Evidence map›Paper›PMID 26942016›Full record

ReviewNeural plasticity2016

Glia and TRPM2 Channels in Plasticity of Central Nervous System and Alzheimer's Diseases.

Jing Wang, Michael F Jackson, Yu-Feng Xie

Open access · goldAbstract readReview
In one paragraph

Review in Neural plasticity, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.7field-weighted citation impact, top 11% 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

20 citing papers in PubMed, 36 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Article
  6. Article
  7. Research progress on transient receptor potential melastatin 2 channel in nervous system diseases.Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2021
    Review
  8. Article
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  12. Review
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  14. Review
  15. Article
  16. Review
  17. Review
  18. Antioxidant activity against HPharmaceutical biology · 2017
    Article
  19. Review
  20. Glial Cells and Synaptic Plasticity.Neural plasticity · 2016
    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

3 authors at 2 institutions in 2 countries.

Jing WangKey Laboratory of Orthopedics of Gansu Province, The Second Hospital of Lanzhou University, No. 82 Cui Ying Men, Lanzhou, Gansu 730030, China.
Michael F JacksonDepartment of Pharmacology & Therapeutics, University of Manitoba, Canada; Kleysen Institute for Advanced Medicine, University of Manitoba, 710 William Avenue, SR426 Winnipeg, MB, Canada R3E 0Z3.
Yu-Feng XieDepartment of Pharmacology & Therapeutics, University of Manitoba, Canada; Kleysen Institute for Advanced Medicine, University of Manitoba, 710 William Avenue, SR426 Winnipeg, MB, Canada R3E 0Z3; Leslie Dan Faculty of Pharmacy, University of Toronto, 144 College Street, Toronto, ON, Canada M5S 3M2.
University of Manitoba · CALanzhou University · CN

Funding

Canadian Institutes of Health Research R4321A07
6 · The paper itself

Abstract

Synaptic plasticity refers to the ability of neurons to strengthen or weaken synaptic efficacy in response to activity and is the basis for learning and memory. Glial cells communicate with neurons and in this way contribute in part to plasticity in the CNS and to the pathology of Alzheimer's disease (AD), a neurodegenerative disease in which impaired synaptic plasticity is causally implicated. The transient receptor potential melastatin member 2 (TRPM2) channel is a nonselective Ca(2+)-permeable channel expressed in both glial cells (microglia and astrocytes) and neurons. Recent studies indicated that TRPM2 regulates synaptic plasticity as well as the activation of glial cells. TRPM2 also modulates oxidative stress and inflammation through interaction with glial cells. As both oxidative stress and inflammation have been implicated in AD pathology, this suggests a possible contribution of TRPM2 to disease processes. Through modulating the homeostasis of glutathione, TRPM2 is involved in the process of aging which is a risk factor of AD. These results potentially point TRPM2 channel to be involved in AD through glial cells. This review summarizes recent advances in studying the contribution of TRPM2 in health and in AD pathology, with a focus on contributions via glia cells.

Indexed as

Neuronal PlasticityAlzheimer DiseaseAnimalsBrainHumansNeurogliaNeuronsOxidative StressTRPM Cation ChannelsTRPM2 protein, humanTRPM Cation Channels

Identifiers

PMID26942016
PMCPMC4749827
OpenAlexW2296402508

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.