Mitoquinone Helps Combat the Neurological, Cognitive, and Molecular Consequences of Open Head Traumatic Brain Injury at Chronic Time Point

dc.creatorHaidar, Muhammad Ali
dc.creatorShakkour, Zaynab
dc.creatorBarsa, Chloe
dc.creatorTabet, Maha
dc.creatorMekhjian, Sarin
dc.creatorDarwish, Hala
dc.creatorGoli, Mona (TTU)
dc.creatorShear, Deborah
dc.creatorPandya, Jignesh D.
dc.creatorMechref, Yehia (TTU)
dc.creatorKhoury, Riyad El
dc.creatorWang, Kevin
dc.creatorKobeissy, Firas
dc.date.accessioned2023-04-06T20:19:12Z
dc.date.available2023-04-06T20:19:12Z
dc.date.issued2022
dc.description© 2022 by the authors. Licensee MDPI, Basel, Switzerland. cc-by
dc.description.abstractTraumatic brain injury (TBI) is a heterogeneous disease in its origin, neuropathology, and prognosis, with no FDA-approved treatments. The pathology of TBI is complicated and not suffi-ciently understood, which is the reason why more than 30 clinical trials in the past three decades turned out unsuccessful in phase III. The multifaceted pathophysiology of TBI involves a cascade of metabolic and molecular events including inflammation, oxidative stress, excitotoxicity, and mito-chondrial dysfunction. In this study, an open head TBI mouse model, induced by controlled cortical impact (CCI), was used to investigate the chronic protective effects of mitoquinone (MitoQ) administration 30 days post-injury. Neurological functions were assessed with the Garcia neuroscore, pole climbing, grip strength, and adhesive removal tests, whereas cognitive and behavioral functions were assessed using the object recognition, Morris water maze, and forced swim tests. As for molecular effects, immunofluorescence staining was conducted to investigate microgliosis, astrocytosis, neuronal cell count, and axonal integrity. The results show that MitoQ enhanced neurological and cognitive functions 30 days post-injury. MitoQ also decreased the activation of astrocytes and microglia, which was accompanied by improved axonal integrity and neuronal cell count in the cortex. Therefore, we conclude that MitoQ has neuroprotective effects in a moderate open head CCI mouse model by decreasing oxidative stress, neuroinflammation, and axonal injury.
dc.identifier.citationHaidar, M.A., Shakkour, Z., Barsa, C., Tabet, M., Mekhjian, S., Darwish, H., Goli, M., Shear, D., Pandya, J.D., Mechref, Y., Khoury, R.E., Wang, K., & Kobeissy, F.. 2022. Mitoquinone Helps Combat the Neurological, Cognitive, and Molecular Consequences of Open Head Traumatic Brain Injury at Chronic Time Point. Biomedicines, 10(2). https://doi.org/10.3390/biomedicines10020250
dc.identifier.urihttps://doi.org/10.3390/biomedicines10020250
dc.identifier.urihttps://hdl.handle.net/2346/92567
dc.language.isoeng
dc.subjectModerate traumatic brain injury
dc.subjectNeurodegeneration
dc.subjectNeuroinflammation
dc.subjectNeurotrauma
dc.subjectOxidative stress
dc.titleMitoquinone Helps Combat the Neurological, Cognitive, and Molecular Consequences of Open Head Traumatic Brain Injury at Chronic Time Point
dc.typeArticle

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