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Brain Sections from Mice with Deletion of Iron Regulatory Protein- 2

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Findings

Dr. Meyron-Holtz and Prof. Rouault are now characterizing the mechanisms leading to the functional iron deficiency observed in the neurons and supporting cells in their mouse model. They are also studying the characteristics of secreted ferritin. This iron-storage protein, found at very high levels in most cells, is normally intracellular, but in mice lacking iron regulatory protein-2, it also occurs in the serum. In addition, they are elucidating possible mechanisms for ferritin secretion and the cellular sources of secreted ferritin.

The work of Dr. Rouault’s group suggests that mitochondrial failure accounts for axon degeneration and, in turn, for the observed neurodegenerative symptoms. They discovered that oral treatment with a stable nitroxide activates the alternative iron- regulatory protein-1, which compensates for loss of iron regulatory protein-2.

 

 In earlier joint studies, these researchers found that iron regulatory protein-1 is not an effective iron regulator under physiologic oxygen concentrations, but can be activated by elevated oxygen levels, in iron-poor cells. Therefore, the present finding -- activation of iron regulatory protein-1 in tissues by a chemically stable compound (nitroxide), for the first time -- is very exciting.

 

 

 

 

Axonal iron accumulation precedes and co-localizes with degeneration in cerebellar axons loaded with ferric iron (as determined by Perls’ DAB stain). Ferritin levels are also elevated (but may be unavailable to the cell, leading to a functional iron deficiency).