How many animals can you name in one minute?
Don’t laugh. It’s a serious question. The Animal Naming Test has proved to be a powerful tool in clinical medicine. A score below 15 may point toward a diagnosis of Alzheimer’s disease.
So too can a brain-imaging study that uses a marker called carbon 11-labeled Pittsburgh Compound B (PiB). The marker binds to beta-amyloid plaques in the brain and shows up on a positron emission tomography (PET) scan. The greater the PiB uptake in the brain, the greater the plaque buildup and the more likely a diagnosis of Alzheimer’s.
Catherine Roe and her colleagues at the Alzheimer's Disease Research Center at the Washington University School of Medicine in St. Louis combined those two diagnostic methods to test the “cognitive reserve hypothesis” of Alzheimer’s. The hypothesis asserts that people with greater cognitive (thinking, learning and memory) abilities can delay the symptoms of Alzheimer's disease, even while beta-amyloid is accumulating in the brain.
Roe and her team studied 198 people, mean age 67, between 2003 and 2008. They compared 161 nondemented subjects with 37 patients whose behavioral and clinical reports led to a diagnosis of Alzheimer’s. Animal naming was only one of the many cognitive tests they used, and all subjects underwent a PiB PET scan. The team used statistical tests to assess how the number of plaques in the brain, clinical and behavioral measures, and cognitive reserve interacted.
Roe used the number of years of education as a measure of cognitive reserve because autopsy studies have shown that people who have stayed in school longer may also exhibit a greater resistance to Alzheimer’s symptoms, even while degenerative changes are occurring in the brain.
Roe’s newest findings, reported in the Nov. 11 issue of the Archives of Neurology, support the cognitive reserve hypothesis. “We found that people who did not have plaques in their brains showed basically no dementia symptoms,” she says. “However, for people who did have plaques in their brains, the severity of dementia symptoms was related to how much education they had completed.” What Roe terms a greater “pathological burden” was required to elicit symptoms of dementia in people with more education. In general, the greater the educational level, the less severe the symptoms.
No one knows exactly how cognitive reserve might work, but experts suggest two possibilities. One is that established networks in the brain are more efficient, have greater capacity or are less susceptible to disruption. The other possibility is that alternative networks may be called into service to compensate for the degenerative changes in previously used networks.
“Roe and her colleagues have demonstrated that high educational attainment reduces the likelihood that amyloid pathology will be associated with manifestations of dementia,” says Paul Aisen, a professor in the Department of Neurosciences at the University of California, San Diego, and director of the Alzheimer’s Disease Cooperative Study.
Roe is quick to point out that years of education may not be the only measure of cognitive reserve. Other indicators include a challenging occupation, engaging hobbies and active social networks. Aisen agrees: “This may encourage people to maximize cognitive activities throughout life [a presumably low-risk approach] to improve resistance to the symptoms of dementia in later life,” he says.
Roe plans to continue her investigations of the cognitive reserve hypothesis. She wants to probe the effects of education and other learning experiences in adulthood to see whether such activities can help maintain cognition when Alzheimer’s pathology is present. “As we obtain more data,” she says, “we will be better able to see whether the association between education and dementia symptoms when plaques are present is similar across different levels of education.”