HYBRID EVENT: You can participate in person at Orlando, USA or Virtually from your home or work.

6th Edition of International Conference on Neurology and Brain Disorders

October 24 -26, 2022

October 24 -26, 2022 | Orlando, Florida, USA
INBC 2022

Reem Ahmad Abedi

Speaker at Neurology and Brain Disorders 2022 - Reem Ahmad Abedi
American University of Beirut, Lebanon
Title : The effect of mitoquinone supplementation on behavioral and neuropathological changes in a mouse model of penetrating brain injury at acute time-point and chronic time-point


Traumatic brain injury (TBI) is a major cause of death and disability worldwide. Penetrating brain injury (PBI), represents ~ 12% of all TBI cases. Typically, PBI is associated with many symptoms including coma. The mechanisms underlying these pathologic changes include excitotoxicity, oxidative stress, neuro-inflammation, and ultimately cell death. Currently, there is no FDA approved drug that targets PBI. Nonetheless, targeting one pathology mechanism must be effective in ameliorating the possible consequences of PBI, and this has been demonstrated in the use of antioxidant drugs. One of the proposed antioxidants is mitoquinone (MitoQ) which is a mitochondria-targeted ubiquinone molecule which synthesized by attaching the latter to a triphenylphosphonium cation (TPP+). In this study, we suggested that MitoQ administration would be beneficial to ameliorate the consequences of PBI at acute time-point (3 days post-injury) and chronic time-point (30 days post-injury). For this purpose, 59 C57BL/6 mice were divided into three groups: sham, PBI, and PBI + MitoQ. Our model of PBI consisted of a hit in the somatosensory area of the right parietal lobe using a modified controlled cortical impact model (CCI). Behavioral and cognitive outcomes were assessed using a battery of behavioral tests. While the cellular outcomes were assessed by immunofluorescence staining of Iba-1 and GFAP for microglia and astrocytes, respectively. In addition to the analysis of the antioxidants SOD2 and CAT expression levels and Nrf-2 that is an antioxidant transcription factor via RT-PCR (qPCR). It has been found that MitoQ reduces muscle strength deficits assessed by the grip strength test, ameliorates depressive-like symptoms by using forced swim test (FST), and lessens learning impairments caused by PBI as assessed by Morris water maze (MWM) at chronic time-point. However, our PBI model did not impair the working/short term memory of the mice as assessed by object recognition test. Moreover, MitoQ was found to reduce astrocytosis and microgliosis in the cortex at chronic time-point as assessed by immunofluorescence staining, and increases SOD expression with no effect on Nrf2 and CAT expression at acute time-point. In conclusion, MitoQ administration following PBI can be an efficient approach to ameliorate the consequences of PBI at acute and chronic time points with no considerable side effects.


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