A WELL BEING JOURNAL FEATURE

Among the millions of Americans who have not fully recovered from COVID-19, or who developed new health challenges following mRNA vaccination, a small number are documenting their experiences in real time.¹

They post symptoms, lab results, and the treatments that brought little relief, alongside the uneven rhythm of daily life: periods of relative function interrupted by stretches when even getting out of bed becomes difficult.

For five years, the X user @HouseLyndseyRN has lived in a body that no longer functions the way it once did. A frontline ICU nurse and former college athlete, she says she became housebound, and at times bedbound, after her third Pfizer COVID vaccine dose in 2021.

Her symptoms resemble what some researchers have described as Post-Vaccine Syndrome (PVS): brain fog, vertigo, neuropathy in her hands and feet, shortness of breath, mast cell activation, and a resting heart rate that climbed into the nineties whenever she stood up.²

In April 2026, Nurse Lyndsey traveled to Tokyo to seek care at Edogawa Hospital and underwent the McCairn-Edogawa Protocol, a two-phase blood treatment developed by neuroscientist Kevin McCairn, PhD, founder of Synaptek-Deep Learning Systems, in collaboration with the Edogawa clinical team.³

The McCairn-Edogawa Protocol combines double filtration plasmapheresis [plaz-muh-feh-REE-sis] (DFPP) with infusions of stem-cell growth factors (SGF), signaling molecules derived from laboratory-grown stem cells.

The protocol Nurse Lyndsey received is not yet approved in the United States and has not been validated in a randomized controlled trial. It is being administered to a small number of patients, most of them Americans, who have traveled privately to Japan to seek care not yet available at home.

Rather than dismissing the McCairn-Edogawa Protocol outright or accepting its claims uncritically, we set out to examine the science behind it.

Several of the biological mechanisms and laboratory findings associated with the McCairn-Edogawa Protocol have already appeared in peer-reviewed literature. At the center of this emerging picture are fibrinaloid microclots, and a growing body of research suggests they may help explain symptoms that have often lacked a clear biological framework.

A Misfolded Protein

In May 2022, a small team of Swedish researchers published a paper that, at the time, received limited attention.⁴ Sofie Nyström and Per Hammarström had been studying the SARS-CoV-2 spike protein, the crown-shaped molecule on the virus’s outer surface. This is the part the immune system recognizes, and the same molecule mRNA vaccines instruct cells to produce. Their aim was to uncover whether portions of the spike protein could fold into amyloid structures.

Amyloids [AM-ih-loyds] are misfolded proteins that aggregate into rigid structures that the body struggles to break down. They form the characteristic plaques of Alzheimer’s disease, the prion deposits associated with Creutzfeldt-Jakob disease, and the abnormal accumulations seen in certain forms of heart failure and type 2 diabetes.

Once a protein adopts an amyloid configuration, it becomes unusually stable and resistant to normal clearance, and in some cases can encourage other proteins to adopt the same misfolded state.

Nyström and Hammarström identified seven sequences within the spike protein that had the potential to misfold into amyloidogenic [am-ih-loy-doh-JEN-ik] structures. When synthesized in the lab and incubated at body temperature, all seven formed aggregates. Three of them met every structural test for true amyloid fibrils, including binding with a dye called Thioflavin T [thigh-oh-FLAY-vin], which fluoresces in the presence of amyloid.

The full spike protein, intact, did not spontaneously misfold. But when the team exposed it to an enzyme called neutrophil elastase, which is released by the immune system during inflammation, the spike was cleaved into a fragment nearly identical to one of those seven sequences. The fragment then formed branched amyloid fibrils.

A 2025 follow-up study from the same Swedish group provided crucial evidence to further narrow down the picture of this process.⁵

Testing all seven spike-derived fragments against the body’s clotting system, the researchers found that two of them disrupted normal clotting biology in different ways. One impaired clot formation by binding to fibrinogen, the precursor protein from which fibrin is made. The second did something more concerning: clots formed in its presence were highly resistant to plasmin, the body’s primary clot-dissolving enzyme, and the same fragment pulled fibrin into dense aggregated structures that resisted normal breakdown.

These findings carry a significant implication.

They suggest that portions of the spike protein—whether produced during infection or after vaccination—may, under inflammatory conditions, contribute to the formation of abnormal amyloid structures. Some of these structures also appear unusually resistant to the body’s normal clearance mechanisms, and at least one fragment appeared to interfere with the body’s ability to dissolve clots once formed.

