Cortical Neuroprotective Mechanisms of Exercise Training in Post-Traumatic Brain Injury: A Systematic Review.

Area of Science:

• Neuroscience
• Molecular Biology
• Exercise Physiology

Background:

• Traumatic brain injury (TBI) induces cortical dysfunction via oxidative stress, neuroinflammation, apoptosis, and impaired neurogenesis.
• Molecular mechanisms underlying TBI include mitochondrial dysregulation and altered neurotrophic signaling.

Purpose of the Study:

• To systematically review the effectiveness of exercise training on molecular dysregulation and motor function in post-TBI.
• To evaluate exercise's impact on oxidative stress, neuroinflammation, apoptosis, neurogenesis, and neurotrophic signaling in TBI models.

Main Methods:

• Systematic review following PRISMA 2020 guidelines, searching PubMed, EMBASE, and Web of Science.
• Inclusion of 35 studies on exercise training in post-TBI animal models (voluntary wheel running, treadmill running, swimming).
• Quality assessment using the CAMARADES checklist.

Main Results:

• Exercise training increased cortical glutathione and Na+/K+-ATPase activity, reducing oxidative stress.
• Exercise reduced microglial and astrocytic reactivity and pro-inflammatory markers (IL-1β, TNF-α).
• Exercise training decreased caspase activity, increased HSP20, reduced apoptosis, enhanced motor function, neurogenesis, and BDNF signaling.

Conclusions:

• Exercise training improves motor function and provides cortical neuroprotection in TBI rodents.
• Benefits are mediated by reduced oxidative stress, neuroinflammation, and apoptosis, alongside enhanced neurotrophic signaling and neurogenesis.
• Regulation of let-7c, IL-6, and mitochondrial function by exercise in TBI requires further investigation.