Evidence map›Paper›PMID 30594047›Full record

ArticleNeurobiology of aging2019

CIP2A-promoted astrogliosis induces AD-like synaptic degeneration and cognitive deficits.

Yang-Ping Shentu, Wen-Ting Hu, Qing Zhang, Yuda Huo, Jia-Wei Liang, Zhen-Yu Liuyang, Huan Zhou, Hui Wei, Dan Ke, Xiao-Chuan Wang and 4 more

Abstract read
In one paragraph

Article in Neurobiology of aging, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 1 pooled it
1.2field-weighted citation impact, top 20% 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

14 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Role of Senescent Astrocytes in Health and Disease.International journal of molecular sciences · 2023
    Review
  6. Review
  7. Article
  8. Review
  9. Article
  10. Chk1 Inhibition Ameliorates Alzheimer's Disease Pathogenesis and Cognitive Dysfunction Through CIP2A/PP2A Signaling.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2022
    Article
  11. Article
  12. Article
  13. Article
  14. 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

14 authors at 2 institutions in 2 countries.

Yang-Ping ShentuDepartment of Pathophysiology, Key Laboratory of Ministry of Education for Neurological Disorders, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Wen-Ting HuDepartment of Pathophysiology, Key Laboratory of Ministry of Education for Neurological Disorders, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Qing ZhangDepartment of Pathophysiology, Key Laboratory of Ministry of Education for Neurological Disorders, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Yuda HuoDepartment of Biology, Boston University, Boston, USA.
Jia-Wei LiangDepartment of Pathophysiology, Key Laboratory of Ministry of Education for Neurological Disorders, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Zhen-Yu LiuyangDepartment of Pathophysiology, Key Laboratory of Ministry of Education for Neurological Disorders, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Huan ZhouDepartment of Pathophysiology, Key Laboratory of Ministry of Education for Neurological Disorders, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Hui WeiDepartment of Pathophysiology, Key Laboratory of Ministry of Education for Neurological Disorders, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Dan KeDepartment of Pathophysiology, Key Laboratory of Ministry of Education for Neurological Disorders, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Xiao-Chuan WangDepartment of Pathophysiology, Key Laboratory of Ministry of Education for Neurological Disorders, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Jian-Zhi WangDepartment of Pathophysiology, Key Laboratory of Ministry of Education for Neurological Disorders, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Heng-Ye ManDepartment of Biology, Boston University, Boston, USA.
Jukka WestermarckTurku Centre for Biotechnology, University of Turku and Åbo Akademi University, Turku, Finland.
Rong LiuDepartment of Pathophysiology, Key Laboratory of Ministry of Education for Neurological Disorders, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China; The Institute for Brain Research, Collaborative Innovation Center for Brain Science, Huazhong University of Science and Technology, Wuhan, China. Electronic address: rong.liu@hust.edu.cn.
Huazhong University of Science and Technology · CNÅbo Akademi University · FI

Funding

Molecular Mechanisms of Homeostatic Synaptic PlasticityR01MH079407 · NIMH · BOSTON UNIVERSITY (CHARLES RIVER CAMPUS) · PI MAN, HENGYE · 2008 to 2018
$3.9M
NIMH NIH HHS R01 MH079407
6 · The paper itself

Abstract

Reactive astrogliosis and early synaptic degeneration are 2 characteristic hallmarks in Alzheimer's disease (AD) brains, but a direct link between the 2 events has not been established. Here, we show that cancerous inhibitor of PP2A (CIP2A), a cancerous protein with high expression level in astrocytes, is upregulated in patients with AD and 3xTg-AD transgenic mice. Overexpression of CIP2A in astrocytes through adeno-associated virus infection both in cultured cells and in mice brains results in activation of astrocytes, increased production of cytokines and Aβ, and synaptic degeneration indicated by decreased levels of synaptic proteins, spine loss, and impairment in long-term potentiation. As a result of synaptic degeneration, CIP2A overexpression in astrocytes in vivo induces significant deficits in visual episodic memory detected by novel objective recognition test and spatial memory detected by Morris water maze. We conclude that CIP2A-promoted astrogliosis induces synaptic degeneration and cognitive deficits in AD.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAmyloid beta-Protein PrecursorAnimalsAstrocytesAutoantigensCognitionCognition DisordersCognitive DysfunctionDisease Models, AnimalHippocampusLong-Term PotentiationMembrane ProteinsMemory DisordersMice, TransgenicSpatial MemoryAmyloid beta-PeptidesAmyloid beta-Protein PrecursorAutoantigensKIAA1524 protein, mouseMembrane ProteinsCIP2ACognitive deficitReactive astrogliosisSynaptic degeneration

Identifiers

PMID30594047
PMCPMC6405315
OpenAlexW2904944085

What OpenQuestion holds

Textmetadata
LicenceTDM
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.