Background and Objectives Social connectedness has been linked prospectively to cognitive aging, but there is little agreement about the social mechanisms driving this relationship. This study evaluated nine measures of social connectedness, focusing on two forms of social enrichment – access to an expansive and diverse set of loosely connected individuals (i.e., social bridging) and integration in a supportive network of close ties (i.e., social bonding). Research Design and Methods This study used egocentric network and cognitive data from 311 older adults in the Social Networks in Alzheimer Disease (SNAD) study. Linear regressions were used to estimate the association between social connectedness and global cognitive function, episodic memory, and executive function. Results Measures indicative of social bridging (larger network size, lower density, presence of weak ties, and proportion non-kin) were consistently associated with better cognitive outcomes, while measures of social bonding (close ties, multiplex support, higher frequency of contact, better relationship quality, and being married) largely produced null effects. Discussion and Implications These findings suggest that the protective benefits of social connectedness for cognitive function and memory may operate primarily through a cognitive reserve mechanism that is driven by irregular contact with a larger and more diverse group of peripheral others.

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Background:We studied the effect of apolipoprotein E (APOE) ε4 status and sex on age of symptom onset (AO) in early-(EO) and late-(LO) onset Alzheimer's disease (AD).Method: A total of 998 EOAD and 2562 LOAD participants from the National Alzheimer's Coordinating Center (NACC) were included. We used analysis of variance to examine AO differences between sexes and APOE genotypes and the effect of APOE ε4, sex, and their interaction on AO in EOAD and LOAD, separately.Results: APOE ε4 carriers in LOAD had younger AO and in EOAD had older AO. Female EOAD APOE ε4 carriers had older AO compared to non-carriers (P < 0.0001). There was no difference for males. Both male and female LOAD APOE ε4 carriers had younger AO relative to non-carriers (P < 0.0001). Conclusion:The observed earlier AO in EOAD APOE ε4 non-carriers relative to carriers, particularly in females, suggests the presence of additional AD risk variants.

Background:We studied the effect of apolipoprotein E (APOE) ε4 status and sex on rates of cognitive decline in early-(EO) and late-(LO) onset Alzheimer's disease (AD). Method:We ran mixed-effects models with longitudinal cognitive measures as dependent variables, and sex, APOE ε4 carrier status, and interaction terms as predictor variables in 998 EOAD and 2562 LOAD participants from the National Alzheimer's Coordinating Center.Results: APOE ε4 carriers showed accelerated cognitive decline relative to non-carriers in both EOAD and LOAD, although the patterns of specific cognitive domains that were affected differed. Female participants showed accelerated cognitive decline relative to male participants in EOAD only. The effect of APOE ε4 was greater in EOAD for executive functioning (p < 0.0001) and greater in LOAD for language (p < 0.0001). Conclusion:We found APOE ε4 effects on cognitive decline in both EOAD and LOAD and female sex in EOAD only. The specific patterns and magnitude of decline are distinct between the two disease variants.

BackgroundSocial connectedness has been linked to decreased rates of cognitive decline particularly among older adults (Fratiglioni et al., 2004). Several studies have demonstrated that access to an expansive network of diverse, and loosely connected individuals (i.e., social bridging) plays a particularly unique role in conferring resilience against cognitive decline (Perry et al., 2021). We explored the association of social bridging with cortical atrophy measured by gray matter density (GMD) in cognitively normal (CN), subjective cognitive decline (SCD), mild cognitive impairment (MCI), and Alzheimer’s Disease (AD) participants from the Social Networks and Alzheimer’s Disease (SNAD) at the Indiana Alzheimer Disease Research Center.Method:We analyzed baseline data of 176 SNAD participants (63 CN, 54 SCD, 47 MCI, 12 AD). Social bridging metrics were collected via in‐person interviews of egocentric social network data. MCI and AD were combined into a cognitively impaired group, resulting in 3 diagnostic groups (CN, SCD, CI). Demographic and biomarker differences across groups were analyzed using ANOVA. Pooled linear regressions were run with ROIs as the dependent variables and diagnosis, age, sex, education, and social bridging as regressors. A voxel‐wise multiple linear regression of GMD images in SPM12 yielded statistical maps across the pooled sample.ResultTable 1 shows the demographic and biomarker comparisons of all groups. The linear regression showed greater social bridging was associated with larger left and right amygdala volume (both p=0.01), and trending larger left frontal thickness (p=0.055), and left and right insula thickness (both p=0.09). Figure 1 and Figure 2 show scatterplot distribution of significant and trending brain regions versus bridging by diagnostic group with regression p‐values and lines. Statistical maps show increasing social bridging is associated with increasing GMD lateralized to the left hemisphere with a frontotemporoparietal pattern (Figure 3).ConclusionWe found that the effects of particular social enrichment on GMD, such as social bridging, are localized to regions primarily involving motivation and emotion. The left lateralization suggests this hemisphere’s propensity for protection against cognitive decline via social mechanisms. Future work should investigate potential associations between social bridging and amyloid and tau deposition.