human brain neurons

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 Health, it affects more than five million Americans and is a leading cause 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. found preliminary evidence that tetrahydrocannabinol (THC) and other compounds found in the cannabis plant can promote cellular elimination of amyloid beta, a toxic protein associated with Alzheimer's disease.

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One of the causes of Alzheimer's disease is the buildup of senile plaques or amyloid plaques between neurons

Although these exploratory studies were conducted on neurons cultured in the laboratory, they may provide a better understanding of the role of inflammation in Alzheimer's disease and provide avenues for the development of 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 our study is the first to show that cannabinoids affect both inflammation and the buildup of beta-amyloid in nerve cells, ”says Professor David Schubert: Professor and head of the cell neurobiology laboratory at Salk.

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

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

Researchers found that high levels of amyloid beta were associated with cell inflammation and higher rates of neuronal death. They demonstrated that exposure of cells to THC reduced levels of beta-amyloid protein and suppressed the inflammatory response in nerve cells elicited by the protein, thus 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 comes 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 for the inflammatory response to beta-amyloid, it became evident that the THC-related compounds produced by nerve cells may be involved in protecting cell death."

Brain cells have switches called receptors that can be activated by endocannabinoids, 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, an activity molecule similar to that of endocannabinoids that can activate the same receptors. Physical activity leads to the production of endocannabinoids, and some studies have shown that exercise may slow the progression of Alzheimer's disease.

Schubert pointed out that his team's findings were 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 discovered an Alzheimer's disease drug candidate called J147 that also removes beta-amyloid from nerve cells and reduces the inflammatory response of nerve cells and the brain. It was the study of J147 that led scientists to discover that endocannabinoids are involved in the elimination of beta-amyloids and the reduction of inflammation.

“Today's results provide insight into 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 from the Society for Neuroscience outlining some of the findings from different research:

  • Prenatal exposure to THC in rats has lasting effects on brain metabolites, making the animal more vulnerable to stress later in life (Robert Schwarcz, abstract 609.12).
  • Rats exposed to synthetic compounds similar to THC during fetal development show an alteration in the formation of neural circuits involved in learning and memory in adolescence (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, abstract 602.07 - survey ).
  • In adolescent rats, cannabinoids can disrupt the development of a protein network important for balancing 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).
  • Prolonged use of cannabinoids alters the metabolism and connectivity of regions of the brain 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 found in marijuana improves memory and reduces neuronal loss, thus 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 clumps of beta-amyloid proteins in the brain. THC has been shown to promote cellular elimination of this toxic Alzheimer's protein from the brain. These results support the continuing evidence for 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. A THC molecule resembles endocannabinoids in that it can activate the same receptors. Endocannabinoids are produced naturally in the body through exercise. Some studies have even shown thatphysical exercise could also slow the progression of Alzheimer's disease. Stepping away from the subject slightly, another study found that exercise also had a beneficial effect on body composition. intestinal bacteria.


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

Tags : AlzheimerEtudeNeuroscience
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