Brains of Estuarine Dolphins Show Signs of Alzheimer’s Disease

A new study shows massive seasonal exposure to a specific neurotoxin originating from harmful algal blooms (HABs) accelerates Alzheimer’s disease (AD) like pathology in the brains of estuarine dolphins, potentially contributing to stranding events.

The research, published in Communications Biology in 2025, examined common bottlenose dolphins (Tursiops truncatus) found stranded in Florida’s Indian River Lagoon (IRL) between 2010 and 2019. The findings provide new insight into how converging factors such as HAB toxins and the natural development of AD pathology in dolphins impact brain health.

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How Do Seasonal Algal Blooms Affect Toxin Levels in Dolphins?

The study focused on the neurotoxin 2,4-diaminobutyric acid (2,4-DAB), which is produced by cyanobacteria, diatoms, and dinoflagellates. HABs in the IRL, often intensifying due to climate warming and nutrient pollution, typically occur during warm-weather bloom seasons (June–November).

Researchers found an extreme difference in toxin concentration based on the date of stranding:

The median concentration of 2,4-DAB in the brains of dolphins stranded during bloom seasons was approximately 2,900 times more concentrated than in those stranded during non-bloom seasons (December–May).

2,4-DAB was detected in all dolphin cerebral cortex samples. The highest concentrations were recorded in dolphins stranded in June and August. This disproportionate seasonal exposure to 2,4-DAB is deemed evidence of the harmful effects of blooms filled with cyanobacteria and is linked to subsequent brain damage.

Seasonal Comparison of 2,4-DAB Toxin Exposure in Dolphins
Bloom Season	June – November
Non-Bloom Season	December – May
Toxin Concentration	Approx. 2,900x higher during Bloom Season
Peak Concentration Months	June and August

Can Algal Blooms Cause Alzheimer’s-Like Brain Damage in Dolphins?

Dolphins are considered a natural model of Alzheimer’s disease (AD) because, like humans, they naturally develop hallmark neuropathological changes, including amyloid beta (Aβ) plaques and tau neurofibrillary tangles (NFTs), as they age. The study found that exposure to 2,4-DAB during bloom seasons exacerbates these issues, inducing concurrent AD-like neuropathological changes and elevated AD gene expression.

Key molecular changes observed in dolphins stranded during bloom seasons included:

Differentially Expressed Genes: A total of 536 differentially expressed (DE) protein encoding genes were identified, with 420 upregulated and 116 downregulated.
Elevated AD Markers: Genes encoding for major AD hallmark changes, such as the amyloid-β precursor protein (APP), microtubule-associated protein tau (MAPT), and TAR DNA binding protein (TARDBP), were elevated with increased brain concentrations of 2,4-DAB and bloom season. This gene elevation was supported by physical pathology, including intracellular Aβ deposits, Aβ plaques, phosphorylated tau, and phosphorylated TDP-43 inclusions.
AD Risk Factors: Transcription of the AD risk factor gene apolipoprotein E (APOE) was increased, in some cases up to 6.5-fold. Other neurodegenerative markers, such as MT-ND1 (linked to mitochondrial dysfunction and early stage AD biomarker), were also increased.

How Does the Algal Neurotoxin Lead to Dolphin Strandings?

Gene enrichment analysis revealed critical functional impairments linked to the toxin exposure:

GABAergic Synapse Impairment: There was significant enrichment for impairment in GABAergic synapses. Dolphins stranded during bloom seasons showed decreased expression of glutamate decarboxylase (GAD), an enzyme essential for GABA synthesis. 2,4-DAB is known to act as a non-competitive inhibitor of GABA transaminase, potentially leading to neurotoxicity and elevated GABA levels in the synapse.
Blood-Brain Barrier Alteration: Upregulation was observed in transcripts associated with the laminin-3 complex. Laminins are part of the basement membrane and interact with integrins.¹⁵ The upregulation of the laminin-3 complex suggests a potential response to blood-brain barrier (BBB) injury and neuroinflammation in the dolphins.

These neurodegenerative changes—including the loss of navigational skills and memory—may be the mechanism leading to the stranding of the dolphins.

Are Algal Blooms a Risk for Alzheimer’s in Humans?

The findings underscore the significant health risks posed by HABs, which produce toxins that bio-magnify in the aquatic food web, affecting marine life, terrestrial mammals, and humans.

As dolphins are a sentinel species for toxic exposures in marine environments, researchers expressed concerns about potential human health issues associated with cyanobacterial blooms, especially as climate warming continues to intensify HABs. While the study focuses on dolphins, the Alzheimer’s-like shifts observed are fundamental, and previous research suggests cyanobacterial exposures may be a risk factor for neurodegeneration in humans, including dementia.