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The brain is particularly vulnerable to oxidative stress due to its high oxygen consumption, abundant polyunsaturated fatty acids, and relatively modest antioxidant defenses compared to other organs [1][2][48]

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Through a number of chemical reactions, mitochondria break down glucose into energy (fuel) known as adenosine triphosphate (ATP)

NSAIDs can delay disease onset, ameliorate symptomatic severity, and slow cognitive decline [15]

111 Additionally, GSTs play a role in antiepileptic drug resistance, with elevated levels of GSTP1 in the brain correlating with medication intractability