Health & Medicine - Posted by Tom Hughes-UNC on Thursday, January 31, 2013 11:50 - 0 Comments
Heart ‘wear and tear’ looks like Alzheimer’s
UNC-CHAPEL HILL (US) — There are striking similarities between heart cells in patients with heart failure and brain cells in patients with Alzheimer’s disease, report scientists.
The findings raise the possibility that some treatment approaches in development for Alzheimer’s may also help reverse the damage from heart failure.
Straight from the Source
Despite a substantial increase in the number of people suffering the debilitating and often deadly effects of heart failure, treatments for the condition have not advanced significantly for at least 10 years.
“We know that Alzheimer’s is a process of wear and tear on the brain, and the same sort of wear and tear affects the heart,” says Cam Patterson, chief of cardiology at University of North Carolina School of Medicine.
“The good news is now that we recognize that—and can understand how the wear and tear actually affects proteins in the heart—it offers us a new chance to identify strategies to reverse that wear and tear. It’s like providing a key to preventing aging of the heart.”
The analysis, co-authored by Patterson and Monte Willis, associate professor of pathology and laboratory medicine, appears in the January 31, 2013 issue of the New England Journal of Medicine.
The researchers say a variety of recent studies point to one conclusion: misfolded proteins in heart cells are a key factor in the process of heart failure. “There’s a convergence of data pointing to this being a real problem,” says Patterson.
Three lines of evidence
First, studies of heart tissue from patients with heart failure reveal large accumulations of misfolded proteins within damaged heart cells, similar to the accumulations found in the brain cells of patients with Alzheimer’s.
Second, recent studies using mice show heart problems can result from defects in the body’s quality-control system for monitoring and maintaining proteins.
Third, studies of a rare genetic disorder link severe heart problems to misfolding of two proteins, known as desmin and CryAB.
Scientists studying Alzheimer’s and other neurological disorders have long focused on ways to correct or prevent protein misfolding, and have even developed drugs that accomplish this feat.
“This raises the possibility that that same type of strategy, and maybe even some of those compounds, will be beneficial in heart failure,” says Patterson. “It’s an entirely new treatment paradigm.”
Heart failure, in which the heart fails to pump as effectively as it should, is a chronic, debilitating, and often-deadly condition affecting millions of adults in the United States. It can result from heart attacks, coronary heart disease, and many other causes.