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CANNABINOIDS ELIMINATE ALZHEIMER PROTEINS FORMING PLATES IN BRAIN CELLS

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Cannabis stimulates the aged brain

Alzheimer's disease is a progressive brain disorder that causes memory loss and can seriously impair a person's ability to perform daily tasks. According to National Institutes of Healthit affects more than five million Americans and is one of the leading causes of death. It is also the most common cause of dementia and its incidence is expected to triple over the next 50 years.

Preliminary laboratory studies at the Salk Institute show that THC reduces beta-amyloid proteins in human brain neurons

Scientists at the Salk Research Institute located in La Jolla, California. have found preliminary evidence that tetrahydrocannabinol (THC) and other compounds found in the cannabis plant may promote the cellular elimination of amyloid beta, a toxic protein associated with Alzheimer's disease.

Result of image search for "beta-amyloid"
One of the causes of Alzheimer's disease is the accumulation of senile plaques or amyloid plaques between neurons

While these exploratory studies have been conducted on laboratory-grown neurons, they may provide insight into the role of inflammation in Alzheimer's disease and provide clues for developing new treatments for the disorder.

"Although other studies have shown that cannabinoids may have an effect neuroprotective against the symptoms of Alzheimer's disease, we believe that our study is the first to demonstrate that cannabinoids affect both inflammation and accumulation of beta-amyloid in nerve cells, "says Professor David Schubert: Professor and Head of Cellular Neurobiology Laboratory at Salk.

It has long been known that beta-amyloid accumulates in nerve cells aging brain well before the onset of symptoms and plaques of Alzheimer's disease. Beta amyloid is a major component of the plaque deposits that characterize the disease. But the precise role of beta-amyloid and the plaques that it forms in the process of the disease remains uncertain.

In a manuscript published in June 2016 on the aging and the mechanisms of the disease , Salk's team studied modified nerve cells to produce high levels of beta-amyloid to mimic aspects of Alzheimer's disease.

The researchers found that high levels of amyloid beta were associated with cellular inflammation and higher rates of neuronal death. They demonstrated that exposure of THC cells reduced levels of beta-amyloid protein and eliminated the inflammatory response of nerve cells caused by the protein, allowing nerve cells to survive.

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"Inflammation in the brain is a major component of the damage associated with Alzheimer's disease, but it has always been assumed that this response came from immune-like cells in the brain, not the nerve cells themselves," says Antonio. Currais, postdoctoral. researcher in Schubert's laboratory and first author of the article. "Once we were able to identify the molecular basis of the inflammatory response to beta-amyloid, it became clear that the THC-related compounds produced by nerve cells could be involved in protecting cell death."

Brain cells have switches called endocannabinoid-activatable receptors, a class of lipid molecules made by the body that are used for intercellular signaling in the brain. The psychoactive effects of marijuana are caused by THC, a molecule of activity similar to endocannabinoids that can activate the same receptors. Physical activity leads to the production of endocannabinoids and some studies have shown that exercise can slow the progression of Alzheimer's disease.

Schubert pointed out that his team's findings had been made on exploratory laboratory models and that the use of THC-like compounds as a treatment should be tested in clinical trials.

In separate but related research, his lab has discovered an Alzheimer's drug candidate called J147 that also removes beta-amyloid from nerve cells and reduces the inflammatory response of nerve cells and the brain. It is the J147 study that has led scientists to discover that endocannabinoids are involved in the elimination of beta-amyloid and the reduction of inflammation.

"Today's results provide a better understanding of the complex effects of cannabis on the brain. Although this may have therapeutic potential in some situations, it is important to better understand the negative aspects as well, especially for pregnant women, adolescents and chronic users. "

Here is a list of the Society for Neuroscience describing some of the findings of different research:

  • Antenatal exposure to THC in rats has long-lasting effects on brain metabolites, making the animal more vulnerable to stress later in life (Robert Schwarcz, 609.12 summary).
  • Rats exposed to synthetic compounds similar to THC during fetal development show an alteration in the formation of neural circuits involved in adolescent learning and memory (Priyanka Das Pinky, abstract 424.17).
  • The consumption of cannabinoids by adolescent rats stimulates the activity of brain pathways responsible for habit formation (José Fuentealba Evans, 602.07 summary - survey ).
  • In adolescent rats, cannabinoids can disrupt the development of a network of important proteins to balance excitatory and inhibitory activity in a region of the brain involved in decision-making, planning, and self-control (Eliza Jacobs-Brichford , abstract 645.09 - abstract abstract ).
  • Long-term use of cannabinoids modifies the metabolism and connectivity of brain regions involved in learning and memory in adult mice (Ana M. Sebastião, abstract 778.08 - study ).
  • Treatment of mice with Alzheimer's disease with the psychoactive compound in marijuana improves memory and reduces neuronal loss, suggesting a possible treatment for human disease (Yvonne Bouter, abstract 467.14 - study summary ).
  • Preliminary laboratory studies conducted at Salk Institute show that THC reduces beta-amyloid proteins in human neurons.
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THC reduces the progression of toxic clusters of beta-amyloid proteins

The progression of Alzheimer's disease is based on toxic clusters of beta-amyloid proteins in the brain. THC has been shown to promote the cellular elimination of this toxic Alzheimer's protein from the brain. These results corroborate the ongoing evidence of the protective effects of cannabinoids, including THC, on patients with neurodegenerative disease.

Activation of endocannabinoids

Receptors are the "switches" of brain cells. These switches (receptors) can be activated by endocannabinoids, a class of lipid molecules made by the body that are used for intercellular signaling in the brain. One molecule of THC resembles endocannabinoids in that it can activate the same receptors. Endocannabinoids are naturally produced in the body through physical exercise. Some studies have even shown thatphysical exercise could also slow the progression of Alzheimer's disease. Moving slightly away from the subject, another study found that exercise also had a beneficial effect on intestinal bacteria.

Conclusion

Scientists stress that the findings of this study alone are not enough to prove that cannabis is a preventative measure or cure for Alzheimer's disease. The use of THC-like compounds as a therapy should still be the subject of clinical trials. However, the chances are good!

Tags : AlzheimerÉtudeNeuroscienceTHC