Dr. Philp McMillan,  John McMillan

The patient was scheduled for a routine PET scan to investigate early signs of dementia when an unexpected coincidence changed science. The day before his brain imaging appointment, he received a Pfizer COVID-19 vaccination. When doctors reviewed his scan results, they discovered something unprecedented: a clear amyloid signal lighting up at his injection site, the telltale signature of misfolded proteins accumulating in his arm.

This wasn’t supposed to happen. Amyloid plaques typically form in the brain during neurodegenerative diseases like Alzheimer’s. Finding them at a vaccine injection site suggested something entirely new was occurring: that the spike protein itself might be triggering the same catastrophic protein misfolding seen in some of medicine’s most devastating conditions.

This single case, analyzed by systems neuroscientist Dr. Kevin McCairn, represents what may be the first direct evidence that spike protein exposure can initiate amyloid cascades in living humans. McCairn, who holds a PhD from The Open University and has extensive publications on brain network interactions, brings unique expertise to this investigation. Best known for developing the first primate model of Tourette Syndrome and pioneering deep brain stimulation techniques, McCairn’s years studying protein misfolding in neurological disorders at Japan’s RIKEN institute provided the foundation for recognizing similar amyloid patterns in COVID-related pathology.

It’s a finding that challenges our understanding of post-viral and post-vaccine pathology and points toward the emergence of a potentially new form of systemic disease.

Meanwhile, across the globe, other troubling patterns were emerging. Interventional cardiologists from the United States to Japan began reporting unusual clots extracted from living patients: massive, white, rubbery structures unlike anything in their experience. Embalmers working independently across multiple countries started documenting similar unprecedented vascular obstructions. By 2022, some reported seeing these anomalous structures in up to 80% of cases.

McCairn’s laboratory evidence suggests these seemingly disparate observations may be connected through a single, alarming mechanism: the misfolding of proteins triggered by SARS-CoV-2 spike protein, creating persistent, system-wide damage that resists the body’s natural clearing mechanisms. While other researchers investigate alternative explanations including traditional thrombosis and inflammatory responses, McCairn’s preliminary findings offer a compelling framework for understanding these puzzling phenomena.

When Proteins Go Rogue

Think of proteins as the body’s molecular machinery, each one folded into a precise three-dimensional shape that determines its job. Like origami, the folding pattern is everything. Change the shape, and you change the function entirely.

Amyloid diseases occur when proteins abandon their normal, functional shapes and misfold catastrophically. These rogue proteins become “sticky,” aggregating into insoluble, harmful structures that the body cannot clear. While most clinicians associate amyloids with neurodegenerative diseases like Alzheimer’s plaques, Parkinson’s Lewy bodies, or prion diseases, McCairn’s research reveals that exposure to SARS-CoV-2 spike protein (present in both the virus and vaccines) can trigger similar misfolding in the circulatory system.

The key player is fibrinogen, the soluble protein that normally converts to fibrin during healthy clot formation. Under spike protein influence, fibrinogen appears to misfold into an amyloid-like structure that resists the body’s natural clot-dissolving mechanisms.

The Seeding Experiment

McCairn’s most alarming finding came from what he calls the “seeding” experiment, designed to test whether these clots possessed prion-like properties. Using RT-QuIC assay technology typically employed for prion detection, he performed carefully controlled studies with multiple sample replicates.

He took a tiny sample from one of the large clots and added it to healthy human plasma, monitoring the mixture for signs of protein conversion. Control samples contained plasma alone or plasma with inert materials. Within 7.5 hours, the clot-seeded plasma showed exponential amyloid formation, converting to the same abnormal, resistant form as the original clot. Control samples remained unchanged.

This demonstrates what scientists call prion-like behavior: misfolded proteins acting as templates that force healthy proteins to adopt the same abnormal shape. Dr. Philip McMillan, a researcher and clinician, uses a magnet analogy: “Just because the magnet is applying a degree of magnetism, this screw, which wasn’t magnetic before, suddenly is. And then it makes this one magnetic and then this one.”

A Disease Without Boundaries

Traditional amyloid diseases like Alzheimer’s face natural constraints. Cellular boundaries limit where the misfolded proteins can spread, keeping damage largely within specific organs like the brain. McCairn has identified a crucial difference with spike-induced amyloidosis that makes it potentially far more dangerous.

“The boundary condition for these amyloidogenic microclots is essentially the system,” McCairn explains. In simpler terms, these protein aggregates form within the bloodstream itself, where no cellular walls exist to limit their growth. This allows them to expand throughout the entire circulatory system, potentially reaching the massive sizes now being discovered.

McCairn’s laboratory can detect microscopic versions of these amyloid structures in blood samples from individuals exposed to spike protein, suggesting the process may be occurring at subclinical levels in many people. His testing has identified these formations in vaccinated individuals and, most concerning, in a three-year-old child whose mother received vaccination during pregnancy.

McCairn raises concerns about potential transmission through blood products and organ transplants. Without systematic screening for these amyloid structures, the safety of such medical procedures may need reevaluation, though this remains speculative pending further research.

Therapeutic Considerations

Current medical approaches may prove inadequate for amyloid-based clotting disorders. Standard anticoagulants target normal clotting pathways, but these resistant amyloid structures likely require different interventions. McCairn’s laboratory work suggests stem cell growth factors can inhibit amyloid cascade formation in test tubes, though clinical applications remain entirely investigational.

The diagnostic challenge is equally significant. Standard tests like D-dimer and other coagulation markers may not detect these abnormal structures. Few laboratories offer the specialized blood analysis that McCairn has developed to identify amyloid burden, leaving most clinicians without diagnostic tools for this potential condition.

The Institutional Response Gap

Perhaps most troubling is the limited institutional response to these findings. Despite the PET scan evidence and reports from medical professionals across multiple specialties and countries, major medical institutions have conducted little systematic investigation of these phenomena.

“There’s so many institutions, entities, individuals who are basically culpable for this mass exposure and this potential mass casualty event that they’ve inflicted on the global population,” McCairn observes. “So no one, there’s no motivation to go and investigate this.”

This has left critical research to private laboratories with limited resources, while institutions with comprehensive capabilities remain largely uninvolved.

Research institutions should prioritize investigating these phenomena with the same rigor applied to other emerging health threats. The collaboration between clinical specialists and research scientists like McCairn demonstrates how medical knowledge can emerge from unexpected observations, but it shouldn’t remain isolated in private laboratories.

As McCairn warns, “We have to recognize that there is this amyloidogenic clotting in extremis that is not being addressed by the institutions which are supposed to be there to be protecting the public.”

The preliminary evidence is substantial enough to warrant immediate, comprehensive investigation. Whether McCairn’s hypothesis proves correct or alternative explanations emerge, the medical mystery demands resolution. The health consequences for millions may depend on how quickly and thoroughly we respond to these troubling signals.

Research Links:

• Amyloidogenesis of SARS-CoV-2 Spike Protein
• SARS-CoV-2 Spike amyloid fibrils specifically and selectively accelerates amyloid fibril formation of human prion protein and the amyloid ß peptide
• Covid-19 Vaccination and Mechanisms of Neurodegenerative Disease
• Severe COVID-19: A multifaceted viral vasculopathy syndrome
• OPEN and CLOSED state of SPIKE SARS-COV-2
• Fibrinogen Mitigates Prion-Mediated Platelet Activation and Neuronal Cell Toxicity
• SARS-CoV-2 Spike Protein and its amyloid properties
• Fibrin drives thromboinflammation and neuropathology in COVID-19