Recognition memory is impacted in atypical “non‐amnestic” Alzheimer’s disease

Abstract

AbstractBackgroundMemory encoding and retrieval deficits have increasingly been identified in atypical phenotypes of AD, including posterior cortical atrophy (PCA) and logopenic variant primary progressive aphasia (lvPPA), despite traditional assumptions that memory is spared in these groups. There is a critical need to better understand relationships between these encoding deficits and recognition memory performance. Here we aim to build on the current literature by investigating recognition memory performance across the atypical AD syndromic spectrum.MethodThirty‐seven amyloid‐positive patients with atypical syndromes of AD (14 PCA, 9 lvPPA, and 14 amnestic dysexecutive) were administered the California Verbal Learning Test (CVLT‐II‐SF). Recognition memory performance (d’) and Total Learning were calculated. Independent samples t‐tests were conducted to test the hypothesis that amnestic dysexecutive patients would show greater d’ impairment compared to non‐amnestic (PCA, lvPPA) groups. Bivariate correlations were conducted to determine if Total Learning was related to d’ performance. Whole‐cortex general linear models, thresholded at p<0.01, were conducted to determine where cortical atrophy was related to d’ and Total Learning across all participants.ResultRecognition memory was poor across both groups but trended toward worse in the amnestic dysexecutive group (mean d’=1.3) compared to the non‐amnestic group (mean d’=1.9; t=1.8, p=0.08). Total Learning was related to d’ in the non‐amnestic group (r=0.72, p=0.0002), but not in the amnestic dysexecutive group (p<0.7). In the full sample, cortical atrophy was related to Total Learning in a strongly left‐lateralized pattern in the medial parietal and lateral temporoparietal cortices, while atrophy in left>right anterior medial temporal cortices was related to d’.ConclusionRecognition memory is not spared in atypical phenotypes of AD traditionally thought to be “non‐amnestic,” such as PCA and lvPPA. In these groups, individuals who showed stronger learning did not show storage decay, while those who struggled to learn showed poor discriminability. In the amnestic dysexecutive group, recognition discriminability was impaired regardless of learning ability, suggesting clearer storage loss. Convergent evidence from this and our prior work (Wolk & Dickerson et al., 2011) shows that when encoding or storage is impaired in atypical or typical AD, it is due to neurodegeneration in common circuits subserving these memory processes.