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Home > Psychiatry and Behavioral Sciences > About Us > Publications > Newsletter > > 2007 - Fall Issue
Alzheimer's: Circulatory Ills Give It a Push
News from the Johns Hopkins Department of Psychiatry and Behavioral Sciences
Could fixing them make the disease less relentless?
Angina. High blood pressure. Heart arrhythmia. A number of studies have singled out flaws in the circulatory system, or combined them even, to see if they raise a person’s likelihood of Alzheimer disease (AD). The most telling ones, the long-term projects that follow large swaths of the adult population, make it clear: So-called vascular factors do increase the risk of the dementing illness.
But what about those who already have the disease? “Once Alzheimer symptoms appear, we haven’t seen much interest, so far, in looking at the effects of vascular problems,” says epidemiologist Michelle Mielke, Ph.D., a researcher in geriatric psychiatry.
That may change, however. Until a cure arrives or AD can be prevented, a focus from within the disease could put some benefits in easy reach. New work by Mielke and her Hopkins colleagues, reported in the November issue of Neurology, first suggests that patients with key signs of circulatory disease undergo a faster Alzheimer-caused decline. But it also leaves open the possibility—one needing study—that improving circulation might slow it.
Mielke’s team analyzed data from 135 men and women over 65, all newly diagnosed with AD. Most of the group was followed for three years and rated every half year on cognitive abilities including memory and on how well they carried out everyday tasks. A physical exam at the time of their diagnosis gave data on circulatory health, with such touchstones as high blood pressure (and having therapy for it), history of the abnormal heart rhythm, atrial fibrillation, heart attack history, diabetes, smoking or angina.
The research is strong, Mielke says, partly because the patients were part of a much-respected and still ongoing study of aging and memory that began in Cache County, Utah, in 1995. That project enrolled more than 5,000 elders, and the expertise of those testing them has made the data extra trustworthy.
“But the fact that it’s a population study is also a strength,” says Mielke. “We’ve watched these participants more than a decade, even before their AD diagnosis, so we know a good deal about their medical history and onset of the disease.” It’s not the same, she adds, as picking already ill patients from a clinic to study them.
In the end, the bad-news trio of dangerous arrhythmia, hypertension or angina are especially obvious in their tie to Alzheimer’s progress. In a group with high blood pressure, for example, rate of memory loss roughly doubled. And though not quite that quick in those with atrial fibrillation, memory decline was still significantly faster.
Could improving circulation slow the disease? “That’s what we’re looking at now,” says Mielke. She’s with a Hopkins team looking at effects of existing drugs that lower blood pressure, among other things. “We’re optimistic that there’s something to it.”
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