For patients who remain ill long after the initial exposure, researchers believe this combination of abnormal protein formation and impaired clearance may represent one possible contributor to ongoing symptoms.

Microclots in Patients

While the Swedish team was working out the chemistry, two other researchers were identifying similar structures in living patients. Etheresia Pretorius and Douglas Kell had spent years studying abnormal fibrin formations in conditions like Alzheimer’s disease, type 2 diabetes, and HIV. When the pandemic arrived, they applied the same methods to blood from people who had not recovered.⁶

What they found has since been documented across a series of peer-reviewed papers. Normal blood clots are built from fibrin. This stringy protein forms a flexible mesh that helps stop bleeding and, once healing is underway, is normally dissolved by the body. The structures Pretorius and Kell were finding looked different.

In the plasma of Long COVID patients, they observed small, abnormal clot structures in which fibrin had set into a rigid amyloid-like configuration rather than its normal flexible mesh. They named these structures fibrinaloid [fih-BRIN-uh-loyd] microclots. When stained with Thioflavin T, the microclots glow under fluorescent light. In healthy controls, they do not.

The microclots range from roughly 2 to 200 micrometers in diameter, small enough to circulate throughout the bloodstream, yet large enough to interfere with the body’s smallest capillaries. Capillaries are where oxygen and nutrients are delivered directly to tissues.

Standard coagulation tests are not designed to detect these structures. Typical D-dimer, fibrinogen, and platelet count tests identify only conventional clotting activity and were not designed to detect microscopic amyloid formations such as those found in the microclots.

In a 2022 study, the Pretorius team analyzed blood samples from a group of Long COVID patients and reported significant fibrin amyloid microclots and platelet abnormalities across the patient group studied.⁷

A separate 2022 study went further, examining what was actually trapped inside the microclots. The researchers identified a range of pro-inflammatory molecules locked within the clot structure.⁸ The microclots appeared to function as more than physical blockages: they also carried inflammatory molecules and disrupted signaling proteins throughout the circulation.

A 2024 paper from Pretorius and Kell went further still. The proteins captured inside microclots, they found, were themselves prone to misfolding into amyloid form. The findings suggested a process known as cross-seeding—the same molecular pattern observed in classical amyloid diseases like Alzheimer’s, where one misfolded protein can encourage other susceptible proteins to adopt the same abnormal shape.⁹

Researchers believe this misfolded protein mechanism may help explain several of the most puzzling features of Long COVID and Post-Vaccine Syndrome: how standard lab tests can return normal even when patients are profoundly unwell, why symptoms wax and wane or seem to migrate through the body, and why anti-inflammatory treatments often provide incomplete relief.

For patients who have spent years being told that nothing is wrong, these findings offer something genuinely important: a biological explanation for what they have been experiencing.

Separate laboratory observations have also raised questions about whether related amyloid-like structures may appear in larger post-mortem clots reported by some embalmers since 2021.

Researchers examining these clots under scanning electron microscopy have reported that the structures fluoresce under ultraviolet light without added dyes—a characteristic often associated with amyloid—and that their fibrin strands appear nodular and twisted rather than smooth, a morphology some have described as resembling structures seen in patients with elevated microclot burden.

Taken together, these observations raise the possibility that related amyloid-forming processes may, in some cases, contribute to the formation of larger fibrous structures within the body.

A note on terminology: The word “microclot” is somewhat metaphorical. These structures are not thrombi in the classical sense. They are not the platelet and fibrin formations that arrest bleeding or cause heart attacks. They are amyloid formations that contain fibrin(ogen), which is why the more precise term is fibrinaloid. Critics have argued that the looser “microclot” framing overstates what is being observed.

Pretorius and Kell themselves use the term to describe a real population of abnormal structures whose clinical significance continues to be examined.

Beyond Long COVID

Fibrinaloid microclots are not unique to COVID. Pretorius and Kell had documented them earlier in patients with type 2 diabetes,¹⁵ Alzheimer’s disease,¹⁶ and Parkinson’s disease,¹⁷ and have since identified them in myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) and rheumatoid arthritis.^10,18,19

If compromised microcirculation from amyloid-forming clot structures contributes to symptoms in post-viral illness, the same mechanism deserves examination in other conditions marked by slow neurological decline, metabolic dysfunction, and unexplained fatigue. Spikeopathy, the umbrella term for chronic conditions believed to be driven by persistent spike protein, may represent one expression of a broader vascular and amyloid-related pattern.

