Heavy metal. ferritin makes it harmless reactive iron in dopaminergic neurons (marked in red).
Locking iron in brain cells may prevent Parkinson's disease, according to a new study. He noted that the prevention of cellular damage caused by iron, using either a naturally occurring protein or a drug iron binding, may slow the progression of the devastating disease. The problem is that the drug, when bound to iron, poisons nerve cells.
Parkinson's disease destroys nerve cells in a brain region called the substantia nigra, which results in jerky movements and tremors that characterize the disease. These neurons seem to deteriorate due to the damage produced by the oxidation of dopamine in the brain chemical. Iron, if not properly restrained in the cell, can accelerate the creation of destructive oxygen molecules. Patients with Parkinson's disease have more iron in their brains than people without the disease, but researchers have not been sure that the disease causes iron buildup or vice versa.
Neurobiologist Julie Andersen of the Buck Institute for Age Research in Novato, California, and colleagues studied two ways to bind iron bulk in the brains of mice with a Parkinson-like disorder . First, they injected mouse embryos with a human gene that encodes a binding protein ferritin iron called. They were designed so that the only cells Niger gene locus and the associated parts of the brain produce the protein. Fewer neurons crashed in mice than in untreated animals. Next, the team tested the effect of clioquinol drug, which binds iron and zinc. Researchers have shown to slow the progression of Alzheimer's disease. Mice given oral clioquinol lost less brain cells than mice that did not receive the drug. . Both ferritin and clioquinol treatments also kept the motor skills of the mice, the researchers report in March 27 number Neuron
Controversy surrounds clioquinol, however; the drug was banned after its use as an antibiotic seemed to cause a neurodegenerative disease in some Japanese patients. Andersen and colleagues suggest that vitamin B-12 deficiency caused toxic effects, and that give patients additional B-12 would eliminate the problem. Yet Jack Arbiser dermatologist at Emory University in Atlanta, Georgia, calls for caution. "They have never proven that B-12 is the issue," he said. Whether clioquinol proves to be useful, "this should certainly stimulate efforts to find ways to intervene in iron," says Alzheimer's disease researcher Gregory Cole of the University of California, Los Angeles.
related sites
Web site laboratory Julie Andersen
lab website Gregory Cole
NIH page of information on Parkinson's disease
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