Neuroprotection after traumatic brain injury

The problem

Traumatic brain injury (TBI) has no FDA-approved treatment — more than 30 phase-III trials in three decades have failed. Its pathology is a cascade of oxidative stress, neuroinflammation, excitotoxicity, and mitochondrial dysfunction, which makes mitochondria-targeted antioxidants a compelling avenue. This work, from my time in molecular neuroscience at the American University of Beirut, tested one directly.

Approach

• Model: controlled cortical impact (CCI) — a moderate open-head TBI — in mice.
• Intervention: mitoquinone (MitoQ), 8 mg/kg intraperitoneally, three times weekly for 30 days, starting 30 minutes post-injury.
• Behavior & cognition: Garcia neuroscore, pole climb, grip strength, adhesive removal, novel object recognition, Morris water maze, and forced swim tests.
• Molecular: immunofluorescence for microgliosis, astrocytosis, neuronal cell count, and axonal integrity (myelin basic protein).

Key findings

• MitoQ enhanced neurological and cognitive function at both 7 and 30 days post-injury — better motor coordination, recognition memory, and spatial learning, and reduced depressive-like behavior.
• It reduced astrocyte and microglial activation while preserving neuronal counts and axonal integrity in the cortex.
• It upregulated antioxidant enzymes (SOD2, CAT) via the Nrf2–ARE pathway.

My role

First author. I led the mechanistic analysis and the data visualization across the behavioral, cognitive, and molecular results — turning a large multi-assay dataset into a clear, defensible story.

Conclusion

MitoQ is neuroprotective in a moderate open-head CCI model by decreasing oxidative stress, neuroinflammation, and axonal injury — with benefits that hold at a chronic, 30-day timepoint.

[This page also stands in for my MSc research on molecular pathways in neurodegeneration — tell me if you’d rather split them into two separate pages.]