Evidence map›Paper›PMID 31024304›Full record

ArticleFrontiers in pharmacology2019

Venlafaxine Improves the Cognitive Impairment and Depression-Like Behaviors in a Cuprizone Mouse Model by Alleviating Demyelination and Neuroinflammation in the Brain.

Yanbo Zhang, Xiaoying Bi, Olubunmi Adebiyi, Junhui Wang, Ali Mooshekhian, Jacob Cohen, Zelan Wei, Fei Wang, Xin-Min Li

Open access · goldAbstract read
In one paragraph

Article in Frontiers in pharmacology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
4.4field-weighted citation impact, top 5% 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

36 citing papers in PubMed, 63 citations in OpenAlex.

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  2. Fisetin Mitigates Ferroptosis and Promotes Remyelination in a Cuprizone Model of Multiple Sclerosis.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025
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  16. Dopamine, Immunity, and Disease.Pharmacological reviews · 2023
    Review
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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

9 authors at 5 institutions in 2 countries.

Yanbo ZhangDepartment of Psychiatry, College of Medicine, University of Saskatchewan, Saskatoon, SK, Canada.
Xiaoying BiDepartment of Neurology, Changhai Hospital, Second Military Medical University, Shanghai, China.
Olubunmi AdebiyiDepartment of Psychiatry, College of Medicine, University of Saskatchewan, Saskatoon, SK, Canada.
Junhui WangDepartment of Physiology, Faculty of Medicine, University of Toronto, Toronto, ON, Canada.
Ali MooshekhianDepartment of Psychiatry, College of Medicine, University of Saskatchewan, Saskatoon, SK, Canada.
Jacob CohenDepartment of Pharmacology, College of Medicine, University of Saskatchewan, Saskatoon, SK, Canada.
Zelan WeiDepartment of Psychiatry, College of Medicine, University of Saskatchewan, Saskatoon, SK, Canada.
Fei WangDepartment of Psychiatry, The First Affiliated Hospital of China Medical University, Shenyang, China.
Xin-Min LiDepartment of Psychiatry, Faculty of Medicine and Dentistry, University of Alberta, Edmonton, AB, Canada.
University of Saskatchewan · CAChina Medical University · CNSecond Military Medical University · CNUniversity of Alberta · CAUniversity of Toronto · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Growing evidence has implicated that myelin deficits and neuroinflammation are the coexisted pathological features that contribute to the mood swing and cognitive decline in major depressive disorder (MDD) and multiple sclerosis (MS). Therefore, attenuation of neuroinflammation and reduction of demyelination became newly emerging treatment strategies for the mood and cognitive symptoms. Antidepressant venlafaxine has been used in depression and anxiety through its multiple neuroprotective effects. However, it is unclear whether venlafaxine can improve myelin integrity and alter inflammation status in the brain. By using a well-established cuprizone-induced acute mouse model of demyelination, we investigated the protective effects of venlafaxine on these facets. The cuprizone-fed animals exhibited cognitive impairment and mood disturbances together with myelin loss and prominent neuroinflammation in the brain. Our present study showed that a high dose of venlafaxine alleviated the loss of myelin and oligodendrocytes (OLs), mitigated depression-like behaviors, and improved cognitive function in cuprizone-fed animals. Data from the present study also showed that venlafaxine reduced microglia-mediated inflammation in the brains of cuprizone-fed animals. These findings suggest that venlafaxine may exert its therapeutic effects

Indexed as

cognitioncuprizonedemyelinationmajor depressive disordermicrogliaoligodendrocytevenlafaxine

Identifiers

PMID31024304
PMCPMC6460225
OpenAlexW2926463281

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.