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Published on: March 9, 2012
by Traci Pederson for Psych Central
Vitamin D3 may activate key genes and networks to help trigger the immune system to get rid of the amyloid beta protein, the core component of destructive plaques in the brain linked to Alzheimer’s disease, according to a new study.
Previous lab work has shown that particular immune cells in people with Alzheimer’s respond well to vitamin D3 and curcumin (found in turmeric spice) by stimulating the immune system to clear the brain of amyloid beta; however, researchers were unsure of exactly how this worked.
Vitamin D3 is the form that is produced by the skin with the help of sunlight and is also found in milk.
“This new study helped clarify the key mechanisms involved, which will help us better understand the usefulness of vitamin D3 and curcumin as possible therapies for Alzheimer’s disease,” said study author Milan Fiala, M.D., a researcher at the David Geffen School of Medicine at UCLA and the Veterans Affairs Greater Los Angeles Healthcare System.
For the study, blood samples were taken from both Alzheimer’s patients and healthy controls; researchers then isolated the macrophages (critical immune cells), which are responsible for clearing out amyloid beta and other waste materials throughout the brain and body.
The scientists incubated these immune cells overnight with amyloid beta. In addition, an active form of vitamin D3 (called 1a,25-dihydroxyvitamin D3 — which is naturally produced in the body through enzymatic conversion in the liver and kidneys) was added to some of the cells to see if it had an effect on amyloid beta absorption.
Prior research by this team revealed that there are at least two types of patients and macrophages: Type I macrophages are improved with the addition of 1a,25-dihydroxyvitamin D3 and curcuminoids (a synthetic form of curcumin), while Type II macrophages are improved with the addition of only 1a,25-dihydroxyvitamin D3.
In both Type I and Type II macrophages, 1a,25-dihydroxyvitamin D3 was critical in opening a specific chloride channel called chloride channel 3 (CLC3), which is important in supporting the uptake of amyloid beta through the process known as phagocytosis. Curcuminoids activated this chloride channel only in Type I macrophages.
“Our findings demonstrate that active forms of vitamin D3 may be an important regulator of immune activities of macrophages in helping to clear amyloid plaques by directly regulating the expression of genes, as well as the structural physical workings of the cells,” said study author Mizwicki, who was an assistant research biochemist in the department of biochemistry at UC Riverside when the study was conducted.
According to the researchers, the next step would include a clinical trial with vitamin D3 to determine its impact on Alzheimer’s patients. Previous studies by other teams have shown that a low serum level of 25-hydroxyvitamin D3 may be tied to cognitive decline.
It is too early to suggest a specific vitamin D3 dosage to help with Alzheimer’s disease and brain health, the researchers said. They add that current studies continue to reveal that Vitamin D3 may be helpful in reducing the incidence of several human diseases.
The study is published in the Journal of Alzheimer’s Disease.
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