Consistent with previous studies on TBI-induced cellular stress and mitochondrial dysfunction our data indicate that repetitive mTBI exacerbates dysregulation of proteins involved in mitochondrial respiration and synaptic plasticity (e.g., Cox6a1, Snca).36–39 This suggests that repetitive injury may intensify vulnerability to neurodegenerative processes observed in conditions like AD and PD, which are often marked by similar proteinopathies.40–43. This evidence concerns the gene COX6A1 and Alzheimer disease.