UCLA scientists have identified the intracellular mechanisms regulated by vitamin D which may help the body clear the brain of amyloid beta, the main component of plaques associated with Alzheimer’s disease.
The research published in the Journal of Alzheimer’s Disease found that vitamin D3 may activate specific genes and cellular signaling networks which help stimulate the immune system to clear the brain of amyloid beta protein.
The researchers drew blood from participants with Alzheimer’s as well as healthy controls. They isolated immune cells from the serum samplesm called macrophages, which are responsible for clearing amyloid beta and other waste products in the brain and body.
The immune cells were incubated overnight with amyloid beta. Then, the researchers added activated vitamin D to some of the cells to gauge the effect it had on amyloid beta absorption.
Previous research by the UCLA team has shown there are two types of patients; those who respond to addition of activated vitamin D and curcuminoids (a synthetic form of curcumin), referred to as Type I macrophages, and those who are improved only by adding activated vitamin D (Type II macrophages).
The researchers found that in both types of patients, the added vitamin D improved uptake of amyloid beta, while curcuminoids alone increased uptake 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, an assistant research biochemist in the department of biochemistry at UC Riverside when the study was conducted.
The researchers suggest the next step in the research is to conduct a clinical trial with vitamin D3 to assess the impact on Alzheimer’s patients.
Mathew T. Mizwicki, Danusa Menegaz, Jun Zhang, Antonio Barrientos-Durán, Stephen Tse, John R. Cashman, Patrick R. Griffin, Milan Fiala. Genomic and Nongenomic Signaling Induced by 1α,25(OH)2-Vitamin D3 Promotes the Recovery of Amyloid-β Phagocytosis by Alzheimer’s Disease Macrophages. Journal of Alzheimer’s Disease, 2012.