One of the most poignant and distressing sights for marine enthusiasts and coastal communities alike is the sight of beached marine mammals—whales, dolphins, or porpoises stranded helplessly on shores. Efforts to rescue these creatures typically involve volunteers and marine biologists working in tandem to shield the animals from the harsh elements, such as relentless sun exposure and drying skin. This often means dousing the animals repeatedly with buckets of seawater or covering them with moist blankets, all in a desperate bid to prevent further suffering while awaiting the rising tide that might facilitate their return to the ocean. However, despite these efforts, many stranded marine mammals are found lifeless, leaving behind haunting questions regarding the underlying causes driving these majestic creatures ashore.
A compelling and novel hypothesis has emerged from a collaborative team of scientists hailing from diverse locations across the United States, spanning from Florida to Wyoming. These researchers propose that the stranding phenomenon may be linked to neurodegenerative conditions akin to Alzheimer’s disease observed in humans. Drawing a parallel between elderly individuals with dementia who sometimes wander disoriented and become lost far from their familiar environments, they suggest that dolphins too might suffer similar cognitive impairments leading to disorientation and stranding. This cognitive decline in marine mammals, they speculate, stems from chronic exposure to neurotoxins produced by cyanobacteria, also known as blue-green algae, whose blooms are increasingly prevalent in marine ecosystems.
Cyanobacteria release a set of potent neurotoxic compounds, foremost among them β-N-methylamino-L-alanine (BMAA) and its chemically related isomers 2,4-Diaminobutyric acid (2,4-DAB) and N-2-aminoethylglycine (AEG). These compounds have been identified as highly neurotoxic, capable of triggering neuropathological hallmarks reminiscent of Alzheimer’s disease in experimental models. Central to Alzheimer’s pathology are misfolded tau proteins and amyloid-beta plaques—abnormal protein accumulations that disrupt normal neuronal function and lead to progressive cognitive decline. Research conducted on human populations, particularly villagers on Guam, has elegantly demonstrated that chronic dietary ingestion of cyanobacterial toxins correlates with these hallmark neuropathologies and the onset of neurological diseases.
In a groundbreaking study focusing on estuarine wildlife, researchers investigated the brains of twenty common bottlenose dolphins (Tursiops truncatus) retrieved following strandings in the Indian River Lagoon, a biodiverse and ecologically significant estuary located along Florida’s eastern coastline. The results were striking. Analytical measurements showed that these dolphins’ brain tissues contained measurable levels of BMAA and its isomers, with 2,4-DAB appearing at the highest concentrations. Notably, dolphins stranded during the summer months, which coincide with prolific cyanobacterial bloom events, exhibited 2,900 times higher levels of 2,4-DAB compared to dolphins found in non-bloom seasons. Such a pronounced seasonal variation strongly implicates cyanobacterial toxins as a significant environmental stressor.
Beyond the chemical presence of these toxins, the dolphins’ neural tissues exhibited pathological features typically associated with Alzheimer’s disease in humans. Microscopic examination revealed deposits of β-amyloid plaques as well as hyperphosphorylated tau proteins—both classical markers of neurodegeneration. Of additional concern was the presence of TDP-43 protein inclusions, which are typically indicative of a more aggressive and severe form of neurological disease akin to certain variants of frontotemporal lobar degeneration and Alzheimer’s. These findings collectively suggest that chronic environmental toxin exposure is capable of inducing profound neuropathological changes in marine mammals.
Furthermore, transcriptome analysis—a comprehensive assessment of gene expression patterns—demonstrated 536 genes differentially expressed during cyanobacterial bloom seasons, with many of these genes implicated in Alzheimer’s pathology. These genetic shifts underscore the biological response elicited by toxin exposure and illuminate the molecular pathways disrupted in affected marine mammals. The convergence of neuropathology, toxin bioaccumulation, and transcriptomic alterations builds a compelling case for cyanobacteria-derived neurotoxins as an environmental driver of neurodegenerative disease-like states in dolphins.
The prevalence and duration of cyanobacterial blooms have risen sharply due to climate change-driven warming and increased nutrient loading from agricultural runoff and sewage discharge. This nutrient enrichment fosters harmful algal blooms that deteriorate water quality not only in coastal waters but also in connected freshwater systems, such as Lake Okeechobee. Discharges from the lake into the St. Lucie River and eventually the Indian River Lagoon carry these toxins downstream, exposing local marine fauna to chronic neurotoxic threats. This environmental dynamic presents a growing concern with direct implications for ecosystem health, biodiversity, and marine mammal welfare.
Dolphins, often regarded as environmental sentinels or bioindicators, provide an early warning system for toxic exposures that potentially affect human health. Dr. David Davis, a researcher at the University of Miami’s Miller School of Medicine, highlights the broader ramifications, emphasizing that the neurotoxic impacts observed in dolphins serve as a harbinger for similar risks to human populations exposed to contaminated water and seafood. The association between cyanobacterial toxins and Alzheimer’s-like neuropathology raises pressing questions about public health, especially in regions with documented high rates of Alzheimer’s disease.
Intriguingly, Miami-Dade County in 2024 reported the highest prevalence of Alzheimer’s disease in the United States. While Alzheimer’s is a multifaceted condition with numerous genetic and environmental factors at play, increasing evidence suggests that chronic cyanobacterial toxin exposure represents a significant and perhaps underappreciated environmental risk factor contributing to its incidence. This convergence of ecological and medical findings intensifies calls for rigorous environmental monitoring and mitigation efforts targeting cyanobacterial blooms.
Historical epidemiological studies reinforce the link between cyanobacteria and neurodegeneration. Research among villagers on Guam—a Pacific island with a documented outbreak of neurodegenerative disorders linked to traditional dietary sources—revealed that chronic exposure to BMAA and related toxins precipitates neurological disease. Dr. Paul Alan Cox from the Brain Chemistry Labs in Jackson Hole, who has led extensive investigations into these connections, reiterates that these toxins serve as a bridge linking environmental change to neurological health in both humans and animals.
The publication of this research in the high-impact journal Communications Biology represents a significant advancement in our understanding of environmental neurotoxicology and the pathological mechanisms underlying marine mammal strandings. The interdisciplinary team includes scientists affiliated with Hubbs-SeaWorld Research Institute, The Blue World Research Institute, The University of Miami Miller School of Medicine, Brain Chemistry Labs, and the Rosenstiel School of Marine, Atmospheric, and Earth Science, underscoring the collaborative nature of this effort.
As marine ecosystems continue to face unprecedented stress from climate change and human activity, the discovery of Alzheimer’s disease signatures in estuarine dolphins compels a reevaluation of how we monitor and protect both wildlife and human communities from harmful algal blooms. With neurological health linked to the quality of aquatic environments, strategies aimed at reducing nutrient pollution, strengthening water quality standards, and enhancing public awareness of cyanobacterial risks must be prioritized to mitigate future neurotoxicity. The dolphins stranded along Florida’s shores serve as tragically poignant reminders that ocean health and human health are inextricably intertwined.
Subject of Research: Animals
Article Title: Alzheimer’s disease signatures in the brain transcriptome of Estuarine Dolphins
News Publication Date: 30-Sep-2025
Web References: http://dx.doi.org/10.1038/s42003-025-08796-0
References: Research published in Communications Biology
Image Credits: Paul Alan Cox
Keywords: Alzheimer’s disease, cyanobacterial toxins, BMAA, 2,4-DAB, neurodegeneration, marine mammals, bottlenose dolphins, environmental neurotoxicology, cyanobacterial blooms, Indian River Lagoon, transcriptomics, neurotoxicology, environmental health
