Let's just say Iron Man was real, and his suit's material was present in his brain; new research would show why he developed Alzheimer's disease.
OK, so Iron Man (for argument’s sake, we’re saying he isn’t a fictional character) hasn’t really developed Alzheimer’s disease, and we don’t really know if the iron from his suit is also present in his brain. But… but, if it were—and, again, if Iron Man was indeed real and had developed Alzheimer’s disease—researchers at Massachusetts General Hospital would know how and why.
The team, reporting on recent study results in the Journal of Biological Chemistry, has determined how iron contributes to the production of plaques that destroy the brain in patients with Alzheimer’s disease. Specifically, they found a very close link between elevated iron levels in the brain and increased amyloid precursor protein (APP) production, which breaks down into a peptide in Alzheimer’s disease that forms destructive plaques.
The findings, according to Dr. Jack T. Rogers, head, neurochemistry lab, Massachusetts General Hospital, “lay the foundation for the development of new therapies that will slow or stop the negative effects of iron buildup" in patients with progressive neurodegenerative disease.
The current research adds to knowledge in the field that too much iron in brain cells leads to APP abundance and the resulting destructive peptide, information that Rogers’ team used to discover the molecular location at which APP and iron interact, and then learn that iron and APP clearly keep one another in check. Now that they’ve “sealed the loop” in the understanding of APP and iron interactions, they’ve also paved the way for the development of medications that can enhance the ability of APP to escort iron out of the cell and restore the iron-APP balance as needed.
The findings don’t end there. Rogers and colleagues also identified IRP1, or iron-regulating protein 1, a molecule that attaches to mRNA and “holds the recipe for making APP.” IRP1, when iron levels in the brain are low, usually hooks up with RNA, preventing the production of APP, but when iron levels are high, the hook up with RNA doesn’t occur, and APP production becomes excessive. Thus, the researchers’ hypothesis that the region where IRP1 binds to mRNA is a potential drug target was solidified.
"With other research teams, we are investigating novel therapies that remove excessive iron, and we're looking at the precise spot on the messenger RNA where IRP1 binds to screen for drugs that specifically prevent APP production," said co-lead author Dr. Catherine Cahill.
It seems that almost every day another potential target for Alzheimer’s disease therapy is discovered. Do you think the findings from this study will actually lead to a marketed drug? If not, how else will they be helpful, or will they? Do you look at such promising studies with a “grain of salt” point of view? Tell us what you think. Get a conversation going!