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The accumulation of amyloid-beta (A) plaques and the hyperphosphorylation of tau proteins contribute to mitochondrial abnormalities and exacerbate oxidative damage

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In addition, GSTs are also involved in conferring multidrug resistance with a non-catalytic mechanism through their inhibition of the JNK signaling pathway, an event that protects tumoral cells from apoptosis, as it will be detailed later

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Stroke subtype-specific interventions address distinct metabolic vulnerabilities: cardioembolic strokes with high TMAO benefit from fecal transplant and CPT1A inhibitors, while lacunar strokes with NAD + depletion respond to NAD + precursors and time-restricted feeding (TRF) (Fig