Friday, April 29, 2011

Remaking Alzheimer’s: A Few Questions

From the NY Times

The newly revised criteria for Alzheimer’s disease, the first change since 1984 in how this dementia is diagnosed, are likely to be most valuable at first to scientists and researchers. The guidelines spring in part from novel research into biomarkers and imaging techniques that may not reach family medical practices for some time.
Still, the new criteria, unveiled on Tuesday by the National Institute on Aging and the Alzheimer’s Association, will have consequences for family caregivers. Informed by research showing that changes in the brain may be under way a decade before any symptoms appear, the guidelines are likely to lead to increasingly early diagnoses.
I spoke with Dr. Gary Kennedy, director of geriatric psychiatry at Montefiore Medical Center in New York, about how that will change the way we look at Alzheimer’s disease.
Q.
What are some of the most important effects of the new criteria? What do families need to understand?
A.
First, that memory impairment doesn’t have to be the first sign of the illness. So older adults who have no problem with recall of recent or remote events, who seem quite up to speed in recalling what they did earlier in the day but have more problems than you’d expect with navigating unfamiliar territory or keeping up with plans or getting tasks started and then finished — all part of what’s called executive function — those actually could be the first signals of dementia.
People with executive dysfunction may also start to misread or ignore other people’s reactions, which can cause interpersonal problems. They’re losing some of their social skills, because they’re failing to perceive cues from the environment that would direct them to behave appropriately.

Q.
The new guidelines establish three distinct stages of Alzheimer’s disease. Could you explain?
A.
They’ve been around for a while, but here they’re simplified so they’re not as confusing.
“Preclinical” dementia is essentially a scientific description. There’s some biological or structural brain evidence that the Alzheimer’s process is under way, but the person’s not disabled and the family doesn’t notice any problem.
The second stage is mild cognitive impairment — someone has problems that don’t cause disability, but they’re evident enough that the patient and a family member or another observer agree, “Yes, it’s noticeable.” You need two sources of information. Mild cognitive impairment progresses to dementia for a little over half the people who meet that criteria.
The overall thrust of the new criteria is to alert people that we need to diagnose this disease much earlier.
Q.
I often hear people say they wouldn’t want to know if they were developing dementia. Given that there’s no cure, why does earlier diagnosis matter?
A.
The reality is, we have a lot of different treatments for Alzheimer’s and the other dementias. No, those treatments are not curative. But we have medications that help maybe 40 percent of people with dementia. We have specific approaches caregivers can use to keep the person with dementia as active and engaged as possible and to keep themselves from getting depressed. We have some evidence that if you optimize the treatments for other diseases that make Alzheimer’s worse, like diabetes and heart disease, that increases the likelihood that Alzheimer’s will not accelerate.
Q.
The guidelines mention biomarkers, found in blood and in spinal fluid, that may help reveal whether symptoms and behavioral changes are caused by Alzheimer’s or something else. They’re being used in research, but it sounds like they won’t yet be available for most patients. Why not?
A.
It’s not like diabetes, where a fasting elevated blood sugar in the morning or hemoglobin A1c above 6 are clear signposts. What we desperately need for Alzheimer’s disease are more accurate biomarkers like that. But the ones we have are not yet standardized outside of laboratories, though if I read the language correctly, there may be individual cases where you might want to use them.
The public could misread these biomarkers of amyloid levels in the spinal fluid or in the blood as real diagnostic criteria, like those we have for diabetes. But we really don’t have a firm connection that’s predictive. We know that high cholesterol, for example, is part of the cause of coronary artery disease, not the result of the disease. We don’t know if amyloid is the cause of Alzheimer’s disease or a byproduct. So these biomarkers are not quite ready for general use in a doctor’s office or hospital.
Q.
It seems, then, that most people accompanying a parent to a doctor’s appointment may not yet see any dramatic developments because of the new criteria. The changes sound more incremental.
A.
That’s true. But because Alzheimer’s has its onset so late in life, if we can push the disability back towards the end of the life span, then the social and personal burdens are very much lessened. We don’t have to cure this disease in order to beat it, in the sense of preventing it from being socially and emotionally crippling.

Paula Span is the author of “When the Time Comes: Families With Aging Parents Share Their Struggles and Solutions.”

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