Association of Performance on the Financial Capacity Instrument-Short Form With Brain Amyloid Load and Cortical Thickness in Older Adults

Maria Vassilaki; Jeremiah A Aakre; Walter K Kremers; Michelle M Mielke; Yonas E Geda; Mary M Machulda; David S Knopman; Prashanthi Vemuri; Val J Lowe; Clifford R Jack Jr; Erik D Roberson; Adam Gerstenecker; Roy C Martin; Richard E Kennedy; Daniel C Marson; Ronald C Petersen

doi:10.1212/CPJ.0000000000001157

Association of Performance on the Financial Capacity Instrument-Short Form With Brain Amyloid Load and Cortical Thickness in Older Adults

Neurol Clin Pract. 2022 Apr;12(2):113-124. doi: 10.1212/CPJ.0000000000001157.

Authors

Maria Vassilaki¹, Jeremiah A Aakre¹, Walter K Kremers¹, Michelle M Mielke¹, Yonas E Geda¹, Mary M Machulda¹, David S Knopman¹, Prashanthi Vemuri¹, Val J Lowe¹, Clifford R Jack Jr¹, Erik D Roberson¹, Adam Gerstenecker¹, Roy C Martin¹, Richard E Kennedy¹, Daniel C Marson¹, Ronald C Petersen¹

Affiliation

¹ Department of Quantitative Health Sciences (MV, JAA, WKK, M.M. Mielke, RCP), and Department of Neurology (M.M. Mielke, DSK, RCP), Mayo Clinic, Rochester, MN; Department of Neurology (YEG), Barrow Neurological Institute, Phoenix, AZ; Department of Psychiatry and Psychology (M.M. Machulda), and Department of Radiology (PV, VJL, CRJ), Mayo Clinic, Rochester, MN; Department of Neurology (EDR, AG, RCM, DCM), Department of Medicine (REK), and Alzheimer's Disease Center (DCM), University of Alabama at Birmingham.

Abstract

Background and objectives: To investigate the association of the Financial Capacity Instrument-Short Form (FCI-SF) performance and timing total scores with brain β-amyloid and cortical thickness in cognitively unimpaired (CU) (at baseline) older adults.

Methods: A total of 309 participants (aged 70 years or older) of the Mayo Clinic Study of Aging underwent ¹¹C-Pittsburgh compound B PET amyloid imaging and MRI, and completed the FCI-SF. Abnormal amyloid PET was defined as standardized uptake value ratio ≥1.48 in an Alzheimer disease (AD)-related region of interest and reduced AD signature cortical thickness as ≤2.68 mm (neurodegeneration). A cohort of 218 (of the 309) participants had follow-up visits (every 15 months) with FCI-SF data for longitudinal analysis (number of visits including baseline, median [range]: 2 [2-4]). In the analysis, we used linear regression and mixed-effects models adjusted for age, sex, education, apolipoprotein E ε4 allele status, global cognitive z score, and previous FCI-SF testing.

Results: Participants' mean age (SD) was 80.2 (4.8) years (56.3% male individuals). In cross-sectional analysis, abnormal amyloid PET (vs normal) was associated with a lower FCI-SF total score and slower total composite time. In longitudinal analysis, FCI-SF total score declined faster (difference in annualized rate of change, beta coefficient [β] [95% confidence interval (CI)] = -1.123 [-2.086 to -0.161]) and FCI-SF total composite time increased faster (difference in annualized rate of change, β [95% CI] = 16.274 [5.951 to 26.597]) for participants with neurodegeneration at baseline (vs those without). Participants who exhibited both abnormal amyloid PET and neurodegeneration at baseline had a greater increase in total composite time when compared with the group without abnormal amyloid and without neurodegeneration (difference in annualized rate of change, β [95% CI] = 16.750 [3.193 to 30.307]).

Discussion: Performance and processing speed on the FCI-SF were associated with imaging biomarkers of AD pathophysiology in CU (at baseline) older adults. Higher burdens of imaging biomarkers were associated with longitudinal worsening on FCI-SF performance. Additional research is needed to delineate further these associations and their predictive utility at the individual person level.

Abstract

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