Inside the McCairn-Edogawa Protocol

The McCairn-Edogawa Protocol unfolds in two phases: the first aims to remove pathological material from the blood, the second is intended to support the body’s repair processes following prolonged illness.

McCairn, whose laboratory work on protein misfolding informed the McCairn-Edogawa Protocol’s design, developed the treatment in collaboration with clinicians at Edogawa Hospital after several years of bench research.

DFPP was introduced in 1980 by Tetsuzo Agishi and colleagues and has been used routinely across Japan and other parts of Asia for decades to treat a range of autoimmune and neurological conditions.¹¹ It is an established medical procedure in those settings, though not approved in the United States for these specific indications.

The procedure draws a patient’s blood through a closed external circuit. A catheter is placed in the jugular vein to support the blood flow required by the system. The blood passes through the first of two filters, which separates the plasma from the cellular components. Red blood cells, white blood cells, and platelets are returned to the patient.

The separated plasma is then routed through a second filter with a pore size roughly ten times smaller than the first. This filter is designed to capture larger molecules believed to contribute to inflammatory and clotting dysfunction, including fibrinaloid microclots, inflammatory cytokines, autoantibodies, and potentially persistently circulating spike protein in the plasma, while allowing smaller proteins like albumin to pass back through to the patient.

A small volume of albumin solution is added to replace the discarded material. By selecting a filter with the appropriate pore size, clinicians can adjust the filtration parameters for different conditions.

Patients in the Edogawa program typically undergo two to four sessions over a roughly two-week stay. Pre- and post-treatment plasma samples are examined under fluorescence microscopy to evaluate changes in microclot burden.

Both patients and clinicians have described visible changes between sessions: plasma that began turbid and orange-tinged returning clearer, apparent reductions in microclot burden, and patients reporting relief within hours of the first treatment

Phase two of the McCairn-Edogawa Protocol involves daily infusions of stem cell growth factors (SGF). The name can be misleading. No live stem cells are placed into the patient. Instead, stem cells, often derived from dental pulp, are grown in laboratory culture.

As they grow, they release a complex mixture of signaling molecules into the surrounding fluid: the chemical messages cells use to communicate with one another. That fluid is collected, filtered, and concentrated. Patients receive this filtered signaling fluid intravenously rather than the stem cells themselves.

The distinction matters. Infusing live cells carries small but real risks of immune rejection or unpredictable cell behavior. Infusing only the chemical signals those cells produce sidesteps some of those concerns while still delivering signaling molecules believed to support repair processes within the body. Researchers believe these signaling molecules may help regulate inflammation, support vascular repair, and encourage tissue recovery.

Both McCairn-Edogawa Protocol phases reflect a coherent physiological rationale: address material the body may be struggling to clear on its own, then support the body’s natural repair processes.

Worth noting what the McCairn-Edogawa Protocol is not: It is not stem cell transplantation; no live cells are administered. It is not standard therapeutic plasma exchange, which removes plasma wholesale and replaces it with donor plasma. It is not gene therapy or pharmaceutical intervention.

And by the developers’ own acknowledgment, it is not a finished medicine, but an investigational protocol with early observational findings and significant gaps that only larger, controlled studies can address. That distinction matters, especially as public interest continues to grow.

A Question About the Blood Supply

A question that follows naturally from this research: If fibrinaloid microclots circulate in the plasma of people who have had COVID-19 or received mRNA vaccines, what might that mean for donated blood?

The American Red Cross and most national blood agencies do not screen donor plasma for fibrinaloid microclots or related amyloid structures. Standard donor screening looks for infectious diseases and basic health markers.

It was not designed to detect the kinds of structures that Pretorius and Kell have been documenting, and the microscopy methods used to identify them are not yet routine outside specialized research settings.

This question has not been formally studied. The peer-reviewed microclot literature is recent, the diagnostic methods are not yet standardized for clinical use, and the implications for transfusion medicine have not been addressed in any published paper.

At the same time, researchers already have access to patient populations, microscopy techniques, and clinical infrastructure that could help clarify these questions in future studies.

What the Research Has Not Yet Answered

The McCairn-Edogawa Protocol has not yet been published as a randomized controlled trial. As of this writing, eighteen patients have completed the full treatment course, with the earliest now nine to twelve months post-treatment.

Their outcomes are documented in their own video and written accounts: meaningful records, though not equivalent to controlled clinical data.

