# Molecular and Cellular Mechanisms Underlying Domoic Acid-Induced Neurotoxicity and Therapeutic Drugs: A Comprehensive Review

**Authors:** Ruoyu Jiang, Zeyu Fan, Xinhao Li, Jiaping Yang, Mingjuan Sun, Binghua Jiao, Lianghua Wang

PMC · DOI: 10.3390/ijms27020867 · 2026-01-15

## TL;DR

This paper reviews how domoic acid harms brain cells and explores new treatment approaches.

## Contribution

The paper provides new insights into the complex mechanisms of domoic acid toxicity and suggests novel therapeutic strategies.

## Key findings

- Domoic acid causes neurotoxicity by overactivating glutamate receptors and causing calcium influx.
- Oxidative stress plays a key role in domoic acid-induced neuronal damage.
- Understanding these mechanisms opens new avenues for developing treatments.

## Abstract

Domoic acid (DA) is a neurotoxic terpenoid compound produced by certain marine algae. It accumulates through the food web and poses a significant threat to humans and animals by selectively targeting hippocampal neurons, leading to neuronal degeneration, necrosis, and subsequent memory impairment. The primary mechanism involves its potent agonism at glutamate receptors, which induces excessive calcium influx, resulting in excitotoxic cell swelling and death. Recent studies have further elucidated the critical role of downstream oxidative stress and other pathogenic factors in DA-induced neurotoxicity. These insights into its multifaceted mechanism have paved the way for novel therapeutic strategies, highlighting promising directions for future treatment development.

## Linked entities

- **Chemicals:** domoic acid (PubChem CID 5282253)

## Full-text entities

- **Diseases:** necrosis (MESH:D009336), memory impairment (MESH:D008569), Neurotoxicity (MESH:D020258), neuronal degeneration (MESH:D009410)
- **Chemicals:** terpenoid (MESH:D013729), calcium (MESH:D002118), DA (MESH:C012301)
- **Species:** Homo sapiens (human, species) [taxon 9606], PX clade (clade) [taxon 569578]

## Figures

2 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12841449/full.md

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Source: https://tomesphere.com/paper/PMC12841449