BACKGROUND: Metabolic syndrome varies by socio-demographic characteristics, with younger (18-29 years) and older (50-69 years) Hispanic/Latino having higher prevalence compared to other groups. While there is substantial research on neighborhood influences on cardiometabolic health, there are mixed findings regarding the effects of gentrification and few studies have included Hispanic/Latinos. The role of neighborhood income inequality on metabolic health remains poorly understood. OBJECTIVES: Examined associations of neighborhood gentrification and income inequality with metabolic syndrome (MetSyn) using data from the Hispanic Community Health Study/Study of Latinos (HCHS/SOL). DESIGN, SETTING AND PARTICIPANTS: The HCHS/SOL is a community-based cohort of adults of Hispanic/Latinos (aged 18-74). Analyses included 6710 adults who did not meet criteria for MetsS at baseline (2008-2011) and completed the visit 2 examination (2014-2017). Poisson regressions estimated odds ratios (IRR) and 95% confidence intervals (CI) for neighborhood gentrification and change in income inequality with MetSyn incidence. MAIN OUTCOME AND EXPOSURE MEASURES: Gentrification was measured with an index that included changes (2000 to 2006-2010) in education, poverty, and income. Change in neighborhood income inequality (2005-2009 to 2012-2016) was measured using the Gini coefficient of income distribution. MetSyn was defined using National Cholesterol Education Program Adult Treatment Panel III criteria. RESULTS: Among 6647 Hispanic/Latino adults, 23% (N = 1530) had incident MetSyn. In models adjusted for socio-demographic, health insurance status, and neighborhood characteristics, gentrification (IRR, 1.00, 95%CI, 0.96-1.03) and income inequality change (IRR, 1.00, 95%CI, 0.99-1.00) were not associated with MetSyn at visit 2. There was no association between cross-sectional income inequality (2005-2009) and MetSyn at visit 2 (IRR, 0.97, 95%CI, 0.82-1.15). CONCLUSION: Neighborhood gentrification and income inequality change were not associated with incidence of MetSyn over 6 years among Hispanic/Latino adults. This study demonstrated that income-based residential changes alone may not be sufficient to explain neighborhood influences on health outcomes among this population.

PURPOSE: Examine the association between neighborhood segregation and 6-year incident metabolic syndrome (MetSyn) in the Hispanic Community Health Study/Study of Latinos. METHODS: Prospective cohort of adults residing in Miami, Chicago, the Bronx, and San Diego. The analytic sample included 6,710 participants who did not have MetSyn at baseline. The evenness and exposure dimensions of neighborhood segregation, based on the Gini and Isolation indices, respectively, were categorized into quintiles (Q). Racialized economic concentration was measured with the Index of Concentration at the Extremes (continuously and Q). RESULTS: Exposure, but not evenness, was associated with higher disease odds (Q1 (lower segregation) vs. Q4, OR = 1.53, 95% CI = 1.082.17; Q5, OR = 2.29, 95% CI = 1.493.52). Economic concentrationprivilege (continuous OR = 0.87, 95% CI = 0.770.98), racial concentrationracialized privilege (Q1 (greater concentration) vs. Q2 OR = 0.75, 95% CI = 0.541.04; Q3 OR = 0.68, 95% CI = 0.441.05; Q4 OR = 0.68, 95% CI = 0.451.01; Q5 OR = 0.64, 95% CI = 0.420.98)(continuous OR = 0.93, 95% CI = 0.821.04), and racialized economic concentrationprivilege (i.e., higher SES non-Hispanic White, continuous OR = 0.86, 95% CI = 0.760.98) were associated with lower disease odds. CONCLUSION: Hispanics/Latino adults residing in neighborhoods with high segregation had higher risk of incident MetSyn compared to those residing in neighborhoods with low segregation. Research is needed to identify the mechanisms that link segregation to poor metabolic health.

Characterization of the genetic landscape of Alzheimer's disease (AD) and related dementias (ADD) provides a unique opportunity for a better understanding of the associated pathophysiological processes. We performed a two-stage genome-wide association study totaling 111,326 clinically diagnosed/'proxy' AD cases and 677,663 controls. We found 75 risk loci, of which 42 were new at the time of analysis. Pathway enrichment analyses confirmed the involvement of amyloid/tau pathways and highlighted microglia implication. Gene prioritization in the new loci identified 31 genes that were suggestive of new genetically associated processes, including the tumor necrosis factor alpha pathway through the linear ubiquitin chain assembly complex. We also built a new genetic risk score associated with the risk of future AD/dementia or progression from mild cognitive impairment to AD/dementia. The improvement in prediction led to a 1.6- to 1.9-fold increase in AD risk from the lowest to the highest decile, in addition to effects of age and the APOE ε4 allele.