Link Between Alzheimer's, Heart Failure
Protein Clusters in Heart Muscle Similar to Amyloid Plaques in Brain Tissue
Nov. 16, 2009 (Orlando, Fla.) -- Researchers report evidence supporting a
link between Alzheimer's disease and chronic heart failure, two of the 10
leading causes of death in the U.S. and Europe.
Heart failure involves a harmful buildup of a protein called desmin, says
Giulio Agnetti, PhD, a postdoctoral research fellow at Johns Hopkins University
School of Medicine and the University of Bologna, Italy.
"Just like pistons have to be in the right place for a car engine to work,
desmins have to be in the right place or the heart will not contract," he tells
Agnetti and colleagues first identified three potentially dangerous changes
in the chemical makeup of desmin in heart muscle cells in dogs.
The changes led to the formation of debris-like protein clusters in heart
muscle, similar to the amyloid plaques seen in the brain tissue of Alzheimer's
patients, he says.
The protein alterations, which were reversed by surgically repairing the
heart, occurred at the onset of heart failure. Since then, the researchers
found the same chemical modifications to desmin in the heart muscle in four
people diagnosed with heart failure.
The research was reported at the American Heart Association Scientific
Sessions 2009, in Orlando, Fla.
Research Ties Desmin to Weakening Heart
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.
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
The new research, Agnetti explains, is believed to be the first to tie
common underlying structural changes in desmin to malformations observed in the
heart as it weakens, strains to pump blood, and starts to fail. Their 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.
In the latest experiment, the researchers analyzed proteins in heart tissue
samples collected from a group of dogs whose hearts had been surgically altered
to beat irregularly, become stressed, and fail -- that is, mimic heart failure.
Additional tissue samples were analyzed from another group of healthy dogs.
The researchers found accumulating amyloid-like debris containing desmin in
the damaged heart tissue but not in the normal tissue.
"In our preliminary research, we found that desmin changed chemically and
structurally and turned into a toxic species," Agnetti says.
Moreover, the debris-like clusters are similar to the amyloid plaques seen
in the brain tissue of Alzheimer’s patients, he says.
"Our study leads us to believe that desmin plays a key role in heart
failure," he says. "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."
American Heart Association spokesman Ralph Sacco, MD, of the University of
Miami, tells WebMD that the research raises the prospect of treating the root
cause of heart failure by preventing the formation of desmin amyloid.