# Social modifiers of the pace of aging across multiple domains and tissues

> **NIH NIH R01** · ARIZONA STATE UNIVERSITY-TEMPE CAMPUS · 2020 · $680,808

## Abstract

Social modifiers of the pace of aging across multiple domains
With a rapidly growing aging population comes a correspondingly rapid increase in the incidence of aging-
related diseases. However, not everyone falls victim to aging-related diseases at the same time – there is
substantial variability in the age at onset and progression of diseases of aging. Evidence suggests that part of
this variation is associated with social adversity, such as low socioeconomic status and social isolation. But
precisely how social adversity “gets under the skin” to alter the pace of aging remains elusive. Progress on this
front lags because comprehensive portraits of individuals' realized biological age are required across the
lifespan in multiple domains and organ systems, a feat largely unfeasible in humans. A suitable animal model,
such a non-human primate, is needed where natural variation in both social behavior and aging are
homologous to that in humans, and can be tracked across the lifespan in different tissues and domains of
aging.
The objective of this proposal is to develop a biological model of the social contributions to aging in a natural
population of nonhuman primates. To do so, it draws on a long-term study of a free-living population of rhesus
macaques. These animals present an unparalleled opportunity to probe aging and its social determinants in a
large population living in naturalistic circumstances because of their phylogenetic proximity to humans,
homologous natural markers of social adversity, including social isolation and low social status represented by
low dominance rank, and considerably shorter (3-4x) lifespans. This project tests the hypothesis that social
adversity accelerates biological aging across multiple tissue types and in three central aging domains: (i)
molecular (e.g., DNA methylation and telomere attrition), (ii) immunological (e.g., inflammation and leukocyte
composition), and (iii) physical (e.g., frailty, including joint mobility and body condition).
Aim 1 of this project aims to generate comprehensive aging profiles across domains and systems by taking an
approach that is: (a) cross-sectional across tissue types and (b) longitudinal over individuals' lifespans. By
tracking aging across tissue types and the lifespan, we will pinpoint modifiable sources of aging variation, as
well as establish the timing and sex-specificity of modifiable aging domains. Aim 2 draws on detailed social
phenotypes to test how, and in what domains, social adversity accelerates aging.
This project will lend transformative insights into two major issues in the biology of aging. First, it will generate
valuable data on molecular, immunological and physical signatures of aging using a naturalistic primate model
for human aging. Second, it will reveal how the social environment alters the pace of aging, which will inform
the targeted development of social and physiological interventions that could reduce the burden of aging-
related disease in ou...

## Key facts

- **NIH application ID:** 10104079
- **Project number:** 7R01AG060931-02
- **Recipient organization:** ARIZONA STATE UNIVERSITY-TEMPE CAMPUS
- **Principal Investigator:** Lauren Johanna Nicole Brent
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $680,808
- **Award type:** 7
- **Project period:** 2019-07-01 → 2024-01-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10104079

## Citation

> US National Institutes of Health, RePORTER application 10104079, Social modifiers of the pace of aging across multiple domains and tissues (7R01AG060931-02). Retrieved via AI Analytics 2026-05-22 from https://api.ai-analytics.org/grant/nih/10104079. Licensed CC0.

---

*[NIH grants dataset](/datasets/nih-grants) · CC0 1.0*