Keeping the mind active may delay symptoms of Alzheimer’s disease; however, the activity does not change the underlying disease in the brain for most people, according to a study published today in the online edition of Neurology, the medical journal of the American Academy of Neurology.
For people who are carriers of a gene linked to Alzheimer’s, the findings differed. People with a gene called APOE4, who had at least 14 years of education and kept mentally active in middle age had lower levels of proteins called amyloid plaques. The proteins can build up in brain tissue and lead to Alzheimer’s disease. People with the gene and a high level of education but did not keep mentally active in middle age had higher levels of amyloid plaques.
“When we looked specifically at the level of lifetime learning, we found that carriers of the APOE4 gene who had higher education and continued to learn through middle age had fewer amyloid deposition on imaging when compared to those who did not continue with intellectual activity in middle age,” says study author Prashanthi Vemuri, Ph.D., a Mayo Clinic dementia researcher.
Dr. Vemuri said the overall findings for people who do not carry the gene should not discourage people from exercising and taking part in activities, such as reading books and magazines, playing games and using computers. “The takeaway message for the general public is that keeping your mind active is very important in delaying symptoms of Alzheimer’s disease,” says Dr. Vemuri.
For the study, researchers evaluated 393 people without dementia who were part of the Mayo Clinic Study of Aging. Of those, 53 had mild cognitive impairment. All were 70 or older. They were divided into two groups: those with more than 14 years of education and those with less. Then, researchers used MRI and positron emission tomography scans to look for biomarkers of Alzheimer’s disease and questionnaires to evaluate weekly intellectual and physical activity in middle age.
Keeping Mind Active May Delay Alzheimer’s Symptoms But Not Underlying Disease
Funding: The study was supported by the National Institutes of Health.
Source: Susan Barber Lindquist – Mayo Clinic
Image Credit: Image is adapted from the Mayo Clinic press release.
Video Source: The video is credited to Mayo Clinic.
Original Research: Abstract for “Effect of intellectual enrichment on AD biomarker trajectories: Longitudinal imaging study” by Prashanthi Vemuri, Timothy G. Lesnick, Scott A. Przybelski, David S. Knopman, Mary Machulda, Val J. Lowe, Michelle M. Mielke, Rosebud O. Roberts, Jeffrey L. Gunter, Matthew L. Senjem, Yonas E. Geda, Walter A. Rocca, Ronald C. Petersen, and Clifford R. Jack, Jr in Neurology. Published online February 24 2016 doi:10.1212/WNL.0000000000002490
Abstract
Effect of intellectual enrichment on AD biomarker trajectories: Longitudinal imaging study
Objective: To investigate the effect of age, sex, APOE4 genotype, and lifestyle enrichment (education/occupation, midlife cognitive activity, and midlife physical activity) on Alzheimer disease (AD) biomarker trajectories using longitudinal imaging data (brain β-amyloid load via Pittsburgh compound B PET and neurodegeneration via 18fluorodeoxyglucose (FDG) PET and structural MRI) in an elderly population without dementia.
Methods: In the population-based longitudinal Mayo Clinic Study of Aging, we studied 393 participants without dementia (340 clinically normal, 53 mild cognitive impairment; 70 years and older) who had cognitive and physical activity measures and at least 2 visits with imaging biomarkers. We dichotomized participants into high (≥14 years) and low (<14 years) education levels using the median. For the entire cohort and the 2 education strata, we built linear mixed models to investigate the effect of the predictors on each of the biomarker outcomes.
Results: Age was associated with amyloid and neurodegeneration trajectories; APOE4 status appears to influence only the amyloid and FDG trajectories but not hippocampal volume trajectory. In the high-education stratum, high midlife cognitive activity was associated with lower amyloid deposition in APOE4 carriers. APOE4 status was associated with lower FDG uptake in the entire cohort and in participants with lower education but not the high-education cohort.
Conclusions: There were minimal effects of lifestyle enrichment on AD biomarker trajectories (specifically rates). Lifetime intellectual enrichment (high education, high midlife cognitive activity) is associated with lower amyloid in APOE4 carriers. High education is protective from the APOE4 effect on FDG metabolism. Differing education levels may explain the conflicting results seen in the literature.
“Effect of intellectual enrichment on AD biomarker trajectories: Longitudinal imaging study” by Prashanthi Vemuri, Timothy G. Lesnick, Scott A. Przybelski, David S. Knopman, Mary Machulda, Val J. Lowe, Michelle M. Mielke, Rosebud O. Roberts, Jeffrey L. Gunter, Matthew L. Senjem, Yonas E. Geda, Walter A. Rocca, Ronald C. Petersen, and Clifford R. Jack, Jr in Neurology. Published online February 24 2016 doi:10.1212/WNL.0000000000002490
