Evidence map›Paper›PMID 32574954›Full record

ReviewEBioMedicine2020

Western diet aggravates neuronal insult in post-traumatic brain injury: Proposed pathways for interplay.

Abdullah Shaito, Hiba Hasan, Karl John Habashy, Walaa Fakih, Samar Abdelhady, Fatima Ahmad, Kazem Zibara, Ali H Eid, Ahmed F El-Yazbi, Firas H Kobeissy

Open access · goldAbstract readReview
In one paragraph

Review in EBioMedicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 2 pooled it
4.5field-weighted citation impact, top 4% 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

21 citing papers in PubMed, 2 syntheses or guidelines pooled it, 47 citations in OpenAlex.

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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

10 authors at 5 institutions in 3 countries.

Abdullah ShaitoDepartment of Biological and Chemical Sciences, Lebanese International University, Beirut, Lebanon and Faculty of Health Sciences, University of Balamand, Beirut, Lebanon.
Hiba HasanInstitute of Anatomy and Cell Biology, Justus-Liebig-University Giessen, 35392 Giessen, Germany.
Karl John HabashyFaculty of Medicine, American University of Beirut, Beirut, Lebanon.
Walaa FakihDepartment of Pharmacology and Toxicology, Faculty of Medicine, American University of Beirut, Beirut, Lebanon.
Samar AbdelhadyFaculty of Medicine, Alexandria University, Alexandria, Egypt.
Fatima AhmadNeuroscience Research Center, Faculty of Medicine, Lebanese University.
Kazem ZibaraBiology Department, Faculty of Sciences-I, Lebanese University, Beirut, Lebanon.
Ali H EidDepartment of Pharmacology and Toxicology, Faculty of Medicine, American University of Beirut, Beirut, Lebanon; Department of Biomedical Sciences, College of Health Sciences, Doha, Qatar.
Ahmed F El-YazbiDepartment of Pharmacology and Toxicology, Faculty of Medicine, American University of Beirut, Beirut, Lebanon; Department of Pharmacology and Toxicology, Faculty of Pharmacy, Alexandria University, Egypt. Electronic address: ae88@aub.edu.lb.
Firas H KobeissyDepartment of Biochemistry and Molecular Genetics, Faculty of Medicine, American University of Beirut, Beirut, Lebanon. Electronic address: fk02@aub.edu.lb.
American University of Beirut · LBAlexandria University · EGLebanese University · LBJustus-Liebig-Universität Gießen · DEUniversity of Balamand · LB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Traumatic brain injury (TBI) is a global health burden and a major cause of disability and mortality. An early cascade of physical and structural damaging events starts immediately post-TBI. This primary injury event initiates a series of neuropathological molecular and biochemical secondary injury sequelae, that last much longer and involve disruption of cerebral metabolism, mitochondrial dysfunction, oxidative stress, neuroinflammation, and can lead to neuronal damage and death. Coupled to these events, recent studies have shown that lifestyle factors, including diet, constitute additional risk affecting TBI consequences and neuropathophysiological outcomes. There exists molecular cross-talk among the pathways involved in neuronal survival, neuroinflammation, and behavioral outcomes, that are shared among western diet (WD) intake and TBI pathophysiology. As such, poor dietary intake would be expected to exacerbate the secondary damage in TBI. Hence, the aim of this review is to discuss the pathophysiological consequences of WD that can lead to the exacerbation of TBI outcomes. We dissect the role of mitochondrial dysfunction, oxidative stress, neuroinflammation, and neuronal injury in this context. We show that currently available data conclude that intake of a diet saturated in fats, pre- or post-TBI, aggravates TBI, precludes recovery from brain trauma, and reduces the response to treatment.

Indexed as

AnimalsBrainBrain Injuries, TraumaticCell DeathDiet, WesternHumansNeuronsOxidative StressMicrobiotaMitochondrial dysfunctionNeuroinflammationOxidative stressTBIWestern diet

Identifiers

PMID32574954
PMCPMC7317220
OpenAlexW3036447201

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.