In a research paper published in the international journal Aging and Mechanisms of Disease, researchers from the Salk Institute found prima facie evidence that tetrahydrocannabinol (THC) and other compounds in cannabis can promote beta starch. The protein is removed from the cell, and beta amyloid is a toxic protein associated with Alzheimer's disease. Although this study was carried out in laboratory-grown neurons, it provides new clues for the development of new therapies for the treatment of Alzheimer's disease.
Researcher David Schubert said that although studies have shown that cannabinol can help fight the symptoms of Alzheimer's disease, we believe that the study first demonstrated that cannabinol can not only affect inflammation, but also affect amyloid beta in nerve cells. The accumulation in the middle. Alzheimer's disease is a progressive brain disorder that causes loss of memory in individuals and severely impairs an individual's ability to perform daily life; according to data from the National Institutes of Health, the disease affects more than 5 million in the United States. Human health, and will directly lead to death of the patient.
Scientists have long been unaware of how beta amyloid accumulates in aging brain cells before Alzheimer's symptoms and plaques appear. Amyloid beta is the major group of plaques deposited in nerve cells. The score, but the precise role played by it and the process researchers of the plaque formed are not clear. In the article, the researchers modified nerve cells to produce high levels of amyloid beta to mimic the onset of Alzheimer's disease.
The researchers found that high levels of amyloid beta are directly associated with cellular inflammation and a high proportion of neuronal death, reducing amyloid levels and eliminating nerve cells triggered by the protein when exposed to tetrahydrocannabinol. An inflammatory response that causes nerve cells to continue to survive. Researcher Antonio Currais believes that inflammation inside the brain is the main cause of brain damage in Alzheimer's patients, and we suspect that this response comes from immune-like cells in the brain, not the nerve cells themselves.
There are receptors called receptors in brain cells that can be activated by endogenous cannabinoids. Physical activity often produces endocannabinoids. Studies have shown that exercise can also help slow the progression of Alzheimer's disease. In another study, the researchers found that an Alzheimer's drug candidate J147 can also remove beta amyloid in nerve cells and reduce inflammatory responses in nerve cells and brain. It can also help scientists to elucidate the role of endogenous cannabinoids in removing beta amyloid and inflammation in the brains of Alzheimer's patients.
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