Their studies have revealed that misfolded proteins in heart cells play a significant role in heart failure and those same misfolded proteins are also present in the brain cells of Alzheimer patients. The work offers hope to heart patients because treatments used to reverse cell damage in Alzheimer’s patients may now be modified to deal with heart patients.
In both heart failure and Alzheimer’s, the disease is now recognised as a process of wear and tear on cell proteins. The North Carolina research team say their study, published in the New England Journal of Medicine, may act as the key to unlocking how to prevent ageing in the heart by devising new treatments.
Heart failure is a serious condition affecting more than 750,000 people in the UK, caused when the heart cannot pump enough blood or cannot fill with enough blood to keep the body functioning. It has a debilitating effect on patients and increased their risk of early death. Alzheimer’s disease is a neurological disorder that is the most common cause of dementia in the UK, affecting around 450,000 people.
Research into Alzheimer’s disease has focused on ways to stop or fix the protein misfolding that causes cell damage and drugs have been developed that can achieve this. The North Carolina team believe those Alzheimer treatments could now be modified for heart failure patients to achieve the same positive outcome.
Their study looked at three factors around heart failure: the evidence of misfolded proteins in patients with heart failure that matched those of Alzheimer’s patients; the results of studies involving mice that revealed monitoring and maintaining proteins can be failed by the body’s own system; and the rare genetic disorder that links heart failure to two specific proteins misfolding in the heart cells.