Evidence map›Paper›PMID 21895523›Full record

ArticleJournal of neurotrauma2012

Lithium ameliorates neurodegeneration, suppresses neuroinflammation, and improves behavioral performance in a mouse model of traumatic brain injury.

Fengshan Yu, Zhifei Wang, Flaubert Tchantchou, Chi-Tso Chiu, Yumin Zhang, De-Maw Chuang

Open access · greenAbstract read
In one paragraph

Article in Journal of neurotrauma, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed
6.9field-weighted citation impact, top 3% 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

71 citing papers in PubMed, 137 citations in OpenAlex.

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  10. Mood and behavior regulation: interaction of lithium and dopaminergic system.Naunyn-Schmiedeberg's archives of pharmacology · 2023
    Review
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11 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

6 authors at 2 institutions in 1 country.

Fengshan YuSection on Molecular Neurobiology, National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland, USA.
Zhifei Wang
Flaubert Tchantchou
Chi-Tso Chiu
Yumin Zhang
De-Maw Chuang
National Institutes of Health · USUniformed Services University of the Health Sciences · US

Funding

Mechanisms Of Action Of Psychoactive DrugsZIAMH002468 · NIMH · NATIONAL INSTITUTE OF MENTAL HEALTH · PI AMARA, SUSAN · 2009 to 2015
$10.1M
Intramural NIH HHS
6 · The paper itself

Abstract

Although traumatic brain injury (TBI) is recognized as one of the leading causes of death from trauma to the central nervous system (CNS), no known treatment effectively mitigates its effects. Lithium, a primary drug for the treatment of bipolar disorder, has been known to have neuroprotective effects in various neurodegenerative conditions such as stroke. Until this study, however, it has not been investigated as a post-insult treatment for TBI. To evaluate whether lithium could have beneficial effects following TBI, lithium at a dose of 1.5 mEq/kg was administered after injury. Assessed at 3 days and 3 weeks post-injury using hematoxylin and eosin staining, lithium treatment was found to reduce lesion volume. Lithium at doses of 2.0 and 3.0 mEq/kg also significantly reduced lesion volume at 3 days after injury, and the therapeutic window was at least 3 h post-injury. TBI-induced neuronal death, microglial activation, and cyclooxygenase-2 induction were all attenuated by lithium at 3 days after injury. In addition, lithium treatment reduced TBI-induced matrix metalloproteinase-9 expression and preserved the integrity of the blood-brain barrier. As for behavioral outcomes, lithium treatment reduced anxiety-like behavior in an open-field test, and improved short- and long-term motor coordination in rotarod and beam-walk tests. Lithium robustly increased serine phosphorylation of glycogen synthase kinase-3β (GSK-3β), suggesting that the underlying mechanisms responsible for lithium's protective effects are triggered by increasing phosphorylation of this kinase and thereby inhibiting its activity. Our results support the notion that lithium has heretofore unrecognized capacity to mitigate the neurodegenerative effects and improve functional outcomes in TBI.

Indexed as

AnimalsBrain InjuriesDisease Models, AnimalInflammationLithium CompoundsMaleMental DisordersMiceMice, Inbred C57BLNerve DegenerationNeuroprotective AgentsLithium CompoundsNeuroprotective Agents

Identifiers

PMID21895523
PMCPMC3261788
OpenAlexW2020311418

What OpenQuestion holds

Textmetadata
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.