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,
Fatimah Ahmad,
Kazem Zibara,
Ali H. Eid,
Ahmed F. El-Yazbi,
Firas H. Kobeissy
Affiliations
Abdullah Shaito
Department of Biological and Chemical Sciences, Lebanese International University, Beirut, Lebanon and Faculty of Health Sciences, University of Balamand, Beirut, Lebanon
Hiba Hasan
Institute of Anatomy and Cell Biology, Justus-Liebig-University Giessen, 35392 Giessen, Germany
Karl John Habashy
Faculty of Medicine, American University of Beirut, Beirut, Lebanon
Walaa Fakih
Department of Pharmacology and Toxicology, Faculty of Medicine, American University of Beirut, Beirut, Lebanon
Samar Abdelhady
Faculty of Medicine, Alexandria University, Alexandria, Egypt
Fatimah Ahmad
Department of Biochemistry and Molecular Genetics, Faculty of Medicine, American University of Beirut, Beirut, Lebanon
Kazem Zibara
Biology Department, Faculty of Sciences-I, Lebanese University, Beirut, Lebanon
Ali H. Eid
Department 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-Yazbi
Department of Pharmacology and Toxicology, Faculty of Medicine, American University of Beirut, Beirut, Lebanon; Department of Pharmacology and Toxicology, Faculty of Pharmacy, Alexandria University, Egypt; Corresponding author at: Department of Pharmacology and Toxicology, Faculty of Medicine, American University of Beirut, Beirut, Lebanon.
Firas H. Kobeissy
Department of Biochemistry and Molecular Genetics, Faculty of Medicine, American University of Beirut, Beirut, Lebanon; Corresponding author.
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.
