By Mary Lide Parker
Two serious conditions: Alzheimer’s disease and heart disease. Could they be prevented with the same drug?
What happens when you have a heart attack? It’s alarmingly simple—part of your heart muscle just dies and just as they can’t bring back the dead, doctors can’t bring back dead parts of the heart.
“We don’t have the ability to repair the heart well once it’s been damaged,” says Cam Patterson, chief of cardiology at the UNC School of Medicine. “More people are surviving heart attacks now, but they’re surviving with heart failure. It’s a big problem.”
Patterson and his colleague, Monte Willis, an associate professor of pathology and laboratory medicine at UNC, are looking for a way to solve this. Their analysis, which appeared in the New England Journal of Medicine on January 31, 2013, proposes that drugs being developed to prevent disease in the brain might also work for preventing heart failure.
Here’s how Patterson describes what happens when things start to go wrong in the heart. Proteins in the heart cells are supposed to fold up into a specific structure. But over time, the repeated contractions of the heart muscle cause stress, and the proteins may no longer fold properly.
Two things can happen when a protein gets worn out and “misfolds.” It simply stops working, and the protein can become toxic to the cell. This cellular damage causes heart failure.
Patterson says a similar cellular damage can occur in the brain. Like the constant contractions of the heart, the constant firing of synapses in the brain can cause wear and tear on brain cells. It’s the same kind of cellular degeneration, except that up in the brain it causes Alzheimer’s.
“The idea that misfolded proteins lead to organ damage has existed in the neurology literature for decades,” Patterson says. “So we’re already far along in terms of identifying therapies that can prevent protein misfolding.”
A drug called a molecular chaperone does just that. Researchers believe that this kind of therapy could prevent Alzheimer’s and cystic fibrosis, another disease caused by protein misfolding. Molecular chaperones for these diseases are in the initial phase of human testing. The logical next step is to test whether some of the drugs could prevent heart failure, effectively knocking out two, or maybe even three, diseases with one type of treatment.