaboratory for Proteolytic Neuroscience, RIKEN Center for Brain Science, Saitama 351-0198, Japan.
Hiroshi KiyamaDepartment of Functional Anatomy and Neuroscience, Nagoya University, Graduate School of Medicine, Aichi 466-8550, Japan.
Hiroki SasaguriLaboratory for Proteolytic Neuroscience, RIKEN Center for Brain Science, Saitama 351-0198, Japan knagata@med.nagoya-u.ac.jp hiroki.sasaguri@riken.jp.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Unique microglial states have been identified in Alzheimer's disease (AD) model mice and postmortem AD brains. Although it has been well documented that amyloid-β accumulation induces the alteration of microglial states, the relationship between tau pathology and microglial states remains incompletely understood because of a lack of suitable AD models. In the present study, we generated a novel AD model mouse by the intracerebral administration of tau purified from human brains with primary age-related tauopathy into

Indexed as

Alzheimer DiseaseDisease Models, AnimalMice, TransgenicMicrogliatau ProteinsAmyloid beta-Protein PrecursorAnimalsBrainFemaleHumansMaleMiceMice, Inbred C57BLTauopathiesAmyloid beta-Protein Precursortau ProteinsAlzheimer's diseaseamyloid-βmicrogliasingle-cell RNA-seqtau

Identifiers

PMID39592224
PMCPMC11628182

What OpenQuestion holds

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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.