Researchers at the Salk Institute for Biological Studies have discovered preliminary evidence that tetrahydrocannabinol and other compounds typically found in marijuana may help reduce the accumulation of toxic proteins commonly associated with Alzheimer’s disease.
The researchers published their findings this month in the journal Aging and Mechanisms of Disease and reported these compounds helped promote the cellular removal of amyloid beta in studies conducted using lab-grown neurons. While the findings are preliminary, they may aid in the development of new ways to treat this common neurodegenerative condition.
In a statement, senior author and Salk professor David Schubert said that while similar studies had “offered evidence that cannabinoids might be neuroprotective against the symptoms” of the disease, he believes his team’s research is “the first to demonstrate that cannabinoids affect both inflammation and amyloid beta accumulation in nerve cells.”
Alzheimer’s disease is a progressive brain disorder that results in memory loss and can severely damage an individual’s ability to perform day-to-day tasks. Currently, the disorder affects more than five million Americans, according to US National Institutes of Health. It is also the primary cause of dementia and one of the leading causes of death among seniors.
David Schubert, the lead author of the study. (Credit: Salk Institute)
Possible link between THC, benefits of exercise in Alzheimer’s patients
Doctors have long known that amyloid beta accumulates in the nerve cells of the aging brain long before the first symptoms of Alzheimer’s disease are detectable. The protein is a primary component of the disease’s trademark plaque deposits, but its exact role in the progression of Alzheimer’s is still not fully known.
In their new study, Schubert and his colleagues altered nerve cells to produce high amounts of amyloid beta in order to mimic aspects of Alzheimer’s disease and found that elevated levels of the protein were associated with cellular inflammation and higher rates of neuron death.
Next, they exposed those cells to THC and found that the marijuana compound not only reduced amyloid beta levels but also reversed the nerve cells’ inflammatory response to the protein, thus allowing those cells to survive. The findings suggest cannabinoid-like compounds produced by the nerve cells themselves could prevent those cells from dying, the authors said.
Furthermore, they explained that receptors in brain cells can be activated by endocannabinoids, a class of lipid molecules which the body produces and uses for intercellular signaling in the brain, Schubert, Salk Institute colleagues Pamela Maher and Daniel Daughtery, and co-authors Oswald Quehenberger and Aaron Armando from the University of California, San Diego added.
While the researchers emphasize that the findings are the result of exploratory laboratory models and that the results need to be verified in clinical trials, they may indicate that endocannabinoids may explain why exercise has been shown to potentially slow Alzheimer’s progression and that the THC found in marijuana could have similar benefits.
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