CBD May Help Limit the “Second Wave” of Brain Damage After Traumatic Brain Injury, Study Finds
- Researchers from Gazi University suggest cannabidiol (CBD) may help reduce the delayed secondary damage following traumatic brain injury (TBI), which involves processes like glutamate excitotoxicity, inflammation, and metabolic disruption.
- CBD is noted for its non-intoxicating properties and potential benefits in restoring blood-brain barrier function, improving long-term potentiation, and reducing cognitive impairment when administered after the initial injury.
- The review emphasizes CBD's effects on metabolism after TBI, including increasing insulin receptor sensitivity, reducing brain insulin resistance, and mitigating high glucose's harmful impacts, as well as lowering tau protein hyperphosphorylation linked to neurodegeneration.
- The conclusions are based on a review of existing research rather than new clinical trials, highlighting CBD as a promising pharmacological tool to prevent secondary brain injury but requiring further experimental validation.
A new study published in Current Opinion in Toxicology by researchers from Gazi University says cannabidiol (CBD) may have potential as a treatment to blunt the delayed “secondary wave” of damage that can follow traumatic brain injury (TBI). The authors explain that while the initial injury is tied to the direct impact site, secondary damage can spread across the brain in the hours and days that follow, driven by processes such as glutamate excitotoxicity, inflammatory signaling, and metabolic disruption, including persistent high blood sugar. This later phase is linked to widespread neuronal death and lasting neurological problems even when the primary injury is localized.
According to the review, CBD could be relevant because it is non-intoxicating and has been associated in prior research with anti-inflammatory and neuroprotective effects. The authors write that CBD given anywhere from hours to months after the initial injury may help restore blood-brain barrier function, improve long-term potentiation, and reduce cognitive impairment. They also point to findings suggesting CBD may reduce neuroinflammation, ease glutamate-related toxicity, and help correct imbalances in excitatory and inhibitory signaling, including glutamatergic and GABAergic pathways.
The review also highlights metabolism as a key issue after TBI, noting that persistent hyperglycemia has been associated with worse outcomes. The authors say CBD may increase insulin receptor sensitivity, reduce brain insulin resistance, and mitigate the harmful effects of high glucose, while also reducing tau protein hyperphosphorylation, a process often linked with neurodegenerative changes.
While the paper frames CBD as a possible pharmacological tool to prevent secondary injury from worsening, it is a review rather than a new clinical trial, meaning its conclusions depend on the strength of existing evidence.