Scientists from UCLA, UC Riverside and the Human BioMolecular Research Institute have found that Vitamin D3 together with Curcumin, a substance found in Turmeric Spice, stimulates the immune system to clear the brain of Amyloid Beta, which is found in the plaques of Alzheimer’s Disease.
In the study, blood samples from Alzheimer’s patients and control subjects were collected. The monocyte cells, which become macrophages of the immune system, were isolated. The cells were incubated with Amyloid Beta, Vitamin D3, and Curcumin (both natural and synthetic Curcumin). The synthetic Curcumin was more readily absorbed and not as easily destroyed as natural Curcumin, and is thus more potent.
The study found that Curcumin enhanced the binding of Amyloid Beta to Macrophages. Vitamin D3 strongly stimulated the uptake and absorption of Amyloid Beta in Macrophages. Some Alzheimer’s patients macrophages respond to Curcumin, some do not. Vitamin D3 and Curcumin may each be used alone or in combination depending on the individual patient.
http://www.ncbi.nlm.nih.gov/pubmed/19433889?
1alpha,25-dihydroxyvitamin D3 Interacts with Curcuminoids to Stimulate Amyloid-beta Clearance by Macrophages of Alzheimer’s Disease Patients.
J Alzheimers Dis. 2009 May 11. Masoumi A, Goldenson B, Ghirmai S, Avagyan H, Zaghi J, Abel K, Zheng X, Espinosa-Jeffrey A, Mahanian M, Liu PT, Hewison M, Mizwicki M, Cashman J, Fiala M.
Patients with Alzheimer’s disease (AD) suffer from brain amyloidosis related to defective clearance of amyloid-beta (Abeta) by the innate immune system. To improve the innate immune system of AD patients, we studied immune stimulation of macrophages by 1alpha,25(OH)-vitamin D3 (1,25D3) in combination with curcuminoids.
AD patients’ macrophages segregate into Type I (positively stimulated by curcuminoids regarding MGAT-III transcription) and Type II (not stimulated). In both Type I and Type II macrophages, 1,25D3 strongly stimulated Abeta phagocytosis and clearance while protecting against apoptosis.
Certain synthetic curcuminoids in combination with 1,25D3 had additive effects on phagocytosis in Type I but not Type II macrophages.
In addition, we investigated the mechanisms of 1,25D3 and curcuminoids in macrophages. The 1,25D3 genomic antagonist analog MK inhibited 1,25D3 but not curcuminoid effects, suggesting that 1,25D3 acts through the genomic pathway.
In silico, 1,25D3 showed preferential binding to the genomic pocket of the vitamin D receptor, whereas bisdemethoxycurcumin showed preference for the non-genomic pocket.
1,25D3 is a promising hormone for AD immunoprophylaxis because in Type I macrophages combined treatment with 1,25D3 and curcuminoids has additive effects, and in Type II macrophages 1,25D3 treatment is effective alone.
Human macrophages are a new paradigm for testing immune therapies for AD.
PMID: 19433889