# Project 3: Cellular and molecular mechanisms underlying effects from early life exposure to HAB toxins

> **NIH ES P01** · WOODS HOLE OCEANOGRAPHIC INSTITUTION · 2026 · $165,193

## Abstract

The overall objective of the proposed research is to elucidate the cellular and molecular mechanisms of toxicity 
from developmental exposure to harmful algal bloom (HAB) toxins. The HAB toxins domoic acid (DA), saxitoxin 
(STX), and anatoxin-a (ATX-a) occur in marine and coastal water bodies as well as in food sources and pose a 
significant threat to public health. Current regulatory guidelines for HAB toxins in seafood are designed to 
protect against acute exposure to adults. However, seafood with HAB toxins below the regulatory limits is 
regularly harvested and the consequences of exposure to low levels of HAB toxins particularly to children and 
young adults are not well understood. It is well known that the early life environment can profoundly influence 
health throughout the life course (the developmental origins of health and disease concept). The central 
hypothesis of the proposed research is that exposure to HAB toxins during early development alters various 
neuronal and glial cell types independently, leading to cell-type specific transcriptional changes, ultimately 
contributing to altered neurobehavioral outcomes. We propose to test this hypothesis using two 
complementary model systems: zebrafish, an established model organism for characterizing molecular, 
cellular, and behavioral changes in vivo, and human iPSC-derived 3D brain systems in vitro for elucidating the 
effects of toxins on differentiating human neural cells. In Aim 1, we will use transgenic zebrafish embryos and 
single-cell RNA sequencing to investigate the cellular and molecular mechanisms underlying the 
neurodevelopmental toxicity of DA, STX, and ATX-a. Building on our previous studies, in Aim 1.1 we will test 
the hypothesis that DA exposure of zebrafish embryos affects oligodendrocyte-neuron interactions in part by 
targeting oligodendrocytes that are necessary for the maturation and survival of axons. In Aim 1.2, we will test 
the hypothesis that STX exposure during developme

## Key facts

- **NIH application ID:** 11360101
- **Project number:** 5P01ES028938-08
- **Recipient organization:** WOODS HOLE OCEANOGRAPHIC INSTITUTION
- **Principal Investigator:** NEELAKANTESWAR  Aluru
- **Activity code:** P01 (R01, R21, SBIR, etc.)
- **Funding institute:** ES
- **Fiscal year:** 2026
- **Award amount:** $165,193
- **Award type:** 5
- **Project period:** 2018-09-30T00:00:00 → 2029-02-28T00:00:00

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/11360101

## Citation

> US National Institutes of Health, RePORTER application 11360101, Project 3: Cellular and molecular mechanisms underlying effects from early life exposure to HAB toxins (5P01ES028938-08). Retrieved via AI Analytics 2026-07-11 from https://api.ai-analytics.org/grant/nih/11360101. Licensed CC0.

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