Evidence map›Paper›PMID 33364525›Full record

ReviewNeurobiology of sleep and circadian rhythms2020

The interaction of the circadian and immune system: Desynchrony as a pathological outcome to traumatic brain injury.

G R Yamakawa, R D Brady, M Sun, S J McDonald, S R Shultz, R Mychasiuk

Open access · goldAbstract readReview
In one paragraph

Review in Neurobiology of sleep and circadian rhythms, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
1.1field-weighted citation impact, top 26% 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

11 citing papers in PubMed, 1 synthesis or guideline pooled it, 28 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Observational
  6. Review
  7. Article
  8. Article
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  10. 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

6 authors at 3 institutions in 1 country.

G R YamakawaDepartment of Neuroscience, Central Clinical School, Monash University, Melbourne, Australia.
R D BradyDepartment of Neuroscience, Central Clinical School, Monash University, Melbourne, Australia.
M SunDepartment of Neuroscience, Central Clinical School, Monash University, Melbourne, Australia.
S J McDonaldDepartment of Neuroscience, Central Clinical School, Monash University, Melbourne, Australia.
S R ShultzDepartment of Neuroscience, Central Clinical School, Monash University, Melbourne, Australia.
R MychasiukDepartment of Neuroscience, Central Clinical School, Monash University, Melbourne, Australia.
Monash University · AUThe University of Melbourne · AULa Trobe University · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Traumatic brain injury (TBI) is a complex and costly worldwide phenomenon that can lead to many negative health outcomes including disrupted circadian function. There is a bidirectional relationship between the immune system and the circadian system, with mammalian coordination of physiological activities being controlled by the primary circadian pacemaker in the suprachiasmatic nucleus (SCN) of the hypothalamus. The SCN receives light information from the external environment and in turn synchronizes rhythms throughout the brain and body. The SCN is capable of endogenous self-sustained oscillatory activity through an intricate clock gene negative feedback loop. Following TBI, the response of the immune system can become prolonged and pathophysiological. This detrimental response not only occurs in the brain, but also within the periphery, where a leaky blood brain barrier can permit further infiltration of immune and inflammatory factors. The prolonged and pathological immune response that follows TBI can have deleterious effects on clock gene cycling and circadian function not only in the SCN, but also in other rhythmic areas throughout the body. This could bring about a state of circadian desynchrony where different rhythmic structures are no longer working together to promote optimal physiological function. There are many parallels between the negative symptomology associated with circadian desynchrony and TBI. This review discusses the significant contributions of an immune-disrupted circadian system on the negative symptomology following TBI. The implications of TBI symptomology as a disorder of circadian desynchrony are discussed.

Indexed as

Clock genesConcussionCytokinesNeuroinflammationSuprachiasmatic nucleus

Identifiers

PMID33364525
PMCPMC7752723
OpenAlexW3093449024

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.