Sandip Verma

Despite being an essential element, iron, if deposited in large quantities in the body could have implications in certain neurodegenerative diseases. But how iron builds up in the body has remained a mystery thus far.

Now, a joint international research team has discovered that the protein that ferries iron across the body collapses into long worm-like fibrils releasing the iron and triggering deposits. The study offers a new insight into how iron builds up in various diseases like Alzheimer’s and Parkinson’s.

Blood protein transferrin safely transports iron via bloodstream to target points and the element is subsequently used by the body. Transferrin seals iron in a way that prevents iron from interacting with anything until delivered to the destined site.

Iron deposition, like mineralization, is a natural biological process. But, controlled iron mineralization in biological systems can be harmful. To test this, the researchers took human transferrin and left it to dry out on mica surface. The transferrin molecules assembled themselves into worm-like fibrils. This triggered the release of iron.

The researchers found electron-rich dark spots along the length of the fibrils while working with iron-bound transferrin. Transferrin devoid of iron showed no dark spots. This linked the dark spots to iron deposition. Some dark spots were 250 nm apart, others 375. Dehydration on the surface of transferrin caused structural change of this iron transporter leading to iron deposition resembling mineralization.

"This is the first experiment to observe that human serum transferrin can form fibrils," says researcher Sandip Verma.