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Protein Alterations in Heart Point Towards Alzheimer's and Heart Disease

by Savitha C Muppala on  November 18, 2009 at 6:02 PM Research News   - G J E 4
Protein  Alterations in Heart Point Towards Alzheimer's  and Heart Disease
Changes in the chemical structure of a protein could point towards Alzheimer's disease and chronic heart failure.
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The international team of biochemists and cardiologists, led by researchers at Johns Hopkins, have said that they have identified three changes in the chemical make-up of a key structural protein, called desmin, in heart muscle cells in dogs.

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The changes led to the formation of debris-like protein clusters, or amyloid-like oligomers containing desmin, in heart muscle, similar to the amyloid plaques seen in the brain tissue of Alzheimer's patients.

The protein alterations, which were reversed by surgically repairing the heart, occurred at the onset of heart failure.

By conducting further experiments, scientists found the same chemical modifications to desmin in the heart muscle in 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 the two chronic diseases.

Researchers say, their latest analysis is believed to be the first to tie common underlying structural changes in desmin to malformations observed in the heart as it weakens and strains to pump blood and starts to fail.

The results are also believed to be the first to suggest that toxic, desmin-like amyloids could form in response to stress placed on the heart.

"Our study leads us to believe that desmin plays a key role in heart failure. Now we have a chemical target to research further and help us investigate what could be the underlying biological cause of heart failure and see if it is like Alzheimer's, an amyloid-related disease," said lead study investigator Dr. Giulio Agnetti.

"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," he added.

Symptoms of heart failure may include fatigue, shortness of breath and enlargement of the heart.

The study was presented at the American Heart Association's (AHA) annual Scientific Sessions in Orlando.

Source: ANI
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