In an interview, the researchers state, "the clinical implications are that vitamin D3 protects the brain through the immune system and that recommended blood levels of the 25-hydroxy vitamin D3 should be maintained in all seasons including winter when the sun is not helping to produce vitamin D in the skin."
Brain clearance of amyloid-beta 1-42 (Aβ-42) by innate immune macrophages (a type of white blood cell, called microglial cell when found in the central nervous system) is required for maintenance of normal brain function. This process of phagocytosis (the process where one cell engulfs/eats something) is defective in AD patients.
In their latest laboratory studies, the research team isolated macrophages from blood samples taken from patients with AD and healthy controls. They incubated the cells overnight with amyloid-beta, some in the presence of vitamin D3 and/or curcuminoids.
The researchers observed that vitamin D3 activates a specific chloride channel that is important in the clearance of Aβ-42 in both types of AD macrophages (type I and type II).
It appears from this work that vitamin D3 can "retune AD macrophages to efficiently phagocytose soluble Aβ-42 by regulating the function of both extranuclear proteins (ie, nongenomic signaling) and expression of genes (genomic signaling)," the researchers report.
Source: Genomic and Nongenomic Signaling Induced by 1α,25(OH)2-Vitamin D3 Promotes the Recovery of Amyloid-β Phagocytosis by Alzheimer's Disease Macrophages
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