Memory Lapses May Herald Early Alzheimer's
But many seniors may function just fine despite brain changes, experts say
TUESDAY, June 27, 2006 (HealthDay News) -- Seniors with no outward signs of dementia but some deterioration in memory could still harbor the accumulated brain plaques that are typical of Alzheimer's disease, a new study suggests.
That doesn't mean elderly Americans should immediately think "Alzheimer's" whenever they have a "senior moment," however.
Barring an actual diagnosis for the illness, "I wouldn't necessarily look at it as something to be extremely concerned about," said Dr. Sam Gandy, chairman of the Alzheimer's Association's Medical and Scientific Advisory Council .
He was not involved in the study, which was led by Dr. David Bennett, director of the Rush Alzheimer's Disease Center in Chicago. His group published its findings in the June 27 issue of Neurology.
Bennett's team studied 134 cognitively normal older adults enrolled in the Memory and Aging Project. The subjects underwent annual clinical evaluation to assess five cognitive domains: Episodic memory, semantic memory, working memory, perceptual speed and visuospatial ability.
After the subjects died, their brains were autopsied and assessed for evidence of Alzheimer's disease.
Bennett and his team identified 50 subjects (37.3 percent) who met the criteria for a pathologic diagnosis of Alzheimer's disease. After adjusting for other factors, they found that these subjects had significantly lower scores for episodic memory (i.e., their ability to recall stories and word lists) than did subjects without Alzheimer's disease. They found no group differences in scores for the other four cognitive domains.
"Even though we couldn't pick it out on a case-by-case basis, when we looked at the group we saw that the presence of the Alzheimer's pathology was associated with this subtle episodic memory deficit," Bennett said.
"What this means is that the very subtle memory loss that people experience that we often call 'normal aging' is probably the beginning of Alzheimer's disease," he said. "I don't want to be an alarmist about it, but we ought to do something about it as a society because it probably means that Alzheimer's disease is much more common than we currently think."
Because treatments are only available for mild-to-moderate Alzheimer's disease, and no treatments are yet available for mild cognitive impairment, Bennett cautioned that the findings should not prompt older adults to seek immediate medical attention for occasional memory lapses.
"I suggest that nobody worry, because worry is bad for you," he said. "What I suggest instead is to write your congressman, because the government is cutting funding for Alzheimer's disease [research]. If you want a treatment 10 years from now, you need to advocate for one now."
The Rush study has good news for seniors, Bennett pointed out: None of the individuals in the study was demented, meaning that many older adults apparently function normally despite the presence of Alzheimer's brain pathology. "We think it's because these people have something else that's protecting them," he said.
Among the possible explanations: A high educational level, which encourages the formation of new brain synapses; an extensive social network; and a neural reserve that may allow older adults to tolerate a large amount of Alzheimer's pathology without developing dementia.
"One of the classic examples is that people tend to use a certain part of the frontal cortex," Bennett said. "Younger people use just one side, but older people tend to use both sides."
Gandy offered another possible explanation. "There's been a recent move away from plaques per se and toward clumps called 'oligomers,' " he said. "The current thinking is that these oligomers -- which are intermediates between the amyloid that exists normally and the part that clumps and forms plaques -- may be the main poison. In the people that Dr. Bennett studied, it's possible that the oligomer levels were not high. Maybe they made plaques but not oligomers."
Although no one knows exactly why Bennett's subjects were spared dementia despite their Alzheimer's pathology, "it's something we'd like to understand because it could possibly provide us with an entirely new avenue of therapy," Gandy said.
"If we could find a drug that mimics what's going on in these people's brains and renders plaques inert, that would be fine," he said. "People don't go to the doctor because their heads are full of plaque. They go because they're demented. You don't really care about the pathology as long as you get a good clinical outcome. "
In a related study, researchers at Duke University Medical Center reported Tuesday that memory deficits typical of early Alzheimer's may be linked to altered activity in more than one brain region.
Reporting in the July Radiology, the team used functional MRI (fMRI) to track brain activity in people with mild cognitive impairment -- a precursor to Alzheimer's. While previous research had linked this memory loss to changes in the brain's temporal lobe, this latest study found alterations in the frontal lobe, as well.
The finding "suggests the possibility of a breakdown in the communication pathway between these two regions, which house short-term and long-term memory, respectively," lead researcher Dr. Jeffrey Petrella said in a prepared statement.
Tracking Alzheimer's progression in the brain may have also gotten easier, according to researchers at Washington University School of Medicine, in St. Louis. Reporting Sunday in the online edition of Nature Medicine, they said they've developed a test that can record the production and clearance of amyloid beta protein -- the plaques that build up in brain tissue as part of Alzheimer's. The new test should prove important for Alzheimer's drug development, the researchers said.
There's more on memory loss at the National Institutes of Health.
SOURCES: David Bennett, M.D., director, Rush Alzheimer's Disease Center, Chicago; Sam Gandy, M.D., Ph.D., chair, Medical and Scientific Advisory Council, Alzheimer's Association, and director, Farber Institute for Neurosciences, Thomas Jefferson University, Philadelphia; June 27, 2006, Neurology, June 27, 2006, news release, Radiological Society of North America