Study Links Heart Disease, Alzheimer's

Toxic Protein Clusters in Heart Disease Like Those in Alzheimer's Brains

From the WebMD Archives

June 22, 2004 -- Toxic protein clusters clog the brains of Alzheimer's patients -- and the hearts of people with heart failure, new research shows.

Abnormally twisted proteins called beta amyloids are the main feature involved in the disruption of thinking in Alzheimer's disease. Similar toxic protein clusters appear in the brains of patients with Huntington's disease and Parkinson's disease, note Jeffrey Robbins, PhD, director of molecular cardiovascular cardiology Cincinnati Children's Hospital, and colleagues.

Now, Robbins says, beta amyloids cluster in the heart muscle cells of people with heart failure.

"The surprising thing is, I don't think anyone really expected to find toxic beta amyloids inside of [heart-muscle cells]," Robbins says in a news release.

The findings appear in the early online edition of the Proceedings of the National Academy of Sciences.

Mutant Mice, Sick People

Robbins' team knew that a mutant form of a small protein causes a specific kind of the heart disease known as cardiomyopathy. In some types of cardiomyopathy, the heart muscles can enlarge, and as a result the heart doesn't pump as well as it should. Eventually the heart muscles get very weak and heart function gets worse and worse.

The researchers studied a strain of mice bred to carry the mutant protein. They showed that the protein forms toxic clumps that cause disease.

A closer look at these clumps showed that they look a lot like the clumps of beta amyloid that clog the brain of patients with Alzheimer's disease and other degenerative brain diseases.

What's happening? Robbins says the normal heart uses one set of proteins to carry harmful proteins out of heart muscle cells. But when the heart gets stressed, this system breaks down. Instead of taking out the trash, defective housekeeping proteins pile up in tangled, toxic clusters. And in the middle of these clusters are beta amyloids.

"Now what does the presence of beta amyloids in the heart muscle cells mean?" Robbins asks. "If you prevent it, will that lessen the severity of the disease? Does it have the potential to become a therapeutic target? At this point, does heart failure become reversible or not?"

The researchers plan follow-up studies to address these questions.

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SOURCES: Sanbe, A. Proceedings of the National Academy of Sciences, Early online edition, June 21, 2004. News release, Cincinnati Children's Hospital Medical Center.
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