Document Type
Article
Language
eng
Format of Original
11 p.
Publication Date
5-2015
Publisher
Elsevier
Source Publication
NeuroImage
Source ISSN
1053-8119
Original Item ID
doi: 10.1016/j.neuroimage.2015.02.011
Abstract
Healthy aging is associated with cognitive declines typically accompanied by increased task-related brain activity in comparison to younger counterparts. The Scaffolding Theory of Aging and Cognition (STAC) (Park and Reuter-Lorenz, 2009; Reuter-Lorenz and Park, 2014) posits that compensatory brain processes are responsible for maintaining normal cognitive performance in older adults, despite accumulation of aging-related neural damage. Cross-sectional studies indicate that cognitively intact elders at genetic risk for Alzheimer's disease (AD) demonstrate patterns of increased brain activity compared to low risk elders, suggesting that compensation represents an early response to AD-associated pathology. Whether this compensatory response persists or declines with the onset of cognitive impairment can only be addressed using a longitudinal design. The current prospective, 5-year longitudinal study examined brain activation in APOE ε4 carriers (N = 24) and non-carriers (N = 21). All participants, ages 65–85 and cognitively intact at study entry, underwent task-activated fMRI, structural MRI, and neuropsychological assessments at baseline, 18, and 57 months. fMRI activation was measured in response to a semantic memory task requiring participants to discriminate famous from non-famous names. Results indicated that the trajectory of change in brain activation while performing this semantic memory task differed between APOE ε4 carriers and non-carriers. The APOE ε4 group exhibited greater activation than the Low Risk group at baseline, but they subsequently showed a progressive decline in activation during the follow-up periods with corresponding emergence of episodic memory loss and hippocampal atrophy. In contrast, the non-carriers demonstrated a gradual increase in activation over the 5-year period. Our results are consistent with the STAC model by demonstrating that compensation varies with the severity of underlying neural damage and can be exhausted with the onset of cognitive symptoms and increased structural brain pathology. Our fMRI results could not be attributed to changes in task performance, group differences in cerebral perfusion, or regional cortical atrophy.
Recommended Citation
Rao, Stephen M.; Bonner-Jackson, Aaron; Nielson, Kristy A.; Seidenberg, Michael; Smith, J. Carson; Woodard, John L.; and Durgerian, Sally, "Genetic Risk for Alzheimer's Disease Alters the Five-Year Trajectory of Semantic Memory Activation in Cognitively Intact Elders" (2015). Psychology Faculty Research and Publications. 173.
https://epublications.marquette.edu/psych_fac/173
Comments
Accepted version. NeuroImage, Vol. 111 (May 2015): 136-146. DOI. © 2015 Elsevier Inc. Used with permission.
NOTICE: this is the author’s version of a work that was accepted for publication in NeuroImage. Changes resulting from the publishing process, such as peer review, editing, corrections, structural formatting, and other quality control mechanisms may not be reflected in this document. Changes may have been made to this work since it was submitted for publication. A definitive version was subsequently published in NeuroImage, Vol. 111 (May 2015): 136-146. DOI.