ACTIVE INGREDIENT IN CANNABIS PROTECTS AGING BRAIN CELLS

Salk researchers find cannabinol preserves mitochondrial function and prevents oxidative damage to cells

LA JOLLA—Decades of research on medical cannabis has focused on the compounds THC and CBD in clinical applications. But less is known about the therapeutic properties of cannabinol (CBN). Now, a new study by Salk scientists shows how CBN can protect nerve cells from oxidative damage, a major pathway to cell death. The findings, published online January 6, 2022, in the journal Free Radical Biology and Medicine, suggest CBN has the potential for treating age-related neurodegenerative diseases, like Alzheimer’s.

“We’ve found that cannabinol protects neurons from oxidative stress and cell death, two of the major contributors to Alzheimer’s,” says senior author Pamela Maher, a research professor and head of Salk’s Cellular Neurobiology Laboratory. “This discovery could one day lead to the development of new therapeutics for treating this disease and other neurodegenerative disorders, like Parkinson’s disease.”

Healthy mitochondria (green); mitochondria showing the effects of oxidative stress (blue); and oxidative stress with CBN (red). Insets show higher magnification of the structure of the mitochondria
Healthy mitochondria (green); mitochondria showing the effects of oxidative stress (blue); and oxidative stress with CBN (red). Insets show higher magnification of the structure of the mitochondria.
Click here for a high-resolution image.
Credit: Salk Institute

Derived from the cannabis plant, CBN is molecularly similar to THC, but is not psychoactive. It’s also less heavily regulated by the FDA. Previous research by Maher’s lab found that CBN had neuroprotective properties, but it wasn’t clear how it worked. Now, this new study explains the mechanism through which CBN protects brain cells from damage and death.

Maher’s team looked at the process of oxytosis, also called ferroptosis, which is thought to occur in the aging brain. Growing evidence suggests that oxytosis may be a cause of Alzheimer’s disease. Oxytosis can be triggered by the gradual loss of an antioxidant called glutathione, causing neural cell damage and death via lipid oxidation. In the study, the scientists treated nerve cells with CBN, and then introduced an agent to stimulate oxidative damage.

They further found that the CBN worked by protecting mitochondria, the cell’s powerhouses, within the neurons. In damaged cells, oxidation caused the mitochondria to curl up like donuts—a change that’s also been seen in aging cells taken from the brains of people with Alzheimer’s disease. Treating cells with CBN prevented the mitochondria from curling up and kept them functioning well.

To confirm the interaction between CBN and mitochondria, researchers then replicated the experiment in nerve cells that had the mitochondria removed. In these cells, CBN no longer demonstrated its protective effect.

“We were able to directly show that maintenance of mitochondrial function was specifically required for the protective effects of the compound,” Maher said.

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