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Salk Institute scientists have found preliminary evidence that tetrahydrocannabinol (THC) and other compounds found in cannabis can promote the cellular removal of amyloid beta, a toxic protein associated with Alzheimer’s disease, reports Caxton Central.
“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.
THC is responsible for the majority of cannabis’ psychological effects, including the high, due to its natural pain-relieving properties.
Salk researchers have found 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 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.”
Brain cells have switches known as receptors that can be activated by endocannabinoids made by the body that are used for intercellular signalling in the brain. THC is 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 slow the progression of Alzheimer’s disease.