Memory loss, decline in brain function and communication skills are all clear indicators of Alzheimer's disease. But the brain's chemistry begins to change long before these telltale signs appear through the accumulation of what are known as amyloid beta proteins. These proteins go on to form brain plaques that correspond with the neurodegenerative disease, but what if it were possible to intervene somehow? Scientists are reporting that exposure to certain compounds in marijuana can cleanse the brain of harmful amyloid beta cells, offering up new clues as to how we might stop the disease in its early stages.
While we are learning more about Alzheimer's everyday, with new insights into its destructive forces, the development of potential blood tests and treatments to reverse its symptoms being just a few recent breakthroughs in the area, there's a whole lot we still don't know.
How exactly the amyloid beta proteins give rise to plaques and in turn wreak havoc on the brain isn't entirely clear, but that hasn't stopped researchers working to avert the process altogether. The development of natural molecules, debris-clearing proteins and drugs inspired by snake venom have all shown promise as tools to stop or slow the buildup of plaques.
And now researchers at the Salk Institute have uncovered new evidence supporting another candidate, tetrahydrocannabinol (THC), the psychoactive ingredient in marijuana. Working with modified nerve cells engineered to produce high levels of amyloid beta, the researchers found that the presence of these proteins caused nerve cell inflammation and higher rates of neuron death.
But by exposing the cells to THC, they reduced levels of the amyloid beta proteins, which also had the effect of stopping inflammation of the nerve cells and allowing more of them to survive.
The idea that THC can put the brakes on amyloid beta proteins isn't entirely new. Another preclinical experiment at the University of South Florida in 2014 found that low doses of the compound could inhibit amyloid beta production. In fact, a 2008 paper demonstrated that THC binds to a key enzyme that induces aggregation of amyloid beta proteins, also inhibiting its buildup.
While the Salk research throws further weight behind the idea that THC can rid the brain of these harmful proteins and is useful for that reason, it also helps our understanding of the disease by identifying a source of brain inflammation: from the nerve cells in response to heightened amyloid beta levels. Research has shown that inflammation in the brain is not just a byproduct of the disease, but can actively worsen it, so understanding how it comes about could open up new avenues to treatment.
"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.
The researchers point out that these early experiments were carried out only on lab-grown cells, and that further testing in clinical trials would be required before such an approach is cleared for therapeutic use.
The research was published in the journal Aging and Mechanisms of Disease.
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