Hackerbrief: Cannabinoids Show Promise in Removing Alzheimer's Plaque-Forming Proteins from Brain Cells, Salk Institute Study Reveals
Preliminary laboratory research from the Salk Institute suggests that tetrahydrocannabinol (THC) and other cannabis compounds may help brain cells remove amyloid beta, a toxic protein associated with Alzheimer's disease. Conducted on human neurons in a lab setting, these exploratory studies indicate cannabinoids could provide insights into inflammation's role in Alzheimer's and potentially lead to new treatments. Salk Professor David Schubert highlighted that this study is believed to be the first to show cannabinoids affecting both inflammation and amyloid beta accumulation in nerve cells. The research observed that THC significantly reduced amyloid beta levels and inflammatory responses in engineered nerve cells, improving cell survival. This mechanism involves brain cell receptors activated by both natural endocannabinoids and THC.
Scientists at the Salk Institute have uncovered preliminary laboratory evidence suggesting that tetrahydrocannabinol (THC) and other compounds found in marijuana can facilitate the cellular removal of amyloid beta, a toxic protein linked to Alzheimer's disease. These exploratory studies, conducted on human neurons grown in the lab, indicate that cannabinoids may offer insights into the role of inflammation in Alzheimer's and could lead to new therapeutic approaches. Salk Professor David Schubert noted, “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.” Alzheimer's disease affects over five million Americans and is projected to triple in incidence over the next 50 years.
The Salk team studied nerve cells engineered to produce high levels of amyloid beta, mimicking aspects of Alzheimer's. They observed that elevated amyloid beta levels correlated with cellular inflammation and increased neuron death. Exposing these cells to THC significantly reduced amyloid beta protein levels and eliminated the associated inflammatory response, thereby enhancing nerve cell survival. Antonio Currais, a postdoctoral researcher and first author, explained, “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 possess receptors activated by endocannabinoids, lipid molecules naturally produced by the body for intercellular signaling; THC activates these same receptors.
