Evidence map›Paper›PMID 34361041›Full record

ArticleInternational journal of molecular sciences2021

3,6'-Dithiopomalidomide Ameliorates Hippocampal Neurodegeneration, Microgliosis and Astrogliosis and Improves Cognitive Behaviors in Rats with a Moderate Traumatic Brain Injury.

Pen-Sen Huang, Ping-Yen Tsai, Ling-Yu Yang, Daniela Lecca, Weiming Luo, Dong Seok Kim, Barry J Hoffer, Yung-Hsiao Chiang, Nigel H Greig, Jia-Yi Wang

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
1.2field-weighted citation impact, top 22% 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

18 citing papers in PubMed, 1 synthesis or guideline pooled it, 17 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Role of chronic neuroinflammation in neuroplasticity and cognitive function: A hypothesis.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2022
    Article
  16. Article
  17. Article
  18. 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

10 authors at 4 institutions in 2 countries.

Pen-Sen HuangGraduate Institute of Medical Sciences, College of Medicine, Taipei Medical University, Taipei 110, Taiwan.
Ping-Yen TsaiGraduate Institute of Medical Sciences, College of Medicine, Taipei Medical University, Taipei 110, Taiwan.ORCID 0000-0001-8863-2966
Ling-Yu YangGraduate Institute of Medical Sciences, College of Medicine, Taipei Medical University, Taipei 110, Taiwan.
Daniela LeccaDrug Design & Development Section, Translational Gerontology Branch, Intramural Research Program, National Institute on Aging, NIH, Baltimore, MD 21224, USA.
Weiming LuoDrug Design & Development Section, Translational Gerontology Branch, Intramural Research Program, National Institute on Aging, NIH, Baltimore, MD 21224, USA.
Dong Seok KimAevis Bio, Inc., Daejeon 34141, Korea.
Barry J HofferDepartment of Neurological Surgery, Case Western Reserve University, Cleveland, OH 44106, USA.
Yung-Hsiao ChiangDepartment of Neurosurgery, Taipei Medical University Hospital, Taipei Medical University, Taipei 110, Taiwan.
Nigel H GreigDrug Design & Development Section, Translational Gerontology Branch, Intramural Research Program, National Institute on Aging, NIH, Baltimore, MD 21224, USA.ORCID 0000-0002-3032-1468
Jia-Yi WangGraduate Institute of Medical Sciences, College of Medicine, Taipei Medical University, Taipei 110, Taiwan.ORCID 0000-0002-9106-3351
National Institute on Aging · USTaipei Medical University · TWTaipei Medical University Hospital · TWNeurological Surgery · US

Funding

Pro-inflammatory cytokine lowering anti-inflammatory drugsZIAAG000994 · NIA · NATIONAL INSTITUTE ON AGING · PI GREIG, NIGEL H. · 2016 to 2025
$16.8M
Ministry of Science and Technology, Taiwan MOST 110-2314-B-038-026-MY3 and MOST 108-2321-B-038-008National Institutes of Health R56 AG057028, USASunny Brain Tumor and Brain Disease Research and Development Fund, Taipei Medical University, Taipei, TaiwanTechnology development Program of MSS S2782046The Intramural Research Program, National Institute on Aging, National Institutes of Health, USAthe National Research Foundation (NRF) grant funded by the Korea government 2021M3A9G2015889
6 · The paper itself

Abstract

Traumatic brain injury (TBI) is a leading cause of disability and mortality worldwide. It can instigate immediate cell death, followed by a time-dependent secondary injury that results from disproportionate microglial and astrocyte activation, excessive inflammation and oxidative stress in brain tissue, culminating in both short- and long-term cognitive dysfunction and behavioral deficits. Within the brain, the hippocampus is particularly vulnerable to a TBI. We studied a new pomalidomide (Pom) analog, namely, 3,6'-dithioPom (DP), and Pom as immunomodulatory imide drugs (IMiD) for mitigating TBI-induced hippocampal neurodegeneration, microgliosis, astrogliosis and behavioral impairments in a controlled cortical impact (CCI) model of TBI in rats. Both agents were administered as a single intravenous dose (0.5 mg/kg) at 5 h post injury so that the efficacies could be compared. Pom and DP significantly reduced the contusion volume evaluated at 24 h and 7 days post injury. Both agents ameliorated short-term memory deficits and anxiety behavior at 7 days after a TBI. The number of degenerating neurons in the CA1 and dentate gyrus (DG) regions of the hippocampus after a TBI was reduced by Pom and DP. DP, but not Pom, significantly attenuated the TBI-induced microgliosis and DP was more efficacious than Pom at attenuating the TBI-induced astrogliosis in CA1 and DG at 7D after a TBI. In summary, a single intravenous injection of Pom or DP, given 5 h post TBI, significantly reduced hippocampal neurodegeneration and prevented cognitive deficits with a concomitant attenuation of the neuroinflammation in the hippocampus.

Indexed as

AnimalsBrain Injuries, TraumaticCognitionGliosisHippocampusImmunologic FactorsMaleMemoryNeuroprotective AgentsRatsRats, Sprague-DawleyThalidomideImmunologic FactorsNeuroprotective AgentspomalidomideThalidomide3,6′-dithiopomalidomideastrogliosiscognitive deficitsimmunomodulatory imide drugsmicrogliosisneurodegenerationneuroinflammationpomalidomidetraumatic brain injury

Identifiers

PMID34361041
PMCPMC8348060
OpenAlexW3189073260

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.