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Neurobiol Aging. 2016 Oct;46:68-75. doi: 10.1016/j.neurobiolaging.2016.06.011. Epub 2016 Jun 25.

Discrepancies between fluid and crystallized ability in healthy adults: a behavioral marker of preclinical Alzheimer's disease.

Author information

1
Center for Vital Longevity, School of Behavioral and Brain Sciences, University of Texas at Dallas, TX, USA. Electronic address: immcdonough@ua.edu.
2
Center for Vital Longevity, School of Behavioral and Brain Sciences, University of Texas at Dallas, TX, USA; Multimodal Neuroimaging Group, Department of Nuclear Medicine, University Hospital Cologne & Cognitive Neuroscience, Institute of Neuroscience & Medicine (INM-3) Research Centre, Juelich, Germany.
3
Center for Vital Longevity, School of Behavioral and Brain Sciences, University of Texas at Dallas, TX, USA.

Abstract

Measures of core cognitive processes (fluid abilities) are highly correlated with measures of knowledge (crystallized abilities) in healthy adults. In early stages of Alzheimer's disease (AD), fluid abilities, however, decline more rapidly than crystallized abilities. We hypothesized that cognitively normal older adults who evidenced lower fluid ability compared with crystallized ability (an ability discrepancy) would show evidence of early AD neuropathology indexed via in vivo measures of amyloid-beta (Aβ) deposition and cortical thickness in AD-vulnerable regions. A sample of older adults (n = 112) aged 65 to 89 underwent a cognitive battery, structural magnetic resonance imaging, and a subset (n = 75) also completed positron emission tomography scanning to measure Aβ deposition using F-18 Florbetapir. Of this sample, 60 older adults (43 with available positron emission tomography scans) evidenced a discrepancy where fluid ability was lower than crystallized ability. The magnitude of the ability discrepancy was independently associated with a greater Aβ deposition and thinner cortex in AD-vulnerable regions, as well as age. The data suggest that such a discrepancy may be a marker of preclinical AD.

KEYWORDS:

Ability discrepancy; Aging; Amyloid-beta; Cortical thickness; Dementia; Preclinical

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