Neuroprotective effect of cannabidiol, a non-psychoactive component from Cannabis sativa, on b-amyloid-induced toxicity in PC12 cells

This study used an animal model and all results are based from the use of lab-bred rats.  
The aim of the present study was to evaluate the neuroprotective effect of cannabidiol (CBD) against the effects of b-amyloid-induced nerve-brain damage.  Heavy accumulation of b-amyloid peptide (Αβ) (a set of base amino acids) has been suggested as one of the central causes of Alzheimer’s disease.  The mechanism by which Αβ induces death of cells in the brain is still unknown, however several mechanisms have been proposed.  

The study evaluated the effect of CBD on brain-nerve cells; specifically focusing on the reactive oxygen species (ROS) formation, cell membrane lipid peroxidation, and cell neuron apoptosis in cultured rat cells exposed to Αβ peptide. 

  • ROS is a natural part of the cellular metabolizing process natural to the body, but in excess can cause cell damage. 
  • Lipid peroxidation is the destruction of lipids/fats due to oxygen contact.  It is the process in which free radicals "steal" electrons from the fats in cell membranes causing cell damage and oxidization.
  • Apoptosis is also known as: 'programmed cellular death'. Apoptosis is considered a vital component of various processes including normal cell turnover, proper development and functioning of the immune system, hormone-dependent atrophy, embryonic development and chemical-induced cell death.

            Previous research indicates that exposure to Αβ peptide increases ROS levels and lipid peroxidation, and leads to brain cell damage; a causing factor in Alzheimer’s disease. Additionally, antioxidants, such as vitamins A, C, E, or those found heavily in carrots, spinach, kale, blueberries are known to reduce Αβ -induced injury from oxidative stress (which causes cell damage).

This study showed an increase in ROS and in lipid peroxidation levels after the introduction of Αβ peptides.  Results from this study suggest that CBD counteracted specific effects Αβ peptide.  Further, the introduction of CBD in b-amyloid effected cells created a reduction in cell death/apoptosis. The results suggest that CBD could exert a protective role at the execution phase of cell death.  Overall, CBD exerts a combination of neuroprotective, anti-oxidative and anti-apoptotic effects against Αβ peptide abuse.