Effect of cannabidiol on traumatic brain injury - related neuronal damage pathways

ENGİN A. B., ENGİN A.

CURRENT OPINION IN TOXICOLOGY, cilt.46, 2026 (ESCI, Scopus)

Özet

In traumatic brain injury (TBI), immediate damage occurs primarily in the brain area affected by the trauma. Late secondary damage develops due to glutamate excitotoxicity, proinflammatory cytokine release, and persistent high glucose effect, in the whole brain. Second wave is characterized by neuronal death leading to neurological disabilities regardless of the primary injury site. Cannabis is the most widely used outlawed drug worldwide however it's non-addictive compound, cannabidiol (CBD) has the potential to be successfully used in the treatment of neuronal damage resulting from the second wave of TBI. CBD treatment from hours to days to months after the primary insult restores blood brain barrier permeability, improves long-term potentiation and cognitive disorder. Moreover, disruption of axonal transmission, autophagy signaling, glutamatergic and y-aminobutyric acidergic (GABAergic) signaling unbalance, glutamate excitotoxicity, neuroinflammation, and synaptic dysfunction alleviate. CBD increases insulin receptor sensitivity, attenuates brain insulin resistance and high glucose effect as well as reduces tau protein hyperphosphorylation. Therefore, CBD could be an effective pharmacological intervention to prevent the enlargement of the secondary wave of TBI.