A two-week course with high-dose center helped restore the function of two proteins, reducing the build-up of beta-amyloid plaque, a feature of Alzheimer’s disease and improved cognition in an experimental model of early onset familial Alzheimer’s – a form of Alzheimer’s that doctors know for sure is linked to genes – say researchers.
The proteins TREM2 and IL-33 are important for the ability of the brain’s immune cells to take up literally dead cells and other debris such as the beta-amyloid plaque that accumulates in patients’ brains – and the levels of both are Alzheimer’s is reduced.
The researchers report for the first time that downtown normalizes levels and functions, which improves cognition more than sevenfold, as it reduces the levels of the immune protein IL-6 in mice, which is accompanied by the high levels of inflammation found in Alzheimer’s, says Dr. Babak Baban, immunologist and co-dean for research at the Dental College in Georgia and the author of the study.
He joined colleagues at the Medical College of Georgia and in the Journal of Alzheimer’s Disease.
“Currently, we have two classes of medications to treat Alzheimer’s,” says Dr. John Morgan, neurologist and director of the movement and memory disorder programs in the MCG department of neurology. One class raises the levels of the neurotransmitter acetylcholine, which is also lowered in Alzheimer’s, and the other works by the NMDA receptors involved in communication between neurons and important for memory.
“But we have nothing to do with the pathophysiology of the disease,” the co-author wrote.
The DCG and MCG researchers have decided to investigate the ability of CBD to address some of the major brain systems that go wrong in Alzheimer’s.
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According to them, it seems that the levels of IL-33 normalize, a protein most of which finds expression in the brain, where it can sound the alarm that there is an invader such as the accumulation of beta-amyloids. There is emerging evidence of its role as a regulatory protein, the function of which is to increase or decrease the immune response depending on the environment, Baban says.
In Alzheimer’s disease, it includes inflammation and restoring the balance of the immune system. The upward and downward expression in health and disease could make IL-33 a good biomarker and treatment target for disease, say investigators.
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CBD also enhances the expression of the trigger receptor expressed on myeloid cells 2 or TREM2, which occurs on the cell surface where it combines with another protein to send out signals that activate cells, including immune cells. In the brain, its expression is on the microglial cells, a special population of immune cells found only in the brain, where it is the key to eliminate invaders such as a virus and irreversibly damaged neurons.
Low levels of TREM2 and rare variations in TREM2 are associated with Alzheimer’s, and in their mouse experiments, supported by the National Institutes of Health, TREM2 and IL-33 were both low.
Increasing useful proteins by 7 and 10 times
According to them, downtown treatment increased elevated levels of IL-33 and TREM2 – sevenfold and tenfold, respectively.
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Both are essential for a natural, continuous cleaning process in the brain, called phagocytosis, in which microglial cells regularly consume beta-amyloid, which is frequently produced in the brain, resulting from the breakdown of amyloid-beta precursor protein, which is important is for the synapses, or connection points, between neurons, and which interrupt the plaque.
The influence of the CBD on brain function in the mouse model of early onset Alzheimer’s is assessed using methods such as the ability to distinguish between a known item and a new one, as well as the movement of the rodents.
People with Alzheimer’s can experience movement problems such as stiffness and impaired gait, says Dr. Hesam Khodadadi, a graduate student working in Baban’s laboratory. Mice with the disease walk in an endless tight circle, behaviors that have stopped treating downtown, says Khodadadi, the first author of the study.
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Next steps include determining optimal doses and administering CBD earlier in the disease process. The compound was given in the late stages for the published study, and now the researchers are using it at the first signs of cognitive decline, Khodadadi says. They are also investigating delivery systems, including the use of an inhaler that can help deliver the CBD directly into the brain. For the published studies, downtown was placed in the abdomen of the mice every other day for two weeks.
A company has developed animal and human inhalers for the investigators who also investigated the effect of CBD on adult respiratory distress syndrome, or ARDS, an accumulation of fluid in the lungs which is a major and deadly complication of COVID-19 , as well as other serious illnesses such as sepsis and severe trauma. The CBD doses used for the Alzheimer’s study were the same as those the researchers successfully used to reduce the “cytokine storm” of ARDS, which could irreversibly damage the lungs.
Familial disease is an inherited version of Alzheimer’s in which symptoms usually occur in the thirties and forties and occur in about 10-15% of patients.
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CBD should be at least as effective in the more common, non-familial type of Alzheimer’s, which is likely to have more targets for CBD, Baban says. They are already looking at its potential in a model of this more common type and are continuing to set up a clinical trial.
Plaques as well as neurofibrillary tangles, a collection of protein tau in neurons, are the major components of Alzheimer’s, Morgan says. Beta-amyloid usually occurs 15-20 years or longer before dementia in the brain, and the occurrence of tau tangles, which can occur up to 10 years later, correlates with the onset of dementia. There is an interaction between beta-amyloid and tau that reduces the dysfunction of each, Morgan says.
The Food and Drug Administration is scheduled to rule by early June on a new drug, aducanumab, which will be the first to attack beta-amyloid and help clean it up, Morgan said.
(Source: Augusta University media)
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