Assessment of Lifecourse Social Exposome in Brain Bank Decedents
Sarah A Keller, W. Ryan Powell, William R. Buckingham, Brittney Lyons Boone, Amanda DeWitt, Joseph A Kramer, Barbara B Bendlin, Amy J. Kind- Psychiatry and Mental health
- Cellular and Molecular Neuroscience
- Geriatrics and Gerontology
- Neurology (clinical)
- Developmental Neuroscience
- Health Policy
- Epidemiology
Abstract
Background
There is increasing evidence that the social exposome impacts the development of Alzheimer’s disease and related dementias (ADRD). The social exposome includes factors such as neighborhood disadvantage, and is thought to impact brain health across the lifecourse, particularly during sensitive life stages such as early childhood. Residential histories are required to assess dosage and timing of exposures, yet are rarely categorized and linked to brain bank cohorts. Our objective was to characterize the lifecourse neighborhood disadvantage across two Alzheimer’s Disease Research Center (ADRC) brain banks.
Method
After abstracting publicly available residential data, we constructed residential histories using validated metrics of neighborhood disadvantage, nationwide Area Deprivation percentile rankings (ADI), constructed for each census timeframe from 1910‐present, to measure lifecourse social exposome time‐concordantly aligned to participant life‐year. ADIs were linked for all available years between birth and death, ranging from age 0 to 103. Greater ADI values denote living in higher neighborhood disadvantage. These ADIs were linked to the residential histories for each decedent and used to calculate two sensitive life stages: ages 0‐19 and 40‐60. A repeated measures one‐way ANOVA determined variance in ADI both within and between these sensitive life stages.
Result
This sample contained 1309 decedents from two brain. To date, 1230 decedents have been linked to at least one ADI timepoint, with an average of 81% (71‐88%) of all life‐course years accounted for via ADI linkage. The mean ADI for the 0‐19 period was 23.5 (SD = 22.3, 5.0‐36.9), while the 40‐60 period was 22.0 (21.6, 5.0‐34.0). A repeated measures one‐way ANOVA found a statistically significant difference in ADI between the two windows of time.
Conclusion
Tissue banked samples are not typically characterized on social determinants of health. Here we show that determining lifecourse social exposomes are feasible using publicly available data. To our knowledge, this is the first time such characterization has been successfully performed. Efforts to link decedents to ADI timepoints are still ongoing, which will reduce missingness, enhance measurement precision, and allow for comparison between all life stages. This work provides a unique methodology for assessing the social exposome in relation to ADRD brain pathology.