Writing in the March 6, 2012 issue of the Journal of Alzheimer's Disease, researchers at the University of California and the Scripps Institute elucidate mechanisms for vitamin D and a synthetic form of curcumin in clearing the brain of amyloid beta, a toxic protein that forms the plaques that are believed to be a major cause of the neurodegeneration that occurs in Alzheimer's disease.
Milan Fiala, MD of UCLA and colleagues studied the effects of vitamin D and curcumin on macrophages derived from the blood of healthy subjects and Alzheimer's disease patients. Macrophages are immune cells that engulf and consume pathogens and waste products (a process known as phagocytosis), including amyloid beta. Previous research conducted by the team demonstrated that the function of type I macrophages in Alzheimer's disease patients is improved by the addition of 1-alpha, 25-dihydroxyvitamin D3, an active form of the vitamin made in the liver and kidneys, as well as by curcuminoids; whereas type II macrophages are improved only by 1-alpha, 25-dihydroxyvitamin D3.
Dr Fiala's team determined that 1-alpha, 25-dihydroxyvitamin D3 is involved in opening a chloride channel which supports the uptake of amyloid beta in phagocytosis by both types of macrophages, and that curcuminoids activate the same chloride channel in type 1 macrophages only. They discovered that 1-alpha, 25-dihydroxyvitamin D3 stimulated the genetic transcription of the chloride channel and the receptor for 1-alpha, 25-dihydroxyvitamin D3 in type II macrophages. The mechanisms were dependent upon calcium and signaling by the MAPK pathway which aids in the communication of signaling from the cell membrane's vitamin D3 receptor to its DNA.
"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," lead author Mathew T. Mizwicki concluded.
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