Amid the rapidly changing political climate surrounding medical marijuana, researchers at University of South Florida (USF) found that low levels of delta-9-tetrahydrocannabinol (THC), a compound in marijuana, have the potential to slow or halt Alzheimer’s disease progression. Extremely low doses of THC were shown to reduce the production of amyloid beta and prevent amyloid aggregates associated with Alzheimer’s.
“Decreased levels of amyloid beta means less aggregation, which may protect against the progression of Alzheimer’s disease,” said lead study author Chuanhai Cao, PhD, a neuroscientist at the Byrd Alzheimer’s Institute and the USF College of Pharmacy, in a news release from USF. “Since THC is a natural and relatively safe amyloid inhibitor, THC or its analogs may help us develop an effective treatment in the future.” Further reading on amyloid and its involvement in Alzheimer’s disease can be found on Alzheimer’s News Today.
Described in “The Potential Therapeutic Effects of THC on Alzheimer’s Disease,” published in Journal of Alzheimer’s Disease, Dr. Cao and colleagues exposed cells that express amyloid to THC and measured the effects with a few different assays. The team found THC directly interacted with amyloid peptide to inhibit aggregation. There were no negative impacts of low-dose THC on cell viability.
On top of these findings, THC also enhanced mitochondrial function in the brain, helping to supply energy, transmit signals, and maintain brain health. The addition of caffeine to THC treatment had no added benefit.
“THC is known o be a potent antioxidant with neuroprotective properties, but this is the first report that the compound directly affects Alzheimer’s pathology by decreasing amyloid beta levels, inhibiting its aggregation, and enhancing mitochondrial function,” said Dr. Cao.
But this by no means suggests Alzheimer’s patients, or individuals who are at a higher risk for Alzheimer’s, should use marijuana. Dr. Cao’s laboratory showed low doses of THC exhibited therapeutic benefits that outweighed the risks of THC toxicity and memory impairment.
“Are we advocating that people use illicit drugs to prevent the disease? No,” said Neel Nabar, a co-author and MD/PhD candidate at USF. “It’s important to keep in mind that just because a drug may be effective doesn’t mean it can be safely used by anyone. However, these findings may lead to the development of related compounds that are safe, legal, and useful in the treatment of Alzheimer’s disease.”
There are compounds in the body that are similar to THC. Naturally-occurring cannabinoid molecules interact with cannabinoid receptors similar to how THC isolated from marijuana interacts. These and any other molecules similar to THC may serve as starting points for finding related compounds with therapeutic benefit.
Dr. Cao and his team will be furthering their research to ensure safety and efficacy of drug compounds. There are plans to move on to a testing platform that involves a genetically-engineered mouse model of Alzheimer’s. “The dose and target population are critically important for any drug, so careful monitoring and control of drug levels in the blood and system are very important for therapeutic use, especially for a compound such as THC,” concluded Dr. Cao.
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