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Reducing iron, adding antioxidants may help prevent Alzheimer's disease

Reducing iron, adding antioxidants may help prevent Alzheimer's disease

Friday, April 13, 2012. A report published online on March 9, 2012 in the Journal of Alzheimer's Disease describes research conducted by Othman Ghribi, PHD of the University of North Dakota and his associates which suggests that lowering iron levels and supplementing with antioxidants could help protect the brain from some of the changes related to the development of Alzheimer's disease.

"The causes of Alzheimer's disease are not well known but a number of environmental and dietary factors are suggested to increase the risk of developing Alzheimer's disease," the authors write in their introduction to the article. "Additionally, altered metabolism of iron may have a role in the pathogenesis of Alzheimer's disease."

In previous research, Dr Ghribi's team demonstrated that the intake of a high cholesterol diet results in Alzheimer's disease-like changes and iron deposition in the brains of experimental animals. In the current study, rabbits were given a high cholesterol diet for 12 weeks, which resulted in the formation of brain plaques containing the protein amyloid beta, which is a characteristic of Alzheimer's disease. The animals also underwent increased phosphorylation of a protein in the brain's neurons known as tau, which is another hallmark of the disease. When some of the rabbits were treated with the iron-chelating agent deferiprone, plasma cholesterol and iron levels were lowered, and even though brain iron levels were not also reduced, amyloid beta and phosphorylated tau were significantly decreased. Treatment with deferiprone did not reduce levels of reactive oxygen species (whose generation by iron causes damage to neurons) in comparison with untreated animals. "These results demonstrate that deferiprone confers important protection against hypercholesterolemia-induced Alzheimer's disease pathology but the mechanism(s) may involve reduction in plasma iron and cholesterol levels rather than chelation of brain iron," the authors conclude. "We propose that adding an antioxidant therapy to deferiprone may be necessary to fully protect against cholesterol-enriched diet-induced Alzheimer's disease-like pathology."

"Our data show that treatment with the iron chelator deferiprone opposes several pathological events induced by a cholesterol-enriched diet," commented Dr Ghribi, who is an associate professor at the University of North Dakota School of Medicine and Health Sciences' department of pharmacology, physiology, and therapeutics. "Deferiprone reduced the generation of amyloid beta and lowered levels of tau phosphorylation."

"It is possible that a higher dose of deferiprone, or combination therapy of deferiprone together with an antioxidant to prevent reactive oxygen species generation would more fully protect against the deleterious effects of cholesterol-enriched diet that are relevant to Alzheimer's disease pathology," he added.

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Mechanisms for vitamin D, curcumin in Alzheimer's disease identified

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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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