Evidence map›Paper›PMID 35426376›Full record

ArticleThe Journal of clinical investigation2022

Aberrant miR-339-5p/neuronatin signaling causes prodromal neuronal calcium dyshomeostasis in mutant presenilin mice.

Hao-Yu Zou, Lin Guo, Bei Zhang, Si Chen, Xin-Rong Wu, Xian-Dong Liu, Xin-Yu Xu, Bin-Yin Li, Shengdi Chen, Nan-Jie Xu and 1 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
3.2field-weighted citation impact, top 7% 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, 26 citations in OpenAlex.

  1. Article
  2. Article
  3. HUWE1 in Skeletal Muscle Prevents Muscle Fatigue via Maintaining Iron and Calcium Homeostasis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  4. Article
  5. Review
  6. Article
  7. Article
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  9. A state-of-the-art review on miRNA in prevention and treatment of AlzheimerZhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2023
    Review
  10. Article
  11. Review
  12. Review
  13. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 3 institutions in 1 country.

Hao-Yu ZouDepartment of Neurology and Institute of Neurology, Ruijin Hospital.
Lin GuoResearch Center of Translational Medicine, Shanghai Children's Hospital, Department of Anatomy and Physiology, and.
Bei ZhangDepartment of Neurology and Institute of Neurology, Ruijin Hospital.
Si ChenResearch Center of Translational Medicine, Shanghai Children's Hospital, Department of Anatomy and Physiology, and.
Xin-Rong WuDepartment of Neurology and Institute of Neurology, Ruijin Hospital.
Xian-Dong LiuDepartment of Neurology and Institute of Neurology, Ruijin Hospital.
Xin-Yu XuResearch Center of Translational Medicine, Shanghai Children's Hospital, Department of Anatomy and Physiology, and.
Bin-Yin LiDepartment of Neurology and Institute of Neurology, Ruijin Hospital.
Shengdi ChenDepartment of Neurology and Institute of Neurology, Ruijin Hospital.
Nan-Jie XuResearch Center of Translational Medicine, Shanghai Children's Hospital, Department of Anatomy and Physiology, and.
Suya SunDepartment of Neurology and Institute of Neurology, Ruijin Hospital.
Ruijin Hospital · CNShanghai Children's Hospital · CNShanghai Jiao Tong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mushroom spine loss and calcium dyshomeostasis are early hallmark events of age-related neurodegeneration, such as Alzheimer's disease (AD), that are connected with neuronal hyperactivity in early pathology of cognitive brain areas. However, it remains elusive how these key events are triggered at the molecular level for the neuronal abnormality that occurs at the initial stage of disease. Here, we identify downregulated miR-339-5p and its upregulated target protein, neuronatin (Nnat), in cortex neurons from the presenilin-1 M146V knockin (PSEN1-M146V KI) mouse model of familial AD (FAD). Inhibition of miR-339-5p or overexpression of Nnat recapitulates spine loss and endoplasmic reticulum calcium overload in cortical neurons with the PSEN1 mutation. Conversely, either overexpression of miR-339-5p or knockdown of Nnat restores spine morphogenesis and calcium homeostasis. We used fiber photometry recording during the object-cognitive process to further demonstrate that the PSEN1 mutant causes defective habituation in neuronal reaction in the retrosplenial cortex and that this can be rescued by restoring the miR-339-5p/Nnat pathway. Our findings thus reveal crucial roles of the miR-339-5p/Nnat pathway in FAD that may serve as potential diagnostic and therapeutic targets for early pathogenesis.

Indexed as

Alzheimer DiseaseMicroRNAsAnimalsCalciumMiceNeuronsPresenilin-1CalciumMicroRNAsPresenilin-1Alzheimer diseaseCalcium signalingCell BiologyNeurodegenerationNeuroscience

Identifiers

PMID35426376
PMCPMC9012292
OpenAlexW4223923090

What OpenQuestion holds

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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.