Cited by 372Dementia and Cognitive Impairment ResearchAlzheimer's disease research and treatmentsMemory Processes and Influences

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fMRI evidence of compensatory mechanisms in older adults at genetic risk for Alzheimer disease

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Bondi, Mark W., Houston, Wes S., Eyler, Lisa T., Brown, Gregory G.·2005·Neurology

DOI 10.1212/01.wnl.0000150885.00929.7ePMC PMC1761695

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Abstract

OBJECTIVE: To determine whether APOE genotype influences brain response and whether nonverbal stimuli generate findings comparable with those of previous studies that used verbal stimuli. The relationship between APOE genotype and blood oxygenation level dependent (BOLD) brain response was examined during a picture-encoding task in nondemented older adults. METHODS: Twenty nondemented participants with normal episodic memory function were divided into two groups based on the presence (n = 10) or absence (n = 10) of the APOE epsilon4 allele. Picture learning was completed during functional MRI in a blocked design alternating between experimental (novel pictures) and control (repeated picture) conditions. RESULTS: Nondemented older adults with an APOE epsilon4 allele showed greater magnitude and extent of BOLD brain response during learning of new pictures relative to their matched epsilon3 counterparts. Different patterns and directions of association between hippocampal activity and learning and memory performance were also demonstrated. CONCLUSIONS: The results suggest that brain response differences are not due to poorer general memory abilities, differential atrophy, or brain response during control conditions, but instead appear to be directly influenced by APOE genotype. Results are consistent with a compensatory hypothesis wherein older adults at genetic risk for Alzheimer disease by virtue of the APOE epsilon4 allele appear to require additional cognitive effort to achieve comparable performance levels on tests of episodic memory encoding.

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Authors: Bondi, M. W., Houston, W. S., Eyler, L. T., & Brown, G. G.
Affiliations: University of California San Diego (US)
ORCID: Bondi, Mark W.
Eyler, Lisa T.
Brown, Gregory G.
Venue: Neurology
Publisher: Ovid Technologies (Wolters Kluwer Health)
Published: 2005-02-08
Volume: 64
Issue: 3
Pages: 501-508
ISSN: 0028-3878 (ISSN-L)
1526-632X
DOI: 10.1212/01.wnl.0000150885.00929.7e
PMC: PMC1761695
OpenAlex: W2152021942
Cited by: 372
References: 57
Citations by year: 2026: 6 · 2025: 6 · 2024: 6 · 2023: 13 · 2022: 8 · 2021: 12 · 2020: 20 · 2019: 9 · 2018: 9 · 2017: 11 · 2016: 14 · 2015: 20 · 2014: 23 · 2013: 24 · 2012: 22
FWCI: 17.17
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Locations: Neurology (publishedVersion)
PubMed (publishedVersion)
PubMed Central (acceptedVersion)
Funders: National Institute on Aging (P50AG005131, R01AG012674)
Topics: Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
Life Sciences › Neuroscience › Cognitive Neuroscience › Memory Processes and Influences
Keywords: APOE ε4, compensatory mechanisms, older adults, BOLD signal, picture encoding, episodic memory encoding, hippocampal activity, nonverbal stimuli, cognitive effort, brain responses
MeSH terms: Adaptation, Psychological, Aged, Aged, 80 and over, Alleles, Alzheimer Disease, Apolipoproteins E, Cerebral Cortex, Cerebrovascular Circulation, Cognition, Female, Genotype, Hippocampus, Humans, Learning, Magnetic Resonance Imaging, Male, Memory, Memory Disorders, Neuropsychological Tests, Photic Stimulation, Prognosis, Reference Values, Disease Progression, Genetic Predisposition to Disease, Early Diagnosis, Apolipoprotein E4

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fMRI evidence of compensatory mechanisms in older adults at genetic risk for Alzheimer disease

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