A new study suggests that marijuana compounds may remove toxic brain proteins associated with Alzheimer’s disease. Researchers from Salk Institute in California lab-grown tests to assess the effect of cannabis properties when clearing up brain plaque.
A new study, published in the journal Aging and Mechanisms of Disease, showed that compounds in marijuana could remove brain damage effects as well as neurological inflammation linked to Alzheimer’s disease. To achieve this purpose, researchers carried out tests in tetrahydrocannabinol (THC), a marijuana agent.
Tetrahydrocannabinol is the main psychoactive chemical found in the cannabis plant. The new study suggests that this component, as well as others marijuana’s compounds, contribute in the removal of the of beta-amyloid protein, which has been associated with Alzheimer’s disease.
The beta-amyloid protein comes from a larger protein found in the fatty membrane surrounding nerve cells, and the proteins present in it lead to the formation of brain plaques in individuals suffering from Alzheimer’s. Former studies have shown that the beta-amyloid protein is highly linked to Alzheimer’s diseases because it interferes with communication between brain neurons.
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The brain plaques cause memory problems (impaired memory) and other classical symptoms of the Alzheimer’s condition. Therefore, considered the recent high rates of the disease, it seems like marijuana treatments may prevent one of Alzheimer’s disease’s key features.
However, Salk Institute researchers do not count with a conclusion about the role the beta-amyloid protein plays in the development of the disease. Preventing beta-amyloid accumulation in the brain seems to be a viable option, but more studies must be conducted before applying medical marijuana to stop the Alzheimer’s process.
The research, which is still at an early stage, has observed only the protective effects of marijuana. Such sort of research has not been carried out yet in living human brains. Clinical trials will be needed to test marijuana effects in human brains. Researchers also must consider the side effects of using marijuana as a drug to treat neurodegeneration.
Increased production of beta-amyloid protein may lead to inflammation and nerve cell death
The lack of clarity in the role of beta-amyloid protein in Alzheimer’s disease is what has encouraged researchers to modify nerve cells to stimulate protein production and assess the feature of beta-amyloid production in the inflammatory process of Alzheimer.
The study’s senior author, Professor David Schubert, of the Salk Institute for Biological Studies in La Jolla, CA, and his colleagues, found that the rising in the production of beta-amyloid led to increased expression of pro-inflammatory proteins in nerve cells. As a consequence, inflammation and nerve cell death are likely to occur.
According to Antonio Currais, a member of Salk Institute for Biological Studies, who worked on the study, inflammation is a key feature linked to Alzheimer’s disease. However, it was believed that inflammation occurs as a result of immune-like cells in the brain and not a cellular process itself.
“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,” said Currais.
Further on, the team of researchers referred to the receptors contained in brain’s nerve cells and how they are activated by lipid molecules known as endocannabinoids. These particles include endogenous cannabinoid receptors which are found in different parts of the body: brain, organs, connective tissues, immune cells, and glands.
Considering that marijuana contains a component called tetrahydrocannabinol (THC), a similar chemical than the one naturally produced by endocannabinoids, researchers have thought about the viability of using THC to prevent nerve cell death.
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Currais explained that when trying to determine the molecular basis of the inflammatory response to amyloid beta, it was appreciated that THC compounds might play a role when preventing the cells from dying. This process occurs because the marijuana compound reduced beta-amyloid levels and acted putting an end to the inflammatory response to the beta-amyloid protein.
Even if the study represents the first step to prove the efficacy of THC in protecting nerve cells against beta-amyloid effects, researchers rely on the certitude that the findings might be a significant contribution for future assessments of Alzheimer’s treatments.
“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,” said senior author David Schubert.
Source: Huffington Post