Twenty-one sick dolphins stranded in Florida between 2010 and 2019. All had one thing in common: brains filled with beta-amyloid plaques and tangled tau proteins. The same markers as human Alzheimer's. The culprit?2,4-diaminobutyric acid, a neurotoxin produced by microscopic algae that thrive in warm, polluted waters.
Sick dolphins exposed during seasonal blooms They had concentrations 2.900 times higher than those who died in other periods. The study, published Biology CommunicationsIt's not just zoology: it's a public health alarm bell. Because those same waters are also frequented by humans.
When the brain shuts down at sea
A beached dolphin isn't always sick in the traditional sense. It has no visible wounds, obvious parasites, or acute infections. It's breathing, moving, but something in its navigation system has gone haywire. Volunteers rush to the beach with buckets of water, douse it, and wait for high tide. They bring it back out to sea. It comes back. Again. It's disoriented, as if it's forgotten where the sea is.
The researchers ofUniversity of Miami and Hubbs-SeaWorld Research Institute They decided to understand what was happening in the brains of these animals. They examined twenty common bottlenose dolphins (Tursiops truncatus) found dead in the Indian River Lagoon on Florida's east coast. Inside those brains, they found a neuropathological picture that eerily resembled that of human Alzheimer's patients: beta-amyloid plaques, neurofibrillary tangles of tau protein, and inclusions of TDP-43, a marker associated with the most aggressive forms of dementia.
But the most worrying discovery was another. In sick dolphins stranded during the algal bloom season (from June to November), the levels of 2,4-diaminobutyric acid were astronomical. We are talking about concentrations up to 2.900 times higher than in specimens that die at other times of the year. This neurotoxin, produced by cyanobacteria that explode in warm, nutrient-rich waters, is a close relative of the infamous BMAA, already linked to neurodegenerative diseases in humans.
Sick Dolphins: Deranged Genes and Fading Memory
When researchers analyzed gene expression in the brains of diseased dolphins, they found that As many as 536 genes behaved abnormallyMany of these are involved in brain inflammation, synapse function, and neuronal communication. The gene apoe, the largest genetic risk factor for Alzheimer's in humans, was found to be hyperactive: in some dolphins it was expressed six times above normal levels.
Other genes of concern included the TNFRSF25, which can induce the self-destruction of brain cells, and the MT-ND1, a mitochondrial gene found in the blood of people in the early stages of Alzheimer's.
The researchers also noted alterations in genes linked to hearing function (MYO1F, STRC, SYNE4), suggesting that exposure to toxins may impair dolphins' ability to communicate and navigate through echolocation.
“Dolphins are considered environmental sentinels for exposure to toxic substances in marine environments,” he explained. David Davis, toxicologist at the University of Miami and co-author of the study.
“There are concerns about human health problems associated with cyanobacterial blooms.”
A detail that does not go unnoticed: in 2024, Miami-Dade County recorded the higher rate of Alzheimer's of all the United States. Just 300 kilometers from the poisoned lagoon.
Algae that thrive in the heat
The Indian River Lagoon is an ecosystem over 250 kilometers long, surrounded by cities, farms, and industrial wastewater. Agricultural fertilizers and wastewater provide abundant nutrients for cyanobacteria, while rising ocean temperatures prolong and intensify algal blooms. This is not a problem unique to Florida. In California, hundreds of sea lions they were found stranded and disoriented due to thedomoic acid, another algal neurotoxin. In Australia, an explosion of Karenia Mikimotoi killed thousands of sea dragons.
Global warming and nutrient pollution are creating ideal conditions for these deadly blooms. And the sick dolphins are just the tip of the iceberg. Second Paul Alan Cox, executive director of the Brain Chemistry Labs In Wyoming, studies on the island of Guam have shown that chronic exposure to cyanobacterial toxins can trigger neurological diseases in humans, including amyloid plaques and tau proteins identical to those found in dolphin brains.
Sick Dolphins: Sentinels with a "Pierced" Mind
Dolphins have complex brains, live long lives, and occupy high positions in the food chain. This makes them excellent models for studying the impact of environmental toxins on neurological health. When they beach themselves, they do so in a consistent pattern: most beachings in the Indian River Lagoon occur in summer, just when algae growth peaks.
The researchers emphasize that 2,4-DAB is likely just one piece of a much more complex puzzle. Other algal toxins, such as domoic acid and okadaic acid, are known to cause memory loss and neuronal death. But in this specific study, 2,4-DAB emerges as the prime suspect.
“There are probably many pathways to Alzheimer’s,” Davis said, “but cyanobacterial exposures increasingly appear to be a risk factor.”
The good news is that we can do something. Reduce agricultural nutrient runoff, improve wastewater treatment, and actively monitor algal blooms. The bad news is that time is running out. With rapidly warming waters, blooms will become more intense and frequent. And sick dolphins will continue to tell us something we perhaps don't want to hear: that what happens to them can happen to us.
For most beachgoers, a stranded dolphin is a tragedy. For scientists, it's a clue. And this clue points straight to our shores, our tables, our brains.
