Scientists have found that the main psychoactive compound in marijuana the tetrahydrocannabinol (THC) and a few other active compounds in marijuana can promote the cellular removal of amyloid beta, a toxic protein associated with Alzheimer’s disease. THC in cannabis activates the same receptors as the body’s endocannabinoids.
The compounds also significantly reduced cellular inflammation, an underlying factor in the disease’s progression.
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“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 Salk Professor David Schubert, the senior author of the paper.
Alzheimer’s disease is a progressive brain disorder that leads to memory loss and can seriously impair a person’s ability to carry out daily tasks. It affects more than five million Americans according to the National Institutes of Health, and is a leading cause of death. It is also the most common cause of dementia and its incidence is expected to triple during the next 50 years.
It has long been known that amyloid beta accumulates within the nerve cells of the aging brain well before the appearance of Alzheimer’s disease symptoms and plaques. Amyloid beta is a major component of the plaque deposits that are a hallmark of the disease. But the precise role of amyloid beta and the plaques it forms in the disease process remains unclear.
The researchers found that high levels of amyloid beta were associated with cellular inflammation and higher rates of neuron death. Exposing the cells to THC reduced amyloid beta protein levels and eliminated the inflammatory response from the nerve cells caused by the protein, thereby 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, ” says 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.”
