Associations between Performance on an Abbreviated CogState Battery, Other Measures of Cognitive Function, and Biomarkers in People at Risk for Alzheimer’s Disease

Abstract

It is not known whether computerized cognitive assessments, like the CogState battery, are sensitive to preclinical cognitive changes or pathology in people at risk for Alzheimer’s disease (AD). In 469 late middle-aged participants from the Wisconsin Registry for Alzheimer’s Prevention (mean age 63.8±7 years at testing; 67% female; 39% APOE4+), we examined relationships between a CogState abbreviated battery (CAB) of seven tests and demographic characteristics, traditional paper-based neuropsychological tests as well as a composite cognitive impairment index, cognitive impairment status (determined by consensus review); and biomarkers for amyloid and tau (CSF phosphorylated-tau/Aβ42 and global PET-PiB burden) and neural injury (CSF neurofilament light protein). CSF and PET-PiB were collected in n=71 and n=91 participants, respectively, approximately four years prior to CAB testing. For comparison, we examined three traditional tests of delayed memory in parallel. Similar to studies in older samples, the CAB was less influenced by demographic factors than traditional tests. CAB tests were generally correlated with most paper-based cognitive tests examined and mapped onto the same cognitive domains. Greater composite cognitive impairment index was associated with worse performance on all CAB tests. Cognitively impaired participants performed significantly worse compared to normal controls on all but one CAB test. Poorer One Card Learning test performance was associated with higher levels of CSF phosphorylated-tau/Aβ42. These results support the use of the CogState battery as measures of early cognitive impairment in studies of people at risk for AD.

Measuring longitudinal cognition: Individual tests versus composites

“…Primary subsample analyses treated Aβ as a binary variable, with 1 representing suprathreshold levels of PiB, CSF‐Aβ 42 , or CSF‐Aβ 42/40 , and 0 representing subthreshold values on each available marker. The processes for determining these thresholds for Aβ positivity have been reported in detail elsewhere [24,36]. To estimate the proportion of variance attributable to Aβ 42 ‐related longitudinal decline, we regressed out covariate effects, and then modeled the residuals as a function of Aβ and Aβ× age.…”

Hypertension and obesity moderate the relationship between β‐amyloid and cognitive decline in midlife

“…Eight bilateral regions of interest (angular gyrus, anterior cingulate gyrus, posterior cingulate gyrus, frontal medial orbital gyrus, precuneus, supramarginal gyrus, middle temporal gyrus, and superior temporal gyrus) were selected from the automated anatomic labeling atlas, standardized, and reverse warped to native space. The mean DVR across these eight regions of interest was calculated for determination of Aβ status (elevated or non-elevated) using a cutoff of 1.19 as previously reported for the WRAP cohort [45].…”

Utility of the NIH Toolbox for assessment of prodromal Alzheimer's disease and dementia

“…As preventive therapies become available [3–5], efficient and sensitive assessments will be needed for longitudinal evaluations of large samples. Computerized measures offer standardized administration, streamlined scoring and analysis, access to large normative data sets, and automated capture of reaction time and other sensitive response parameters, making them highly effective for detection of subtle cognitive impairment [2,6].…”