Dolphins Are Getting Alzheimer’s: What Marine Neuroscience Reveals About Environmental Neurodegeneration
New research confirms wild dolphins develop the same brain pathology as human Alzheimer’s patients, and environmental toxins may be accelerating it.
Alzheimer’s disease was long considered uniquely human. Other species develop bits and pieces of the pathology (dogs with cognitive dysfunction, aged primates with amyloid deposits), but the full constellation of amyloid plaques, neurofibrillary tangles, and neuritic pathology? That appeared to be our burden alone.
Until researchers started examining dolphin brains.
The Discovery
A 2023 study in the European Journal of Neuroscience examined brains from 22 stranded odontocetes (toothed whales, including dolphins) across five species.¹ The findings were striking: all aged animals had amyloid plaque pathology, and three individuals from three different species showed the complete Alzheimer’s signature: co-occurring amyloid-beta plaques, intraneuronal hyperphosphorylated tau, neuropil threads, and neuritic plaques.
This wasn’t partial pathology. This was full Alzheimer’s disease-like neuropathology developing spontaneously in wild marine mammals.
The researchers proposed an unsettling hypothesis: this pathology might explain some mass strandings. The “sick-leader” theory suggests that when a pod’s navigational leader develops cognitive impairment, healthy members strand alongside them due to the species’ intense social bonds.
The Environmental Connection
A separate line of research has been tracking why dolphins might be so vulnerable. A 2019 study in PLOS ONE examined stranded dolphins from Florida and Massachusetts, regions known for recurring harmful algal blooms (HABs).²
The researchers measured levels of BMAA (β-methylamino-L-alanine), a cyanobacterial neurotoxin that bioaccumulates through the marine food chain. BMAA has been linked to Alzheimer’s, ALS, and other neurodegenerative diseases in humans. It crosses the blood-brain barrier and becomes incorporated into brain proteins, inducing misfolding and aggregation.
The results were alarming: 13 of 14 dolphins had high BMAA levels in their brains (ranging from 20 to 748 μg/g). Neuropathological examination revealed increased β-amyloid plaques and dystrophic neurites concentrated in the auditory cortex, the brain region dolphins rely on for echolocation and navigation.
As apex predators, dolphins accumulate these toxins from every fish, squid, and crustacean they consume. Each meal adds to the lifetime dose.
Geographic Spread
This isn’t isolated to U.S. waters. A November 2024 study examined 43 dolphins (bottlenose and striped) stranded along Italian coasts, the first study of its kind for the Mediterranean.³ Researchers found amyloid plaques in aged animals of both species, with significant correlations between plaque presence, advanced age, and concurrent viral infections.
The pathology appears wherever researchers look for it.
Why This Matters for Companion Animals
Dolphins and dogs share a relevant trait: long post-reproductive lifespans. Both species live well beyond their reproductive years, which increases the window for cumulative neurodegenerative pathology to develop.
We already know dogs develop canine cognitive dysfunction (CCD), which shares features with human Alzheimer’s: behavioral changes, sleep disturbances, disorientation, and yes, amyloid-beta deposits in the brain. The dolphin research adds a new dimension: environmental exposures may accelerate or trigger these processes.
Consider the parallels:
- Bioaccumulation: Dogs drinking from algae-contaminated lakes, swimming in affected waters, or eating fish from toxin-laden environments face similar exposure routes
- Chronic low-dose exposure: Like dolphins, companion animals experience lifetime cumulative doses rather than single acute events
- HABs are increasing: Climate change is expanding the frequency, duration, and geographic range of harmful algal blooms
The dolphin data suggests we should be asking harder questions about environmental neurotoxin exposure in our patients.
The Broader Implication
Dolphins occupy a unique position as marine sentinels. Their long lifespans, apex predator status, and cognitive sophistication make them canaries in the oceanic coal mine. When dolphins develop Alzheimer’s pathology at increasing rates, it signals something about environmental neurotoxin loads that applies beyond the ocean.
The research doesn’t prove causation between BMAA and dolphin Alzheimer’s pathology (correlation across 14 stranded animals isn’t definitive), but the biological plausibility is strong. BMAA causes tau tangles and amyloid plaques in primate feeding studies. It bioaccumulates. It’s present at high levels in affected dolphins.
For veterinary professionals, the takeaway is both sobering and actionable: neurodegenerative disease in animals may have environmental contributors we’re only beginning to understand. As HABs expand and toxin exposure increases, we should expect to see more of this pathology, not less.
For a comprehensive review of neurological assessment, localization, and common conditions in companion animals, join Dr. Susan Arnold for Neurology In A Nutshell on February 21, 2026. This 4-hour RACE-approved CE session covers the neurological exam, lesion localization, and practical approaches to seizures, vestibular disease, and spinal cord disorders.
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References
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Vacher MC, Durrant CS, Rose J, et al. Alzheimer’s disease-like neuropathology in three species of oceanic dolphin. Eur J Neurosci. 2023;57(7):1161-1179. doi:10.1111/ejn.15900. PMID: 36514861
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Davis DA, Mondo K, Stern E, et al. Cyanobacterial neurotoxin BMAA and brain pathology in stranded dolphins. PLoS One. 2019;14(3):e0213346. doi:10.1371/journal.pone.0213346. PMID: 30893348
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Orekhova K, Testori C, Giorda F, et al. Amyloid-β and phosphorylated tau screening in bottlenose dolphin (Tursiops truncatus) and striped dolphin (Stenella coeruleoalba) brains from Italy reveals distinct immunohistochemical patterns correlating with age and co-morbidity. PLoS One. 2024;19(11):e0314085. doi:10.1371/journal.pone.0314085. PMID: 39591474