Evidence map›Paper›PMID 29863022›Full record

ArticleNeural regeneration research2018

Association between Alzheimer's disease pathogenesis and early demyelination and oligodendrocyte dysfunction.

Yu-Xia Dong, Hui-Yu Zhang, Hui-Yuan Li, Pei-Hui Liu, Yi Sui, Xiao-Hong Sun

Open access · goldAbstract read
In one paragraph

Article in Neural regeneration research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
3.4field-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

45 citing papers in PubMed, 66 citations in OpenAlex.

  1. Article
  2. Article
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  4. Article
  5. Emerging Role of Oligodendrocytes Malfunction in the Progression of Alzheimer's Disease.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025
    Review
  6. Review
  7. Review
  8. Review
  9. Article
  10. Article
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  14. White Matter Injury in Central Nervous System Disorders.Neuropsychiatric disease and treatment · 2025
    Review
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  16. Review
  17. Article
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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

6 authors at 3 institutions in 1 country.

Yu-Xia DongDepartment of Neurology, The Fourth Affiliated Hospital of China Medical University, Shenyang; Department of Neurology, Fushun Second Hospital, Fushun, Liaoning Province, China.
Hui-Yu ZhangDepartment of Neurology, The Fourth Affiliated Hospital of China Medical University, Shenyang, Liaoning Province, China.
Hui-Yuan LiDepartment of Neurology, The Fourth Affiliated Hospital of China Medical University, Shenyang, Liaoning Province, China.
Pei-Hui LiuDepartment of Neurology, The Fourth Affiliated Hospital of China Medical University, Shenyang; Department of Neurology, Huludao Central Hospital, Huludao, Liaoning Province, China.
Yi SuiDepartment of Neurology, The Fourth Affiliated Hospital of China Medical University; Department of Neurology, Shenyang First People's Hospital, Shenyang, Liaoning Province, China.
Xiao-Hong SunDepartment of Neurology, The Fourth Affiliated Hospital of China Medical University, Shenyang, Liaoning Province, China.
Fourth Affiliated Hospital of China Medical University · CNChina Medical University · CNFuzhou Second Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The APPSwe/PSEN1dE9 (APP/PS1) transgenic mouse model is an Alzheimer's disease mouse model exhibiting symptoms of dementia, and is commonly used to explore pathological changes in the development of Alzheimer's disease. Previous clinical autopsy and imaging studies suggest that Alzheimer's disease patients have white matter and oligodendrocyte damage, but the underlying mechanisms of these have not been revealed. Therefore, the present study used APP/PS1 mice to assess cognitive change, myelin loss, and corresponding changes in oligodendrocytes, and to explore the underlying mechanisms. Morris water maze tests were performed to evaluate cognitive change in APP/PS1 mice and normal C57BL/6 mice aged 3 and 6 months. Luxol fast blue staining of the corpus callosum and quantitative reverse transcription-polymerase chain reaction (qRT-PCR) for myelin basic protein (MBP) mRNA were carried out to quantify myelin damage. Immunohistochemistry staining for NG2 and qRT-PCR for monocarboxylic acid transporter 1 (MCT1) mRNA were conducted to assess corresponding changes in oligodendrocytes. Our results demonstrate that compared with C57BL/6 mice, there was a downregulation of MBP mRNA in APP/PS1 mice aged 3 months. This became more obvious in APP/PS1 mice aged 6 months accompanied by other abnormalities such as prolonged escape latency in the Morris water maze test, shrinkage of the corpus callosum, upregulation of NG2-immunoreactive cells, and downregulation of MCT1 mRNA. These findings indicate that the involvement of early demyelination at 3 months and the oligodendrocyte dysfunction at 6 months in APP/PS1 mice are in association with Alzheimer's disease pathogenesis.

Indexed as

Alzheimer's diseaseAPP/PS1 micecorpus callosumdemyelinationmonocarboxylic acid transporter 1Morris water maze testmyelin basic proteinnerve regenerationneural regenerationoligodendrocytes

Identifiers

PMID29863022
PMCPMC5998637
OpenAlexW2805598377

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.