Targeting neuroinflammation and oxidative stress improves cognitive and sensorimotor outcomes following experimental traumatic brain injury

Repeated impacts induce acute neurobehavioral and molecular deficits in a mouse model of traumatic brain injury

Differential consequences of traumatic brain injury in male rat hippocampus hemispheres and the beneficial effect of neuropeptide Y.

Traumatic brain injury (TBI) initiates a complex cascade of secondary injury mechanisms, including neurovascular dysfunction, neuroinflammation, and glial activation, which progressively contribute to long-term neurological deficits. Although the primary mechanical insult is typically unilateral, secondary pathological...

Mas receptor activation promotes mitophagy and preserves neuronal function after traumatic brain injury.

Findings identify MasR as an endogenous regulator of PINK1/Parkin-mediated mitophagy and mitochondrial homeostasis following TBI and demonstrate that MasR signaling is required for preserving mitochondrial function and neurological outcomes after injury.

Potential neuroprotective effects of resveratrol against traumatic brain injury in rodent models: a systematic review and meta-analysis

ABSTRACT Background Oxidative stress, inflammation, and apoptosis following traumatic brain injury (TBI) cause secondary damage that leads to long-term neurological impairments. Though its effectiveness in TBI remains largely underexplored, the natural polyphenol resveratrol (RES) shows neuroprotective effects. This me...

Neuroprotective Effects of Nanocurcumin in Spinal Cord Injury: Modulation of Inflammatory and Inflammasome-Associated Signaling in an Integrated In Vivo, In Silico, and Machine-Learning Study.

Spinal cord injury (SCI) triggers secondary neuroinflammatory and inflammasome-associated responses that contribute to tissue damage and functional impairment. This study evaluated nanocurcumin in experimental SCI using integrated experimental, computational, and exploratory machine-learning approaches. Adult male Wist...

Hinokitiol Promotes Neural Repair After Spinal Cord Injury by Reprogramming Microglial Inflammatory and Redox Responses.

Hinokitiol supports neural repair after SCI by reprogramming microglial inflammatory-redox states, at least partly through Nrf2 signaling, which justifies further pharmacokinetic, sex-inclusive, and long-term safety studies.