Evidence map›Paper›PMID 40437286›Full record

ArticleMolecular neurobiology2025

Late-Stage Activation of Toll-like receptor 3 Alleviates Cognitive Impairment and Neuropathology in an Alzheimer's Disease Mouse Model.

Taiyang Zhu, Fanyu Shen, Xiao Jia, Hui Zhou, Wanyan Ni, Shang Wang, Di Wu, Huimin Gao, Zhenying Shang, Yan Zhou and 8 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular neurobiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
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

18 authors.

Taiyang ZhuDepartment of Neurology, Xuzhou Medical University, Xuzhou, 221004, China.
Fanyu ShenDepartment of Neurology, Xuzhou Medical University, Xuzhou, 221004, China.
Xiao JiaDepartment of Neurology, Xuzhou Medical University, Xuzhou, 221004, China.
Hui ZhouDepartment of Neurology, Xuzhou Medical University, Xuzhou, 221004, China.
Wanyan NiDepartment of Neurology, Xuzhou Medical University, Xuzhou, 221004, China.
Shang WangDepartment of Human Anatomy, Kangda College of Nanjing Medical University, Lianyungang, 222000, China.
Di WuSuqian First People's Hospital of Nanjing Medical University, Suqian, 223800, China.
Huimin GaoDepartment of Neurology, Xuzhou Medical University, Xuzhou, 221004, China.
Zhenying ShangDepartment of Neurology, Affiliated Hospital of Xuzhou Medical University, Xuzhou, 221002, China.
Yan ZhouDepartment of Neurology, Xuzhou Medical University, Xuzhou, 221004, China.
Jingjing HanDepartment of Neurology, Xuzhou Medical University, Xuzhou, 221004, China.
Guoliang JinDepartment of Neurology, Xuzhou Medical University, Xuzhou, 221004, China.
Fuxing DongPublic Experimental Research Center, Xuzhou Medical University, Xuzhou, 221004, China.
Jie ZuDepartment of Neurology, Xuzhou Medical University, Xuzhou, 221004, China.
Xinxin YangDepartment of Neurology, Xuzhou Medical University, Xuzhou, 221004, China.
Hongjuan ShiDepartment of Neurology, Xuzhou Medical University, Xuzhou, 221004, China.
Chao ZhouDepartment of Neurology, Xuzhou Medical University, Xuzhou, 221004, China. zhouchao@njglyy.com.
Fang HuaDepartment of Neurology, Xuzhou Medical University, Xuzhou, 221004, China. fhua@augusta.edu.

Funding

National Nature Science Foundation of China 82171420
6 · The paper itself

Abstract

This study was to investigate the effects of Toll-like receptor-3 (TLR3) activation on cognitive impairment and neuropathology in late-stage of Alzheimer's disease in a mouse model. Amyloid protein precursor (APP)/presenilin-1 (PSEN1) (APP/PSEN1) mice were treated with Poly (I:C), a specific for TLR3. A panel of neurobehavioral tests were conducted to evaluate their cognitive functions. Aβ deposition, plasma Aβ levels, neuropathological changes, and activation of TLR3- TIR-domain-containing adapter-inducing interferon-β (TRIF) signaling were assessed by magnetic resonance imaging (MRI), electrophysiological recordings, transmission electron microscopy, Western blotting, immunofluorescence staining, and qPCR. The data demonstrated that Poly (I:C) significantly attenuated cognitive and neuropathological impairments, compared with APP/PSEN1 mice without Poly (I:C) treatment. Administration of Poly (I:C) significantly reduced brain Aβ

Indexed as

Alzheimer DiseaseCognitive DysfunctionToll-Like Receptor 3Adaptor Proteins, Vesicular TransportAmyloid beta-PeptidesAnimalsBrainDisease Models, AnimalMaleMiceMice, Inbred C57BLMice, TransgenicPoly I-CSignal TransductionAdaptor Proteins, Vesicular TransportAmyloid beta-PeptidesPoly I-CTLR3 protein, mouseToll-Like Receptor 3Alzheimer’s diseaseMouse modelPoly (I:C)Toll-like receptor-3TRIF

Identifiers

PMID40437286
PMCPMC12433446

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.