Antisaccade task reflects cortical involvement in mild cognitive impairment
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Abstract
Objective: The aims of this study were to examine executive dysfunction using an antisaccade (AS) task in normal elderly (NE) and patients with mild cognitive impairment (MCI) and Alzheimer disease (AD) as well as to evaluate the relationship between AS performance and cortical thinning within AD-associated regions.
Methods: We recorded eye movements in 182 subjects (NE: 118; MCI: 36; AD: 28) during an AS task. We also performed neuropsychological measures of executive function for comparison. Brain MRI scans were collected on most subjects, and cortical thickness was determined in 9 regions known to exhibit atrophy in AD dementia (“AD signature”). We investigated the relationships between AS and neuropsychological performance, as well as possible correlations between AS performance and cortical thickness.
Results: AS performance in MCI resembled that in NE; subjects with AD were impaired relative to both MCI and NE. In all subjects, AS performance correlated with neuropsychological measures of executive function, even after controlling for disease severity. In the subjects with MCI but not in NE, cortical thickness in frontoparietal AD signature regions correlated with AS performance.
Conclusions: The AS task is a useful measure of executive function across the AD spectrum. In MCI, AS performance may reflect disease burden within cortical brain regions involved in oculomotor control; however, AS impairments in NE may have etiologies other than incipient AD.
GLOSSARY
- AD=
- Alzheimer disease;
- AS=
- antisaccade;
- CDR-SB=
- Clinical Dementia Rating–Sum of Boxes;
- EF=
- executive function;
- MCI=
- mild cognitive impairment;
- MMSE=
- Mini-Mental State Examination;
- NE=
- normal elderly;
- ROI=
- region of interest;
- UCSF=
- University of California, San Francisco
Footnotes
Go to Neurology.org for full disclosures. Funding information and disclosures deemed relevant by the authors, if any, are provided at the end of the article.
Supplemental data at www.neurology.org
- Received April 22, 2013.
- Accepted in final form July 1, 2013.
- © 2013 American Academy of Neurology
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