# Understanding the developmental impact of environmental risk factors on brain and cognitive systems vulnerable to Alzheimers disease in children

> **NIH NIH F99** · UNIVERSITY OF NEBRASKA MEDICAL CENTER · 2024 · $49,974

## Abstract

Alzheimer's disease (AD) is a pressing issue in the United States, affecting over 6 million Americans and
ranking as the fifth-leading cause of death in 2020 for persons 65 and over. Approximately 90% of AD cases
are sporadic, reflecting an established contribution to AD risk of environmental and lifestyle risk factors (ERF).
ERF impact AD risk throughout the lifespan, but ERF during critical developmental periods may influence late-
life disease risk beyond what is currently appreciated. This may be demonstrated by abnormal brain maturation
(structural or functional) due to ERF exposure. While late onset AD is not often diagnosed until one’s mid 60s,
utilizing a lifespan approach acknowledges early life ERF that may influence risk to disease. Utilizing an AD
lens can help investigate these early life influences, with the goal of identifying early interventions for reducing
neurodegenerative risk. The F99 phase of my proposal will investigate prenatal and childhood ERF and their
association with memory. The central hypothesis is that AD associated ERF (AD-ERF) during childhood are
linked to the neurodevelopment of AD associated brain systems (hippocampus, hippocampal dependent
memory), and these links affect AD vulnerability in late life. There is a notable gap in understanding how early-
life AD-ERF bias cognitive development towards neurodegenerative risk. To investigate this, I will measure
how a person’s environmental exposures (stress, socioeconomic status, neighborhood deprivation index) in
the prenatal, personal, and parental environments (as identified through a factor analysis using the Adolescent
Brain and Cognitive Development study: Aim1A) controlling for familial AD risk (via grandparent/great
grandparent blood biomarker assay: collected from parent study) influence hippocampal dependent RM in
children. The F99 phase will include training in reproducible neuroimaging, advanced statistics, and scientific
communication. Completion of the F99 phase lays a strong intellectual, technical, and professional foundation
for the postdoctoral (K00) phase of this award. During the K00 phase, training in epigenetics and AD-
associated biological aging will develop knowledge, expertise, and skills essential to becoming an independent
investigator. It is my long-term goal to establish a multi-disciplinary research laboratory focused on studying
modifiable AD risk factors in order to develop and implement treatments or preventative programs that might
reduce AD risk in populations with high vulnerability due to their environment. This research will shed light on
the relationship between environments and development, offering insights into the predictive power of the
environment in shaping AD risk. Ultimately, this work could lead to early interventions for AD, addressing the
looming public health crisis posed by an aging, AD-vulnerable US population.

## Key facts

- **NIH application ID:** 11075542
- **Project number:** 1F99NS139537-01A1
- **Recipient organization:** UNIVERSITY OF NEBRASKA MEDICAL CENTER
- **Principal Investigator:** Meghan Ramirez
- **Activity code:** F99 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2024
- **Award amount:** $49,974
- **Award type:** 1
- **Project period:** 2024-09-17 → 2026-08-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/11075542

## Citation

> US National Institutes of Health, RePORTER application 11075542, Understanding the developmental impact of environmental risk factors on brain and cognitive systems vulnerable to Alzheimers disease in children (1F99NS139537-01A1). Retrieved via AI Analytics 2026-05-26 from https://api.ai-analytics.org/grant/nih/11075542. Licensed CC0.

---

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