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| Diseases in Heart and Brain Linked |
| Sam Ohmen/John Hopkins Newsletter |
| 12/3/2009 |
| Scientists at the Hopkins School of Medicine, working with colleagues in Canada and Italy, have recently uncovered a surprising biochemical link between Alzheimer's disease and heart failure. The link seems to be tied to protein abnormalities - specifically, abnormal protein folding that leads to the aggregation of large masses of misfolded proteins that can interfere in both the brain's and the heart's normal functioning. Alzheimer's and heart failure are not linked by causation, but rather by parallel causes, and this link may help scientists to characterize and treat similar medical disorders in the future. It is known that the brains of Alzheimer's sufferers, when examined post-mortem, display irregular protein tangles and plaques called tau tangles and beta amyloid plaques. These tangles or plaques are formed when misfolded proteins clump together, and such clumps can cause serious damage when they interact with, and get stuck in, brain tissues. The scientific team credited with this latest discovery has found that, at least in the canine model they have studied, heart failure can sometimes be caused by the same scenario. Protein plaques form in heart muscle and may ultimately play a role in heart failure. By surgically engineering animals that had malfunctioning hearts, the team was able to elicit a stress response from the heart muscles, a response in which protein plaques formed. "In both cases (the brain and heart, respectively) it takes time for these plaques to build up and exert their toxic effect," said Giulio Agnetti of Hopkins' Heart and Vascular Institute and the National Institute for Cardiovascular Research at the University of Bologna in Italy, "It's a slow, chronic process in both cases. Due to these analogies, I started thinking that something similar to what's going on in Alzheimer's disease could also be occurring in the heart." Previous research had found that a protein called desmin formed plaques in genetically engineered mice hearts. David March of Hopkins and his team found that desmin also begins to form toxic plaques in the hearts of dogs whose hearts do not beat regularly. The desmin plaques are thought to be analogues of amyloid plaques found in the brains of Alzheimer's patients. Desmin plaques seem to aggregate and play a toxic role, perhaps exacerbating the original stress that had been inflicted on the heart itself. Interestingly, when the dogs' hearts underwent surgery, the toxic desmin plaques began to dissipate, the hearts began pumping normally, and the irregular protein folding was no longer observed. * * * Understanding how the desmin works to exacerbate heart failure is an important step in combating the devastating effects of heart failure. Instead of just treating the symptoms of heart failure, scientists and doctors may now be able to move towards treating the actual biochemical cause of heart failure. Indeed, the Hopkins team has already identified similar plaques within the hearts of human patients suffering from heart failure. By understanding desmin plaques in mice and in dogs, and their associated treatments, scientists may one day better understand Alzheimer's amyloid plaques and ways to treat them or address their toxic and damaging effects. This is great news for the millions of Americans and others around the world who suffer or die each year from these two diseases. For complete article go to: http://www.jhunewsletter.com/home/index.cfm?event=displayArticle&uStory_id=25b74cd4-ae7b-4846-827c-936ef03c33e5 |
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