The active ingredient of Marijuana prevents the formation of tetrahydrocannabinol alzheimer plates

Scientists from the Salk Institute have found the first evidence showing that tetrahydrocannabinol (THC) and other components in marijuana eliminate the cellular amyloid beta protein that causes Alzheimer's disease. Experimental studies are being studied in neurons developed in the laboratory and unique therapies are developed for inflammation in Alzheimer's disease.
Although other studies have presented evidence that cannabinoids may be neuroprotective against Alzheimer's symptoms, we believe that our study demonstrates the initial accumulation of both inflammation and neuronal cells in the neuron cells, diğer says David Schubert, Professor of Salk Institute. Alzheimer's is a brain disorder that causes memory loss. This disease, which affects only 5 million people in the US, is expected to triple in the next 50 years. Amyloid beta accumulation is the most important constituent of plaque formation. Amyloid beta is a phenomenon which is still being investigated by helping the formation of plaques and developing the disease. In June 2016, the Aging and Mechanisms of Disease magazine published a study that simulated Alzheimer's disease by producing large amounts of amyloid beta.

Researchers found that large amounts of amyloid beta were associated with cellular inflammation and high neuronal death. The researchers who gave tetrahydrocannabinol (THC) to the cells were able to lower the amyloid beta level and prevent the death of nerve cells by eliminating inflammation in the nerve cells. Inin Since the main cause of inflammation in the brain is thought to be associated with Alzheimer's disease, nerve cells have been ignored because it is assumed that the cause comes from immune-like cells in the brain for a long time. When we describe the molecular response of amyloid beta, it will be clear how THC-like compounds protect the cell from dying, k says postdoctoral researcher Antonio Currais. It was known that brain cells were activated by receptors called endocannabinoids. These lipid molecules produced by the body are used for the transmission of intracellular signaling in the brain. The psychoactive effects of THC in cannabis may activate the same receptors as endocannabinoids. It has been shown in some studies that endocannabinoids produced as a result of physical activity slow the progression of Alzheimer's disease. The findings of Schubert and his team on discovery lab models suggest that THC-like compounds may need to be tested clinically before use. In a different, but related study, Alzheimer's drug candidate J 147 showed that by removing the amyloid beta from the nerve cells, it reduced the inflammation response in both the nerve and the brain. J147 was instrumental in discovering that endocannabiods were effective in amyloid beta pavement and in reducing inflammation. The Salk Institute David Schubert In Alzheimer's research, it's a good thing to say.


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