Neuroprotective

Neuroprotection refers to mechanisms that preserve neuronal structure or function against ischemic, excitotoxic, oxidative, or inflammatory injury. Preclinical work dating to Hampson, Mechoulam and colleagues (1998, PNAS) showed that CBD and THC attenuate glutamate-induced neurotoxicity in cortical cultures via antioxidant activity independent of CB1 receptors, and subsequent rodent studies have reported benefits in models of stroke, Huntington's disease, and traumatic brain injury. In humans, however, clinical evidence remains insufficient to limited (NASEM 2017): trials in Parkinson's disease, Alzheimer's disease, amyotrophic lateral sclerosis, and Huntington's disease have been small, short, or underpowered for disease-modification endpoints. Proposed mechanisms include reduction of oxidative stress, modulation of mitochondrial calcium handling, CB2-mediated suppression of microglial activation, and adenosine-mediated inhibitory tone. Regulatory agencies have not approved any cannabinoid for a neurodegenerative indication, and claims of neuroprotection in consumer products are not evidence-based as of April 2026. → See also: CBD, THC, Endocannabinoid System.