When Richard Watt came to BYU as a professor in 2006, he was determined to understand iron in such a way that it would lead to something significant. And now, finally, almost eight years later, the hard work is paying off.
Watt and his research team are working on a new unified model for ferritin iron loading that, if successful, could help in curing today’s major diseases, including Alzheimer’s and diabetes. When iron roams free in our bodies, it can be damaging.
“Our bodies are designed to absorb iron from our diet, but once iron enters our bodies it is important to always have it packaged and protected. And, if those systems fail, it leads to disease,” Watt said.
The ferritin iron-loading model seeks to understand how subcellular levels of iron are controlled during inflammation. Our bodies seek to package iron in non-reactive forms, and when iron is free, the body should send it back to its assigned place so that there is less oxidative stress happening in the body. When there is free iron, it’s like a “wrinkle” in the system and results in oxidative stress and disease. The iron needs to stay in its appropriate, assigned place for us to be healthy. In most cases the safe location is hemoglobin, which is essential for our blood to carry oxygen.
If the model is accurate, it could contribute in keeping our bodies “wrinkle-free” with all iron organized neatly in its place, thereby reducing inflammation and disease that comes from oxidative stress (when the iron and oxygen molecules react with one another).
Watt studied the components of nickel in cells as a graduate student and then went on to study manganese in plants. Now at BYU, he focuses on iron. In developing this groundbreaking model, Watt has involved the help of other professors on campus.
“We were working with Chad Hancock in nutrition and Jon Wisco in PD Bio. Chad studies diabetes and Jon studies Alzheimer’s disease. . . . It has been an ongoing project . . . [and] when you can finally put it all together in a model, that’s pretty exciting,” Watt explained.
Now that the model has been formed, these scientists are putting their research to the test.
“We’re actually doing tests with both our collaborators now. . . . We are treating mice and rats with chemicals that trigger iron to be free, and then we’re trying to use treatments or drugs that will put the iron back into the safe locations we call iron-chaperones,” Watt said.
Sometimes thinking outside the box is the key to success, and that has proven true in developing this iron model. Watt said, “It’s really exciting. A lot of people are looking at inflammation from different directions and not including iron, and so looking at free iron, we are able to explain a lot of the symptoms with inflammation. . . . We’re coming at it from a different direction, and that’s helping us to be successful.”
Watt and his collaborators are hoping that with more time and funding, the model will become a sure success, and that in controlling the free iron, scientists could better understand the processes of controlling subcellular concentrations of iron during inflammation. In doing so, there would be a possible guide to proper treatments for Alzheimer’s disease and diabetes.