Evidence map›Paper›PMID 32664974›Full record

ArticleJournal of neuroinflammation2020

BDNF reverses aging-related microglial activation.

Shih-Ying Wu, Bo-Syong Pan, Sheng-Feng Tsai, Yi-Ting Chiang, Bu-Miin Huang, Fan-E Mo, Yu-Min Kuo

Open access · goldAbstract read
In one paragraph

Article in Journal of neuroinflammation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 95 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
95citing papers in PubMed, 1 pooled it
7.7field-weighted citation impact, top 2% 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

95 citing papers in PubMed, 1 synthesis or guideline pooled it, 171 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Article
  5. Hepatocyte BDNF Acts as a Novel Immune Checkpoint to Restrain TLR4-Mediated Acute Hepatitis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
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  8. Comprehensive Review of Anesthetic Strategies for Patients With Neurodegenerative Diseases.Medical science monitor : international medical journal of experimental and clinical research · 2026
    Review
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35 more citing papers are in PubMed but not listed here.

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

7 authors at 1 institution in 1 country.

Shih-Ying WuInstitute of Basic Medical Sciences, College of Medicine, National Cheng Kung University, Tainan, Taiwan.
Bo-Syong PanInstitute of Basic Medical Sciences, College of Medicine, National Cheng Kung University, Tainan, Taiwan.
Sheng-Feng TsaiInstitute of Basic Medical Sciences, College of Medicine, National Cheng Kung University, Tainan, Taiwan.
Yi-Ting ChiangDepartment of Cell Biology and Anatomy, College of Medicine, National Cheng Kung University, 1 Ta Hsueh Road, 70101, Tainan, Taiwan.
Bu-Miin HuangInstitute of Basic Medical Sciences, College of Medicine, National Cheng Kung University, Tainan, Taiwan.
Fan-E MoInstitute of Basic Medical Sciences, College of Medicine, National Cheng Kung University, Tainan, Taiwan.
Yu-Min KuoInstitute of Basic Medical Sciences, College of Medicine, National Cheng Kung University, Tainan, Taiwan. kuoym@mail.ncku.edu.tw.
National Cheng Kung University · TW

Funding

Ministry of Science and Technology, Taiwan 04-2320-B-006-039-MY3Ministry of Science and Technology, Taiwan 101-2320-B-006-006-MY3
6 · The paper itself

Abstract

backgroundExcessive microglial activation is implicated in the pathogenesis of various age-related neurodegenerative diseases. In addition to neurons, brain-derived neurotrophic factor (BDNF) and its receptor TrkB are also expressed in microglia. However, the direct effect of BDNF on age-related microglial activation has rarely been investigated.

methodsWe began to address this question by examining the effect of age on microglial activation and the BDNF-TrkB pathway in mice. By using pharmacological and genetic approaches, the roles of BDNF and downstream signaling pathways in microglial activation and related neurotoxicity were examined in microglial cell line and primary microglial cells.

resultsWe showed that microglial activation was evident in the brains of aged mice. The levels of BDNF and TrkB in microglia decreased with age and negatively correlated with their activation statuses in mice during aging. Interestingly, aging-related microglial activation could be reversed by chronic, subcutaneous perfusion of BDNF. Peripheral lipopolysaccharide (LPS) injection-induced microglial activation could be reduced by local supplement of BDNF, while shTrkB induced local microglial activation in naïve mice. In cultured microglial cell line and primary microglial cells, BDNF inhibited LPS-induced microglial activation, including morphological changes, activations of p38, JNK, and NF-кB, and productions of proinflammatory cytokines. These effects were blocked by shTrkB. BDNF induced activations of ErK and CREB which then competed with LPS-induced activation of NF-кB for binding to a common coactivator, CREB-binding protein.

conclusionsDecreasing BDNF-TrkB signaling during aging favors microglial activation, while upregulation BDNF signaling inhibits microglial activation via the TrkB-Erk-CREB pathway.

Indexed as

AgingAnimalsBrain-Derived Neurotrophic FactorCells, CulturedMaleMembrane GlycoproteinsMiceMice, Inbred C57BLMicrogliaProtein-Tyrosine KinasesReceptor, trkBBdnf protein, mouseBrain-Derived Neurotrophic FactorMembrane GlycoproteinsNtrk2 protein, mouseProtein-Tyrosine KinasesReceptor, trkBAgingBDNFCREBMicroglial activationNF-кBTrkB

Identifiers

PMID32664974
PMCPMC7362451
OpenAlexW3042372355

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.