Scientists at Salk Institute have uncovered preliminary evidence that tetrahydrocannabinol (or THC) as well as other compounds that are found in marijuana can promote the cellular removal of amyloid beta, which is a toxic protein associated with Alzheimer’s disease. During the conducted studies, tests were done on neurons that were grown in the laboratory. The findings may offer insight into the role of inflammation in Alzheimer’s disease and could offer some clues into the development of new therapeutics for the disorder.

Salk Professor David Schubert, senior author of the study says although the studies have offered evidence that cannabinoids might be neuroprotective against Alzheimer’s symptoms; we believe the study 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 eventually leads to memory loss and can seriously impair the individual’s ability to carry out everyday tasks. It affects as many as five million Americans according to the National Institutes of Health and is a top cause of death in the country. It is also the most common cause of dementia and its incidence is expected to triple within the next 50 years or so. Scientists have long known that amyloid beta accumulates inside the nerve cells of the aging brain many years before Alzheimer’s disease symptoms arise. Amyloid beta is a major component of the plaque deposits that are a hallmark for the disease, but the role of the amyloid beta and the plaques it forms in the disease process is still not clear.

The team published a manuscript in the June 2016 issue of Aging and Mechanism of Disease journal, where Salk and his team studied nerve cells altered to produce high levels of amyloid beta to mimic aspects of Alzheimer’s disease. Researchers quickly realized that high levels of amyloid beta were associated with cellular inflammation and higher rates of neuron death. They demonstrated that exposing the cells to THC actually reduced amyloid beta protein levels and eliminated the inflammatory response from the nerve cells caused by the protein, which allowed the nerve cells to continue to survive.

First author of the paper Antonio Currais, a postdoctoral researcher in Schubert’s laboratory said 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. 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.

Brain cells have receptors, which are basically like switches that can be activated by endocannabinoids which are a class of lipid molecule that are created by the body that are used for intercellular signaling in the brain. The psychoactive effects of marijuana are caused by THC, a molecule similar in activity to endocannabinoids that can activate the same receptors. Physical activity results in the production of endocannabinoids and some studies have shown that exercise may be able to slow down the progression of Alzheimer’s disease.

The team made it clear that their findings were conducted in exploratory laboratory models and that the use of THC-like compounds as a therapy would need to be tested in clinical trials before it could possibly become something used on a wide scale.

In separate research conducted, the lab found that Alzheimer’s drug candidate known as J147 that also is known to remove amyloid beta from nerve cells and reduces the inflammatory response in both nerve cells and within the brain. During the study of J147, scientists were led to the discovery that endocannabinoids are involved in the removal of amyloid beta and the reduction of inflammation.