Alzheimer Disease Cerebrospinal Fluid Biomarkers Moderate Baseline Differences and Predict Longitudinal Change in Attentional Control and Episodic Memory Composites in the Adult Children Study. (29th September 2015)

• Record Type: Journal Article
• Authors: Aschenbrenner, Andrew J.; Balota, David A.; Fagan, Anne M.; Duchek, Janet M.; Benzinger, Tammie L.S.; Morris, John C.
• Is Part Of: Journal of the International Neuropsychological Society. Volume 21:Number 8(2015:Aug.)
• Page Start: 573
• Page End: 583
• Publication Date: 2015-09-29
• Subjects: Neuropsychology -- Periodicals; 616.8
• DOI: 10.1017/S1355617715000776
• Languages: English
• ISSNs: 1355-6177

Abstract

<abstract abstract-type="normal"> <title>Abstract</title> <p>Cognitive measures that are sensitive to biological markers of Alzheimer disease (AD) pathology are needed to (a) facilitate preclinical staging, (b) identify individuals who are at the highest risk for developing clinical symptoms, and (c) serve as endpoints for evaluating the efficacy of interventions. The present study assesses the utility of two cognitive composite scores of attentional control and episodic memory as markers for preclinical AD pathology in a group of cognitively normal older adults (<italic>N</italic>=238), as part of the Adult Children Study. All participants were given a baseline cognitive assessment and follow-up assessments every 3 years over an 8-year period, as well as a lumbar puncture within 2 years of the initial assessment to collect cerebrospinal fluid (CSF) and amyloid tracer Pittsburgh compound-B scan for amyloid imaging. Results indicated that attentional control was correlated with levels of Aβ42 at the initial assessment whereas episodic memory was not. Longitudinally, individuals with high CSF tau exhibited a decline in both attention and episodic memory over the course of the study. These results indicate that measures of attentional control and episodic memory can be used to evaluate cognitive decline in preclinical AD and provide support that CSF tau may be a key mechanism driving longitudinal cognitive change. (<italic>JINS</italic>, 2015, <italic>21</italic>, 573–583)</p> </abstract>