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(Ivanhoe Newswire) -- New evidence supports a link between Alzheimer's disease and chronic heart failure, two of the ten leading causes of death in the United States.
A team of biochemists and cardiologists led by researchers at Johns Hopkins identified three changes in the chemical make-up of a key structural protein called desmin in heart muscle cells in dogs. The changes led to the formation of debris-like protein clusters containing desmin in the heart muscle, similar to the amyloid plaques seen in the brain tissue of Alzheimer's patients.
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The protein alterations, which were reversed by surgically repairing the heart, occurred at the onset of heart failure. Further experiments by the Hopkins scientists found the same chemical modifications to desmin in the heart muscles of four people already diagnosed with the disease.
Misshaped desmin proteins and amyloid-like debris had been previously reported in 2005 in mice genetically altered to develop chronic heart failure, providing the first biological link between Alzheimers and chronic heart failure. Studies since have also reported desmin changes in failing animal hearts, but none detailed what the chemical changes were or how they might affect organ function.
"Our study leads us to believe that desmin plays a key role in heart failure," lead study investigator and protein biochemist Giulio Agnetti, Ph.D., was quoted as saying. "Now we have a chemical target to research further and help us investigate what could be the underlying biological cause of heart failure and if it is like Alzheimer's, an amyloid-related disease."
"Just as significantly, our study raises the prospect of testing new treatment options for heart failure by moving beyond treating symptoms of the disease and getting to the root of the matter, preventing these desmin amyloids from forming and impairing heart function from the start," said Agnetti, a postdoctoral research fellow at both the Johns Hopkins University School of Medicine and its Heart and Vascular Institute, and the University of Bologna and its National Institute for Cardiovascular Research, in Italy.
The team's latest investigation began with an analysis of proteins contained in heart tissue samples collected from a group of dogs whose hearts had been surgically altered to beat irregularly, become stressed and fail. Additional tissue samples were taken from another group of healthy controls.
The team's analysis yielded at least three chemical differences in each desmin protein in response to heart failure. They also found accumulating amyloid-like debris containing desmin in the damaged heart tissue.
When researchers performed surgery restoring the dogs' heart pumping function to normal, they found phosphorylated sites mostly reverted to normal. The amlyoid-like oligomers also began to disappear. Tissue samples from four people with heart failure showed similar desmin modifications.
Jennifer Van Eyk, PhD, a Johns Hopkins professor and director of Hopkins' NHLBI Proteomics Group and the Proteomics Center at Johns Hopkins Bayview Medical Center, was quoted as saying, "But what is most interesting about our findings is that we have shown that these chemical changes and debris are related to impaired heart function, which, ultimately, may explain how and why the heart can fail."
SOURCE: Presented at the American Heart Association Annual Scientific Sessions, Orlando, FL, November 15, 2009
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