Mentally Challenging Tasks Don’t Prevent Alzheimer’s, But They May Slow It Down

 
07 13 mentally challenging tasks Mentally Challenging Tasks Don’t Prevent Alzheimer’s, But They May Slow It Downt prevent alzheimer s but they may slow it downPhoto credit: Tatyana Kazakova

Intelligence and education may offer a cognitive “head start” that could keep the minds of people with Alzheimer’s functioning better temporarily, research finds.

Put another way, the investigators say, those who start out with greater cognitive reserve—a baseline of higher mental functioning—may have more they can afford to lose before Alzheimer’s disease symptoms begin to interfere with their daily lives compared with those who don’t have as much schooling or participate regularly in mentally challenging tasks.

“…more education seems to play a role as a form of cognitive reserve that helps people do better at baseline, but it doesn’t affect one’s actual level of decline.”

The findings, which appear in the Journal of Alzheimer’s Disease, suggest—but don’t prove—that exercising your brain might help keep you cognitively functional longer, but won’t ward off the inevitable decline of Alzheimer’s disease.

“Our study was designed to look for trends, not prove cause and effect, but the major implication of our study is that exposure to education and better cognitive performance when you’re younger can help preserve cognitive function for a while even if it’s unlikely to change the course of the disease,” says Rebecca Gottesman, professor of neurology at the Johns Hopkins University School of Medicine and of epidemiology at the Bloomberg School of Public Health.

Tracking changes over time

About 5 million people in the US live with Alzheimer’s disease, a number expected to triple by 2060, according to the US Centers for Disease Control and Prevention.

Because effective treatment options aren’t available for Alzheimer’s disease or other forms of dementia, researchers are interested in identifying ways to prevent or delay disease. Earlier studies suggested that people with higher intelligence or more education might have lower rates of these diseases, and Gottesman’s team designed a study to test the idea.

For the study, the researchers used data from the federally funded Atherosclerosis Risk in Communities (ARIC) study, in which nearly 16,000 healthy participants in midlife from Washington County, Maryland; Forsyth County, North Carolina; Jackson, Mississippi; and Minneapolis, Minnesota were enrolled from 1987 to 1989 and followed over the next decades. Twenty years into the study, participants were an average of 76 years old. About 57 percent were women, and 43 percent were African American, with the remaining participants white.


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The investigators focused on a group of 331 participants without dementia who were part of an additional study, the ARIC-PET study, in which participants underwent specialized brain imaging. Some 54 had less than a high school education, 144 had completed high school or earned their GED diploma, and 133 had some college or more formal education.

Twenty years in, all participants underwent MRIs and positron emission tomography (PET) scans of their brains to measure levels of amyloid beta protein accumulated in the brain, a standard marker of Alzheimer’s disease. The average PET scan score indicating the amount of amyloid beta protein in the brain after being compared with a part of the brain where amyloid beta doesn’t accumulate was 1.2. Researchers categorized some 171 participants as having elevated values greater than this standard, and they assigned the remaining participants to the non-elevated amyloid beta values category.

In late life (ages 65–84), researchers assessed each participant’s cognition with 10 standard tests of memory, language, and other intellectual function. Researchers administered three of these tests at about the 10-year timepoint as well. The average score indicating normal cognition was set to zero for statistical purposes, with a value of 1 indicating an above-average score, and -1 indicating a below average score.

Searching for an Alzheimer’s disease biomarker

Participants with any level of amyloid beta and with college, postgraduate, or professional schooling had average cognitive scores of about one or more standard units higher than those who had less than a high school education, regardless of beta amyloid levels in the brain. Gottesman says these data suggest that education seems to help preserve cognition, since those with education scored higher.

Gottesman notes that cognition scores in midlife weren’t associated with elevated levels of amyloid beta protein in the brain in late life. White participants with higher late-life cognition scores had a 40 percent lower risk of having elevated amyloid beta protein in the brain. Researchers observed this general trend in African American participants too, but to a lesser degree (around 30 percent lower risk).

“Our data suggest that more education seems to play a role as a form of cognitive reserve that helps people do better at baseline, but it doesn’t affect one’s actual level of decline,” says Gottesman.

“This makes studies tricky because someone who has good education may be less likely to show a benefit of an experimental treatment because they are already doing well.”

What this means for future research into developing therapies for Alzheimer’s disease, Gottesman says, is that it’s important to focus on some sort of independent and specific biomarker to show actual treatment benefit. She also says studies must look at trends in performance over time rather than at one timepoint.

Additional coauthors are from Oregon State University, Johns Hopkins, the University of Mississippi, and the Mayo Clinic.

Support for the ARIC-PET study came from the National Heart, Lung, and Blood Institute, as well as the National Institute on Aging. NHLBI and the NIA supported this particular research. Avid Radiopharmaceuticals provided the radioactive brain tracer the researchers used in the study.

Knopman is an investigator in clinical trials sponsored by Biogen and Lilly pharmaceuticals. Coauthor Dean Wong has received funding from Johnson & Johnson, Avid Radiopharmaceuticals/Eli Lilly, Roche Neurosciences, and Lundbeck.

Source: Johns Hopkins University

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