Academics and Research / Magazine Feature

DU prof says nothing about Alzheimer’s disease research is easy

Nothing has been easy in the scientific community’s battle against Alzheimer’s disease: not finding a cure, not settling on a cause, not figuring out who might become afflicted, and not even diagnosing it, assistant professor Christina Coughlan told visitors Feb. 10 at DU’s Division of Natural Sciences and Mathematics winter luncheon.

And even after researchers succeeded in developing a vaccine that appeared to reverse the damage done by the brain-ravaging ailment in mice, new setbacks were encountered when human testing began and some subjects died.

“The good news is that we know that this is the right therapeutic approach,” Coughlan said of the vaccine. “The bad news is that death is a large side effect.”

Coughlan’s light touch belies the serious work she and scientists in DU’s Department of Biological Sciences and the Eleanor Roosevelt Institute do in search for a cure. But her underlying message is that it’s been a long and difficult struggle against a disease that afflicts some 5 million Americans. Even identifying patients who truly have Alzheimer’s, not another form of dementia, is difficult, often possible only in autopsies after the patient has died.

“It’s a horrible disease,” she said.

Coughlan’s research areas focus on understanding protein folding and the diseases that result when the process goes awry. Her particular areas of interest are Alzheimer’s disease and dementia in diabetes.

When it comes to Alzheimer’s, the sobering news is that there is at least one risk factor no one is immune to: aging.
At 65 years old, Americans have a 10 percent chance of developing the disease. That figure doubles every 10 years. By 85, the risk is 40 percent.

Plaques made up of protein are present in everyone’s brains as they age. For some reason, Alzheimer’s patients have an immune response develop to these plaques that is responsible for at least some of the brain destruction caused by the disease. Another pathology that scientists have found is that “tangles” in the brain block neurons from communicating with each other, and this in turn causes neurons to die.

Other risk factors, she said, include high cholesterol in mid life, a lack of anti-oxidants in the diet and even plain old lack of brain stimulation — dubbed the “use it or lose it” risk factor. Genetic predisposition, she said, accounts for only 5 percent of all cases.

There are tests, but Coughlan mused that for some, knowing test results when there is not yet a cure might be counterproductive.

But on a more hopeful note, Coughlan said scientists continue to make breakthroughs, and large pharmaceutical companies are intensely interested in finding a cure. Coughlan’s own lab hopes to test its amyloid specific dendrimers, designed to be detectors and protectors against Alzheimer’s, in mice within the next few months.

Meanswhile, there are things individuals can do to stave off the disease.

Stay healthy and active, Coughlan said. Learn new things and keep the brain working, and eat right and exercise to reduce cholesterol.

“Definitely there is evidence in favor of not letting your brain turn to mush,” she said. “What’s good for the heart is good for the brain as well.”

For more information, visit Coughlan’s Web site.


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