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Cortical thickness in the Alzheimer’s disease signature regions among superagers
Author(s) -
Dev Sheena Isha,
Savoca Paul,
Wong Bonnie,
Andreano Joseph M,
Katsumi Yuta I,
Barrett Lisa F,
Dickerson Brad C,
Touroutoglou Alexandra
Publication year - 2020
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1002/alz.045480
Subject(s) - audiology , cognitive decline , atrophy , psychology , medicine , cognition , dementia , disease , neuroscience
Background Normal aging is usually associated with decline in several cognitive domains and atrophy across most brain regions. Some older adults who show exceptionally preserved memory performance (dubbed Superagers (SA)) exhibit preserved cortical thickness in key regions of the salience and default mode networks, which are important for memory and implicated in both aging and Alzheimer’s disease (AD). Although studies suggest SA have a similar prevalence of cerebral amyloidosis compared with typical older adults (TOA), none have investigated aging‐selective vs. AD‐selective atrophy in these groups. Here we compare cortical thickness in our aging‐selective and AD‐selective cortical signatures in TOA and SA. Method 41 young adults (YA), 21 TOA, and 17 SA were included. SA were older adults (aged 60‐80) who a) performed at or above average for YA on the California Verbal Learning Test‐2 long delay free recall; and b) were within expectations for their age group on the Trail Making Test‐B. Structural scans were acquired for all participants and average cortical thickness in Aging‐ and AD‐Signatures were extracted. Independent t‐tests determined differences between young adults (YA) and combined older adult groups in the Aging‐ and AD‐Signature. One‐way ANOVAs examined cortical thickness between all groups. All effects reported met a‐priori alpha value of 0.05 uncorrected. Result Groups were matched on education and gender. There was no difference in age between TOA and SA. There were large reductions in cortical thickness in the entire older adult sample compared to YA in both Aging‐signature (t=12.5, Cohen’s d=2.8) and AD‐Signature (t=8.14, d=1.84). Compared to YA, TOA showed very large reductions in cortical thickness in Aging‐Signature (t=12.5, d= 3.20) and AD‐Signature (t=8.2, d= 2.15), while SA showed lesser reductions in Aging‐Signature (t=8.5, d= 2.6) and AD‐Signature (t=5.6, d= 1.64). SA showed thicker cortex than TOA in both Aging‐signature (t=8.4, d = 0.88) and AD‐signature (t=2.1, d = 0.64). Conclusion Superagers are resilient to atrophy in regions affected by normal aging and AD. Preliminary analyses suggest that most of these effects were driven by large global effects of age, but work is ongoing to adjust the AD‐signature measure for cortical age as we have done previously.