(HealthDay News) – Vitamin D stimulates macrophages from patients with Alzheimer’s disease to allow phagocytosis of amyloid beta (Aβ42) through genomic and non-genomic signaling.

Noting that 1α,25-dihydroxyvitamin D3 (1,25D3) has been shown to stimulate Aβ42 phagocytosis recovery in macrophages, Mathew T. Mizwicki, PhD, from the University of California in Riverside, and colleagues investigated the intracellular mechanisms associated with this recovery using macrophages from Alzheimer’s patients and healthy individuals. The role of the vitamin D receptor bisdemethoxycurcumin was also explored.

The researchers found that, in macrophages from Alzheimer’s patients, 1,25D3 potentiated the 4,4-diisothiocyanostilbene-2,2-disulfonic acid-sensitive chloride channel (CIC-3) currents in type I and II cells. In addition, 1,25D3 upregulated CIC-3 mRNA expression in type II peripheral blood mononuclear cells. The CIC-3 blocker was attenuated by 1,25D3-induced Aβ42 phagocytosis. Mass spectrometry and computational results showed differences in the regulation of gene expression based on vitamin D receptor helices stability induced by 1,25D3 and curcuminoids.

“In closing, this work suggests that 1,25D3 can retune Alzheimer’s disease macrophages to efficiently phagocytose soluble Aβ42 by regulating the function of both extranuclear proteins (ie, non-genomic signaling) and expression of genes (genomic signaling),” Mizwicki and colleagues write.

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