For several years, researchers have been looking for a way to defer the early onset of Alzheimer’s. As the only disease in the top 10 causes of death unable to be prevented, cured, or even slowed, Alzheimer’s disease is a top priority for many researchers, scientists, and doctors. Several conclusions and proposals have been brought up in the past decades, and several of them slipped out of our reach or are still being tested and evaluated. However, Salk Institute scientists have found preliminary evidence that tetrahydrocannabinol (THC) and other compounds found in marijuana can promote the cellular removal of amyloid beta (Aβ), which happens to be a toxic protein associated with Alzheimer’s disease. THC is the principal psychoactive constituent in marijuana and is the chemical responsible for most of marijuana’s psychological effects.
In a news article from Salk Institute, Salk Professor David Schubert, the senior author of the paper, states that their study is the first to be able to demonstrate their conclusion.
“Although other studies have offered evidence that cannabinoids might be neuroprotective against the symptoms of Alzheimer’s, we believe our study is the first to demonstrate that cannabinoids affect both inflammation and amyloid beta accumulation in nerve cells,”says Schubert.
Even though the studies were conducted on neurons grown in the laboratory, this discovery nonetheless offers insight on the role of inflammation in Alzheimer’s disease and paves a pathway for developing novel therapeutics for the serious disorder.
The disease is induced by amyloid beta proteins that accumulate within nerve cells as the brain ages. The heaping of these toxic proteins leads to the formation of plaque deposits in the brain, which is a large characteristic of Alzheimer’s. Alzheimer’s disease is a grave progressive brain disorder, destroying nerve connections in the brain, which makes it continuously more difficult to perform simple and basic tasks such as moving around, swallowing, and feeding yourself. Although there are several complications in the brain, this alone does not kill you. What does, is the complications that stem from it — some common examples being aspiration pneumonia, bedsores, malnutrition, and sepsis infections.
Salk researchers had found that high levels of amyloid beta (Aβ ) were heavily associated with cellular inflammation and higher rates of neuron death. They also successfully demonstrated that exposing the cells to THC reduced the amyloid beta protein levels and eradicated the inflammatory response from the nerve cells induced by the protein, allowing the nerve cells to survive.
“Inflammation within the brain is a major component of the damage associated with Alzheimer’s disease, but it has always been assumed that this response was coming from immune-like cells in the brain, not the nerve cells themselves,” states Antonio Currais, a postdoctoral researcher in Schubert’s laboratory and first author of the paper. “When we were able to identify the molecular basis of the inflammatory response to amyloid beta, it became clear that THC-like compounds that the nerve cells make themselves may be involved in protecting the cells from dying.”
To add, physical activity results in the production of endocannabinoids and some studies have successfully shown that exercise may slow the progression of Alzheimer’s disease. In a separate but relevant research study led by Schubert, his lab had found an Alzheimer’s drug candidate called J147 producing similar results. This study had led the scientists to discover the beneficial effect of endocannabinoids like THC.
Although these results are only the beginning to finding a way to successfully fight Alzheimer’s, the data from other existing research involving marijuana and Alzheimer’s support these findings and make this a plausible treatment in the near future.