Evidence map›Paper›PMID 38658772›Full record

ArticleMolecular psychiatry2024

Thy1-ApoE4/C/EBPβ double transgenic mice act as a sporadic model with Alzheimer's disease.

Zhengjiang Qian, ZhiHao Wang, Bowei Li, Xin Meng, Zhonghua Kuang, Yanjiao Li, Yongfeng Yang, Keqiang Ye

Abstract read
In one paragraph

Article in Molecular psychiatry, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing 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

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

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
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  17. GnRH and Cognition.Endocrinology · 2025
    Review
  18. Review
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  20. Neuroscience and addiction research: current advances and perspectives.Journal of neural transmission (Vienna, Austria : 1996) · 2024
    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

8 authors.

Zhengjiang QianFaculty of Life and Health Sciences, Brain Cognition and Brain Disease Institute (BCBDI), Shenzhen Institute of Advanced Technology (SIAT), Chinese Academy of Sciences, Shenzhen, 518055, Guangdong, China.ORCID 0000-0003-1306-6829
ZhiHao WangDepartment of Neurology, Renmin Hospital of Wuhan University, Wuhan, Hubei Province, 430060, China.
Bowei LiShenzhen Institute of Advanced Technology, University of Chinese Academy of Science, Shenzhen, Guangdong Province, 518055, China.
Xin MengFaculty of Life and Health Sciences, Brain Cognition and Brain Disease Institute (BCBDI), Shenzhen Institute of Advanced Technology (SIAT), Chinese Academy of Sciences, Shenzhen, 518055, Guangdong, China.
Zhonghua KuangPaul C. Lauterbur Research Center for Biomedical Imaging, Institute of Biomedical and Health Engineering, Shenzhen Institute of Advanced Technology (SIAT), Chinese Academy of Sciences, Shenzhen, 518055, Guangdong, China.
Yanjiao LiFaculty of Life and Health Sciences, Brain Cognition and Brain Disease Institute (BCBDI), Shenzhen Institute of Advanced Technology (SIAT), Chinese Academy of Sciences, Shenzhen, 518055, Guangdong, China.
Yongfeng YangPaul C. Lauterbur Research Center for Biomedical Imaging, Institute of Biomedical and Health Engineering, Shenzhen Institute of Advanced Technology (SIAT), Chinese Academy of Sciences, Shenzhen, 518055, Guangdong, China.
Keqiang YeFaculty of Life and Health Sciences, Brain Cognition and Brain Disease Institute (BCBDI), Shenzhen Institute of Advanced Technology (SIAT), Chinese Academy of Sciences, Shenzhen, 518055, Guangdong, China. kq.ye@siat.ac.cn.ORCID 0000-0002-7657-8154

Funding

National Natural Science Foundation of China (National Science Foundation of China) 32200928National Natural Science Foundation of China (National Science Foundation of China) 32330040
6 · The paper itself

Abstract

Early onset familial Alzheimer's disease (FAD) with APP, PS1/2 (presenilins) mutation accounts for only a small portion of AD cases, and most are late-onset sporadic. However, majority of AD mouse models are developed to mimic the genetic cause of human AD by overexpressing mutated forms of human APP, PS1/2, and/or Tau protein, though there is no Tau mutation in AD, and no single mouse model recapitulates all aspects of AD pathology. Here, we report Thy1-ApoE4/C/EBPβ double transgenic mouse model that demonstrates key AD pathologies in an age-dependent manner in absence of any human APP or PS1/2 mutation. Using the clinical diagnosis criteria, we show that this mouse model exhibits tempo-spatial features in AD patient brains, including progressive cognitive decline associated with brain atrophy, which is accompanied with extensive neuronal degeneration. Remarkably, the mice display gradual Aβ aggregation and neurofibrillary tangles formation in the brain validated by Aβ PET and Tau PET. Moreover, the mice reveal widespread neuroinflammation as shown in AD brains. Hence, Thy1-ApoE4/C/EBPβ mouse model acts as a sporadic AD mouse model, reconstituting the major AD pathologies.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesBrainDisease Models, AnimalMice, Transgenictau ProteinsAmyloid beta-Protein PrecursorAnimalsApolipoprotein E4CCAAT-Enhancer-Binding Protein-betaFemaleHumansMaleMiceMutationNeurofibrillary TanglesAmyloid beta-PeptidesAmyloid beta-Protein PrecursorApolipoprotein E4CCAAT-Enhancer-Binding Protein-betatau Proteins

Identifiers

PMID38658772
PMCPMC11449781

What OpenQuestion holds

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Registered trials

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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.