Evidence map›Paper›PMID 30579834›Full record

ArticleNeuroscience2019

ADAMTS18 Deficiency Affects Neuronal Morphogenesis and Reduces the Levels of Depression-like Behaviors in Mice.

Rui Zhu, Yi-Hsuan Pan, Lijie Sun, Tianhao Zhang, Caiyun Wang, Shuai Ye, Ning Yang, Tiantian Lu, Thomas Wisniewski, Suying Dang and 1 more

Open access · greenAbstract read
In one paragraph

Article in Neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

13 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Frontiers in behavioral neuroscience · 2026
    Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Neural plasticity and depression treatment.IBRO neuroscience reports · 2023
    Article
  12. Article
  13. 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

11 authors at 3 institutions in 2 countries.

Rui ZhuKey Laboratory of Brain Functional Genomics, Ministry of Education, Shanghai Key Laboratory of Brain Functional Genomics, School of Life Science, East China Normal University, China.
Yi-Hsuan PanKey Laboratory of Brain Functional Genomics, Ministry of Education, Shanghai Key Laboratory of Brain Functional Genomics, School of Life Science, East China Normal University, China.
Lijie SunKey Laboratory of Brain Functional Genomics, Ministry of Education, Shanghai Key Laboratory of Brain Functional Genomics, School of Life Science, East China Normal University, China.
Tianhao ZhangKey Laboratory of Brain Functional Genomics, Ministry of Education, Shanghai Key Laboratory of Brain Functional Genomics, School of Life Science, East China Normal University, China.
Caiyun WangKey Laboratory of Brain Functional Genomics, Ministry of Education, Shanghai Key Laboratory of Brain Functional Genomics, School of Life Science, East China Normal University, China.
Shuai YeKey Laboratory of Brain Functional Genomics, Ministry of Education, Shanghai Key Laboratory of Brain Functional Genomics, School of Life Science, East China Normal University, China.
Ning YangKey Laboratory of Brain Functional Genomics, Ministry of Education, Shanghai Key Laboratory of Brain Functional Genomics, School of Life Science, East China Normal University, China.
Tiantian LuKey Laboratory of Brain Functional Genomics, Ministry of Education, Shanghai Key Laboratory of Brain Functional Genomics, School of Life Science, East China Normal University, China.
Thomas WisniewskiDepartments of Neurology, Pathology and Psychiatry, New York University School of Medicine, New York, NY 10016, USA.
Suying DangDepartment of Biochemistry and Molecular Cell Biology, Shanghai Jiao Tong University School of Medicine, Shanghai, China. Electronic address: suyingdang@shsmu.edu.cn.
Wei ZhangKey Laboratory of Brain Functional Genomics, Ministry of Education, Shanghai Key Laboratory of Brain Functional Genomics, School of Life Science, East China Normal University, China. Electronic address: wzhang@sat.ecnu.edu.cn.
East China Normal University · CNNew York University · USShanghai Jiao Tong University · CN

Funding

Research Education ComponentP30AG066512 · NIA · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI Mary Sherman Mittelman · 2020 to 2026
$28.4M
Transgenic/Behavior CoreP01AG060882 · NIA · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI WISNIEWSKI, THOMAS M · 2020 to 2024
$12.0M
Characterization of Rapidly Progressive Alzheimer's DiseaseRF1AG058267 · NIA · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI HAINES, JONATHAN L, SAFAR, JIRI G. · 2017 to 2017
$4.0M
NIA NIH HHS P01 AG060882NIA NIH HHS P30 AG066512NIA NIH HHS RF1 AG058267
6 · The paper itself

Abstract

The ADAMTS (a disintegrin and metalloproteinase with thrombospondin motifs) enzymes are secreted, multi-domain matrix-associated zinc metalloendopeptidases that modify extracellular matrix components and play crucial roles in development and numerous diseases. ADAMTS18 is a member of the ADAMTS family, and genome-wide association studies made an initial association of ADAMTS18 with white matter integrity in healthy people of 72-74 years old. However, the potential roles of ADAMTS18 in central nervous system remain unclear. In this study, we showed that Adamts18 mRNA is highly abundant in developing brains, especially in the cerebellum granular cell layer and the hippocampus dentate gyrus (DG) granular cell layer. Adamts18 knockout (KO) mice displayed higher dendritic branching complexity and spine density on hippocampal DG granular cells. Behavioral tests showed that Adamts18 KO mice had reduced levels of depression-like behaviors compared to their wild-type (WT) littermates. The increased neurite formation could be attributed in part to reduced phosphorylation levels of the collapsin response mediator protein-2 (CRMP2) due to activation of the laminin/PI3K/AKT/GSK-3β signaling pathway. Our findings revealed a critical role of ADAMTS18 in neuronal morphogenesis and emotional control in mice.

Indexed as

ADAMTS ProteinsAnimalsBrainDepressive DisorderDisease Models, AnimalMaleMice, 129 StrainMice, Inbred C57BLMice, KnockoutNeuronal PlasticityNeuronsRNA, MessengerADAMTS18 protein, mouseADAMTS ProteinsRNA, MessengerADAMTS18dendritic branchingdepressionlaminin

Identifiers

PMID30579834
PMCPMC8006808
OpenAlexW2905688073

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.