People often recognize and remember faces of individuals within their own race more easily than those of other races. While behavioral research has long suggested that the Other-Race Effect (ORE) is due to extensive experience with one’s own race group, the neural mechanisms underlying the effect have remained elusive. Predominant theories of the ORE have argued that the effect is mainly caused by processing disparities between same and other-race faces during early stages of perceptual encoding. Our findings support an alternative view that the ORE is additionally shaped by mnemonic processing mechanisms beyond perception and attention. Using a “pattern separation” paradigm based on computational models of episodic memory, we report evidence that the ORE may be driven by differences in successful memory discrimination across races as a function of degree of interference or overlap between face stimuli. In contrast, there were no ORE-related differences on a comparable match-to-sample task with no long-term memory load, suggesting that the effect is not simply attributable to visual and attentional processes. These findings suggest that the ORE may emerge in part due to “tuned” memory mechanisms that may enhance same-race, at the expense of other-race face detection.

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Introduction:We tested whether Alzheimer's disease (AD) pathology predicts memory deficits in non-demented older adults through its effects on medial temporal lobe (MTL) subregional volume. Methods: Thirty-two, non-demented older adults with cerebrospinal fluid (CSF) (amyloid-beta [Aβ] 42 /Aβ 40 , phosphorylated tau [p-tau] 181 , total tau [t-tau]), positron emission tomography (PET; 18F-florbetapir), high-resolution structural magnetic resonance imaging (MRI), and neuropsychological assessment were analyzed. We examined relationships between biomarkers and a highly granular measure of memory consolidation, retroactive interference (RI). Results: Biomarkers of AD pathology were related to RI. Dentate gyrus (DG) and CA3 volume were uniquely associated with RI, whereas CA1 and BA35 volume were related to both RI and overall memory recall. AD pathology was associated with reduced BA35, CA1, and subiculum volume. DG volume and Aβ were independently associated with RI, whereas CA1 volume mediated the relationship between AD pathology and RI. Discussion: Integrity of distinct hippocampal subfields demonstrate differential relationships with pathology and memory function, indicating specificity in vulnerability and contribution to different memory processes.

White matter hyperintensities are a marker of small vessel cerebrovascular disease that are strongly related to cognition in older adults. Similarly, medial temporal lobe atrophy is well-documented in aging and Alzheimer's disease and is associated with memory decline. Here, we assessed the relationship between lobar white matter hyperintensities, medial temporal lobe subregional volumes, and hippocampal memory in older adults. We collected MRI scans in a sample of 139 older adults without dementia (88 females, mean age (SD) = 76.95 (10.61)). Participants were administered the Rey Auditory Verbal Learning Test (RAVLT). Regression analyses tested for associations among medial temporal lobe subregional volumes, regional white matter hyperintensities and memory, while adjusting for age, sex, and education and correcting for multiple comparisons. Increased occipital white matter hyperintensities were related to worse RAVLT delayed recall performance, and to reduced CA1, dentate gyrus, perirhinal cortex (Brodmann area 36), and parahippocampal cortex volumes. These medial temporal lobe subregional volumes were related to delayed recall performance. The association of occipital white matter hyperintensities with delayed recall performance was fully mediated statistically only by perirhinal cortex volume. These results suggest that white matter hyperintensities may be associated with memory decline through their impact on medial temporal lobe atrophy. These findings provide new insights into the role of vascular pathologies in memory loss in older adults and suggest that future studies should further examine the neural mechanisms of these relationships in longitudinal samples.

Background Amyloid‐beta (Aβ) plaques are among the hallmark pathologies of Alzheimer’s disease (AD) and could potentially influence the aggregation of tau pathology, which is associated with neurodegeneration in AD. Prior work has demonstrated that left hippocampal atrophy is present in both Alzheimer’s disease (AD) and mild cognitive impairment (MCI). However, these relationships are not clear in preclinical AD (i.e. those with Aβ biomarkers but no clinical impairment). This study assesses the relationship between Aβ pathology and hippocampal volume in nondemented older adults without clinical impairment. Method Data from 54 adults (60‐85 years of age, 41 female) enrolled in the Biomarker Exploration for Aging, Cognition, and Neurodegeneration (BEACoN) study were included in this analysis. Participants underwent T1‐weighted MRI scans (MPRAGE) and PET amyloid scans with F18‐florbetapir (AV‐45) at the University of California, Irvine. Aβ status (+ or ‐) was determined by the composite score defined by Jack et al (Alz Dem 2017). Each subject’s T1 weighted MRI image was skull stripped and run through the joint label fusion (JLF) pipeline in ANTs to obtain medial temporal lobe subregion volumes and surface area. Cortical reconstruction was performed using Freesurfer 6.0 to obtain estimated total intracranial volume (ICV). All scans were then subjected to visual QC to ensure high quality segmentations. Of the sample of 54, 39 (29F) were Aβ‐ and 15 (12F) were Aβ+. We used two multiple regressions to determine if Aβ status was associated with left hippocampal volume. The first treated Aβ status as a binary variable and the second used the continuous SUVR measure in the AD composite region. Both models accounted for the effect of age and gender. Result We found a significant association between left hippocampal volume and Aβ status, which remained significant after adjusting for age and gender. The result was further corroborated by using the continuous SUVR measures. Conclusion Our results suggest that the association between amyloid deposition and hippocampal atrophy may begin years before the onset of Alzheimer’s disease and can be detected even in nondemented older adults. Future work is needed to examine whether these relationships change longitudinally.