The patients who have traveled to Tokyo also represent a specific subset of the affected population: those motivated to seek out the treatment, the financial resources to pursue it, and the physical capacity to make a transcontinental trip. Out-of-pocket costs run roughly $20,000 to $40,000, not including travel and accommodation.

The procedure itself carries considerations worth understanding. DFPP can temporarily deplete fibrinogen and other plasma proteins, which may briefly affect normal clotting. Drops in blood pressure during sessions are common. And the catheter required for the procedure carries the same risks as any line placed in a major vein, including infection and localized bleeding, though these complications are routinely managed by Japanese clinicians.

In one early case in the Tokyo program, clinicians placed the catheter through the femoral vein rather than the jugular and inadvertently nicked an artery, requiring overnight observation. The patient’s treatment outcomes were unaffected, but it reflects the kind of complication that can arise in any honest accounting of an investigational medical procedure.²⁰

A 2023 Cochrane review reached three substantive conclusions: that the term “microclots” overstates what the particles are, that amyloid fibrin(ogen) particles have been observed in healthy individuals and patients with other conditions, and that plasmapheresis for this indication should not be administered outside a randomized controlled trial.¹²

That review was based on five laboratory studies and was published before two of the foundational papers cited in this article: the Kell and Pretorius 2024 cross-seeding paper and the 2025 Westman follow-up on plasmin resistance.

It also examined a different procedure than DFPP and has not been updated since. Readers encountering the Cochrane review in public discussion should understand both its full conclusions and the scope and timing of the evidence it evaluated.

A separate 2023 case series by Jaeger and colleagues documented successful treatment of Long COVID patients using a different apheresis technique, heparin-mediated extracorporeal LDL precipitation, or HELP apheresis, suggesting that targeted blood-purification approaches for this patient population are being explored along multiple tracks.¹⁴

McCairn has been openly candid about the limits of his understanding.²⁰ The stem cell growth factor infusion delivers roughly one hundred different signaling molecules into the patient at once, and which combination of those signals does the most therapeutic work has not been isolated.

He has stated plainly that determining the active mechanism would require institutional-level research funding that has not been available. The McCairn-Edogawa Protocol has appeared to work in the patients who have received it. Exactly why it works is still a question.

A separate critique sometimes raised against this body of research is that fibrinaloid structures have also been observed in samples from healthy individuals and from patients with conditions other than Long COVID, including type 2 diabetes.

This is true, and Pretorius and Kell were themselves the first to publish on it. The relevant question is not whether amyloid-form fibrin can occur outside of Long COVID, since it can, but whether its prevalence, persistence, and protein composition differ in ways that matter clinically. The published proteomic findings suggest they may.

The scientific framework underlying the McCairn-Edogawa Protocol draws from published, peer-reviewed research, while the filtration procedure used as part of the McCairn-Edogawa Protocol has long been used in Japan and other parts of Asia for a range of conditions. Early patient outcomes have been publicly documented, though controlled clinical data remain limited.

What comes next is the difficult work of larger, carefully designed studies: the kind that could help clarify which patients benefit, what mechanisms are involved, and whether the approach withstands broader scientific scrutiny.

What Comes Next

The science of microclots is advancing independently of any single institutional decision. The researchers behind this work continue to publish. New diagnostic methods are being developed and refined. Independent laboratories are beginning to offer microclot testing to patients who want a clearer picture of what may be circulating in their blood.

Clinicians are referring motivated patients to the Edogawa program. Efforts to bring an Institutional Review Board–approved version of the McCairn-Edogawa Protocol to the United States are actively underway.

In May 2026, a little over a month after her treatment, Nurse Lyndsey posted a video to X with the caption: “I’m a SURVIVOR. 90% RECOVERED.” The footage shows her on a ball field, an activity that would have been unthinkable a year earlier.

What the early patients who have undergone the McCairn-Edogawa Protocol have demonstrated is that these findings deserve serious scientific attention, the procedure appears feasible, and the outcomes warrant careful study. The evidence remains early, imperfect, and largely observational, but for now, it is what patients and clinicians have to work with.

Some patients are not waiting for larger studies or institutional consensus. They are organizing privately, paying out of pocket, and traveling across the Pacific in search of treatment options they believe may help.

For the millions still searching for answers, the challenge ahead is whether these observations can move from private networks and patient accounts into the larger clinical studies needed to evaluate them rigorously and transparently.

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For a complete list of references, visit: wellbeingjournal.com/mj26-references/