Depending on age and medical condition, marijuana can have therapeutic benefits or it can be harmful. Seeing as marijuana is growing in popularity and becoming legal in many places around the world, there has been a growing necessity to really understand its effects on humans. Researchers have been conducting more in-depth studies to make sure people know when, and in what conditions, consuming marijuana could be useful, and when it could be detrimental.
One such study has revealed that compounds found in marijuana, such as the psychoactive compound delta-9-tetrahydrocannabinol (THC), may improve memory in Alzheimer’s patients and mitigate some of the disease’s symptoms. On the contrary, marijuana exposure in the womb or during adolescence has a negative effect. It has been found to disrupt learning and memory, damage communication between brain regions, and disturb levels of key neurotransmitters and metabolites in the brain. These findings were presented at Neuroscience 2018, the annual meeting of the Society for Neuroscience and the world’s largest source of emerging news about brain science and health.
Press conference moderator Michael Taffe, PhD, of Scripps Research Institute and an expert in substance abuse research, said:
“Today’s findings lend new understanding of the complex effects that cannabis has on the brain. While it may have therapeutic potential in some situations, it is important to get a better understanding of the negative aspects as well, particularly for pregnant women, teens, and chronic users.”
The Good And The Bad
Here’s a list by the Society for Neuroscience outlining some of the findings from different research:
- Prenatal exposure to THC in rats has lasting effects on metabolites in the brain, making the animal more vulnerable to stress later in life (Robert Schwarcz, abstract 609.12).
- Rats exposed to synthetic compounds that are similar to THC during fetal development show impaired formation of the neural circuits involved in learning and memory as adolescents (Priyanka Das Pinky, abstract 424.17).
- Cannabinoid use by adolescent rats boosts activity in brain pathways responsible for habit formation (José Fuentealba Evans, abstract 602.07 – study).
- In adolescent rats, cannabinoids may disturb the development of a protein lattice important for balancing excitatory and inhibitory activity in a brain region involved in decision-making, planning, and self-control (Eliza Jacobs-Brichford, abstract 645.09 – study abstract).
- Long-term cannabinoid use alters metabolism and connectivity of brain regions involved in learning and memory in adult mice (Ana M. Sebastião, abstract 778.08 – study).
- Treating Alzheimer’s disease mice with the psychoactive compound found in marijuana improves memory and reduces neuronal loss, suggesting a possible therapy for the human disease (Yvonne Bouter, abstract 467.14 – study abstract).
- Preliminary lab studies at the Salk Institute find THC reduces beta-amyloid proteins in human neurons.
THC Helping With Alzheimer’s Disease
The kickstarter to the progression of Alzheimer’s disease is toxic clumps of amyloid beta protein in the brain. THC – tetrahydrocannabinol, an active compound in marijuana – has been found to promote the cellular removal of this toxic Alzheimer’s protein from the brain. These findings support standing evidence of the protective effects of cannabinoids, THC included, on patients with neurodegenerative disease.
Senior author of the paper, David Schubert, from the Salk Institute for Biological Studies in California, said:
“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.”
Schubert and his colleagues conducted exploratory studies on the effects of THC on human neurons grown in the lab that mimic the effects of Alzheimer’s disease. They were searching for clues to developing novel therapeutics for the disorder.
The Salk Institute team studied nerve cells altered to produce high levels of amyloid beta to mimic aspects of Alzheimer’s disease. What they discovered was that high levels of amyloid beta were associated with cellular inflammation and higher rates of neuron death. Then, by exposing the cells to THC, they were able to reduce amyloid beta protein levels and eliminated the inflammatory response from the nerve cells caused by the protein, thereby allowing the nerve cells to survive.
Antonio Currais, a postdoctoral researcher in Schubert’s laboratory and first author of the paper, said:
“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. 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.”
Receptors are the “switches” of brain cells. These switches (receptors) can be turned on (activated) by endocannabinoids, a class of lipid molecules made by the body that are used for intercellular signaling in the brain. A THC molecule is similar to endocannabinoids in the way that it can activate the same receptors. Endocannabinoids are naturally produced in the body through physical exercise. Some studies have even shown that exercise too may slow the progression of Alzheimer’s disease. Jumping off topic slightly, a different study revealed that exercise also has a beneficial effect on gut bacteria composition.
These findings were conducted in exploratory laboratory models. The scientists make it a point to state that this study’s findings alone are not enough to prove that marijuana is a preventative measure or a cure to Alzheimer’s disease. The use of THC-like compounds as a therapy would need to be tested further in clinical trials. However, the odds are looking good!
Correction: The previous version of this article stated that the research was published by Neuroscience, it has been corrected to the Society for Neuroscience.