# Molecular interception and immunological characterization of age-associated disease

> **NIH NIH P01** · STANFORD UNIVERSITY · 2021 · $638,723

## Abstract

PROJECT SUMMARY
In developed countries, noncommunicable diseases such as cancer, cardiovascular disease, chronic respiratory
illness, and diabetes account for the majority of deaths among people aged 70 and older. The global economic
burden to care for patients with noncommunicable diseases is astronomical. In 2010, it cost an estimated 47
trillion dollars in 2010-2030, which is equivalent to 75% of global gross domestic product in 2010, to provide care
for patients with chronic disease. Clearly, we need a better strategy to identify patients at greatest risk so that
we can prevent disease development or provide earlier intervention. Our recent work has suggested that a
decline in immune function is a major, potentially modifiable, risk factor for the development of cardiovascular
disease. It remains unclear, however, at what point in the patient’s lifespan does the immune system age and
contribute to disease, how genetic and environmental factors affect immune age, and whether decline in immune
function is also associated with the development of other noncommunicable diseases associated with
chronological aging. Project 2 is designed to understand the relationship between immune-aging (whose
deepened understanding and relationship to flu response we assess in Project 1) and the development of
diseases associated with chronological aging - an association that we hypothesize begins in middle-age but
extends throughout the individual’s life span. In Project 2, first, we add a middle age cohort of twins (MAT-SELA)
demographically similar to the SELA cohort, to not only expand the age range of patients to be profiled, but also
to disentangle the effects of genetics and the environment to immune aging. To further isolate the environmental
effects on immune age, we will also compare the immune age of a super fit older cohort (AL-SELA) with that of
the SELA cohort, who are normal, older patients leading sedentary lifestyles. Second, we perform an in-depth
analysis of how immune age affects the development of cardiovascular disease, building from our previous work,
by serially profiling the immune age of patients who are at greatest risk for developing atherosclerosis (e.g.,
plaque build-up, heart attack or stroke), monitoring these patients by non-invasive imaging for the development
and/or progression of cardiovascular disease, and documenting any major adverse clinical events. Furthermore,
we apply advanced immune-based assays developed by our lab to interrogate the molecular and cellular
components of the atherosclerotic plaque, extending our recent finding that flu specific T cells are found in the
atherosclerotic plaque, in order to better understand the underlying mechanisms behind recent clinical
observations that having the flu increases the risk of heart attack and stroke. Lastly, we will determine if immune
age contributes to other non-communicable diseases by comparing the immune gene signatures associated with
advanced aging in our cohorts w...

## Key facts

- **NIH application ID:** 10190562
- **Project number:** 1P01AI153559-01A1
- **Recipient organization:** STANFORD UNIVERSITY
- **Principal Investigator:** Mark Morris Davis
- **Activity code:** P01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2021
- **Award amount:** $638,723
- **Award type:** 1
- **Project period:** 2021-09-21 → 2026-08-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10190562

## Citation

> US National Institutes of Health, RePORTER application 10190562, Molecular interception and immunological characterization of age-associated disease (1P01AI153559-01A1). Retrieved via AI Analytics 2026-05-26 from https://api.ai-analytics.org/grant/nih/10190562. Licensed CC0.

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