The main Amyloid Fibrin Microclots review covers the mechanism, the patient-cohort detection, the Edogawa clinical pathway, and the treatment landscape in depth. This page covers the adjacent literature that the main review references but does not expand on:
It also preserves the curated paper list and media archive that previously lived here, with citation details corrected to canonical form.
SDF-1 (stromal-cell derived factor-1, also called CXCL12) is a chemokine that mobilises CXCR4-positive cells from bone marrow. It is best known for its role in haematopoietic stem-cell trafficking, but the same axis has been studied in neurodegeneration because CXCR4 is expressed on microglia and several neural cell populations.
Key peer-reviewed finding. In a rat model of Alzheimer's disease, combination of SDF-1 with G-CSF (granulocyte colony-stimulating factor) reduced amyloid-beta plaque burden, lowered apoptosis markers, and improved cognition, with the proposed mechanism being microglial mobilisation and M1-to-M2 polarisation. [AN] CONFIDENCE: MODERATE for the preclinical effect; no human replication in the PASC / spikeopathy context.
This is the axis that connects the SDF-1 / stem-cell literature to the fibrinaloid microclot literature: if fibrinaloid clots are driving microvascular obstruction and secondary ischaemia-reperfusion injury (see below), then endogenous repair requires both clearance of the clots and mobilisation of regenerative cells. SDF-1 sits on the mobilisation side; DFPA (double filtration plasmapheresis) sits on the clearance side.
Two MSC sources dominate this literature:
Bone-marrow MSCs (BM-MSCs). Documented to inhibit neuroinflammation, shift microglia from M1 to M2 phenotype, and reduce amyloid-beta and tau burden in AD models. The effect is largely paracrine (mediated by secreted factors) rather than through cell replacement. [AN + SR] CONFIDENCE: MODERATE for the mechanism; limited human translation in neurodegeneration.
Sources: BM-MSC mechanisms in AD, PMID 34566422; HP-BMSCs post-CPR, PMID 37246833; Stem cells in neurodegeneration review, PMC3025439.
SHED (Stem cells from Human Exfoliated Deciduous Teeth). A well-characterised dental-pulp MSC source whose conditioned medium contains IL-10, BDNF, NGF, VEGF, and IGF-1. This is the secretome used in the Edogawa Hospital clinical pathway as regenerative support after DFPA. The terminology matters here: what McCairn / Edogawa call "SGF" or "SCGF" informally is SHED-conditioned medium, not isolated Stem Cell Growth Factor / CLEC11A (a single specific cytokine). See the main review's Edogawa Clinical Pathway section for the full discussion.
Sources: El Moshy 2020 SHED-CM review, PMID 32089709; de Cara 2019 angiogenic properties, Heliyon; Engineered MSCs in ischemia, PMC11554727.
The ischaemia-reperfusion (I/R) angle is what links fibrinaloid microvascular obstruction to tissue-level damage. The chain is straightforward:
This is the textbook I/R injury mechanism applied to the fibrinaloid context. The Pretorius / Kell group formalised the connection in a 2022 Biochemical Journal paper, arguing that fibrinaloid-driven microvascular obstruction creates the conditions for chronic, low-grade I/R injury across multiple vascular beds. [SR + MECHANISTIC] CONFIDENCE: MODERATE .
Source: Kell & Pretorius 2022 on I/R in Long COVID, Biochem J 479:1653.
Two peer-reviewed threads are relevant here.
Spike binds fibrinogen directly. Ryu et al. (2024, Nature) localised the binding site on the fibrinogen alpha chain and showed the interaction is necessary for much of spike's thromboinflammatory effect in mouse models. [PR] CONFIDENCE: HIGH . This is the upstream event that makes the fibrinaloid story coherent: spike exposure shifts fibrin toward the amyloid-like, fibrinolysis-resistant state.
Source: Ryu et al. 2024, Nature.
Fibrinogen interacts with prion protein (PrP). A separate literature documents that fibrinogen mitigates PrP toxicity and PrP stabilises clot structure. This is a two-way interface between clotting biology and prion-related biology, and is one of the reasons the fibrinaloid story overlaps with prion-like and CJD discussions in the broader literature.
For the prion-like acceleration claims specific to spike (Wang 2024 on amyloid-beta acceleration, Nystrom 2022 on alpha-synuclein), see the main review's Amyloid cross-seeding section.
All citations below are in canonical form (PubMed / PMC / publisher DOI). The table is the persistent part of this page; the prose above interprets the most important rows.
| Paper | Title / Topic | Takeaway | Relevance |
|---|---|---|---|
| PMC8924615 | SDF-1 + G-CSF in rat AD model | Combo reduced amyloid-beta plaques and apoptosis; improved cognition via microglial mobilisation | Direct amyloid-beta reduction; stem-cell mobilisation |
| PMC3025439 | Stem cells in neurodegeneration | Trophic and repair effects beyond cell replacement | Supports repair mechanisms despite plaques |
| PMID 34566422 | BM-MSC mechanisms in AD | Inhibits neuroinflammation; shifts microglia M1 to M2; reduces amyloid-beta and tau | Targets inflammatory drivers |
| PMID 37246833 | HP-BMSCs post-CPR | Suppresses pyroptosis and ROS-driven inflammation | Indirectly favours clearance |
| PMC9543648 | Stem-cell angiogenesis and wound healing | Angiogenesis and extracellular vesicles improve repair | Vascular repair aids clearance |
| PMC11554727 | Engineered MSCs in ischemia | eMSCs and their EVs reduce infarct size; boost repair | Applicable repair pathways |
| PMID 32089709 | El Moshy 2020 SHED-CM review | Dental-pulp MSC secretome composition established (IL-10, BDNF, NGF, VEGF, IGF-1) | Direct bearing on Edogawa SHED-CM component |
| Heliyon 5:e01560 | de Cara 2019 SHED-CM angiogenesis | SHED-conditioned medium promotes endothelial proliferation, migration, VEGF production | Mechanistic support for SHED-CM regenerative use |
| Biochem J 479:1653 | I/R injury in Long COVID | Microclot-hypoxia loop; targets ROS, iron, clot burden | Connects fibrinaloid clots to tissue damage |
| Biochem J 479:537 | Kell & Pretorius 2022 fibrinaloid review | Formalises fibrinaloid microclots as the PASC clot phenotype | Names the clinical entity |
| Nature 2024 | Ryu et al. spike-fibrinogen binding | Crystallised binding site; antibody 5B8 blocks effect | Upstream cause of fibrinaloid transformation |
| PMC8977893 | Fibrinogen-prion interactions | Fibrinogen mitigates PrP toxicity; PrP stabilises clots | Prion / amyloid clot interface |
| Vaccines 11(7):1139 | COVID and amyloidosis review | Serum amyloid A / inflammation link; case reports | Pro-amyloid inflammatory context |
| PMC8456430 | COVID-related amyloidogenesis | Inflammatory-driven amyloid formation context | Background mechanism |
| PMID 35579205 | Spike and amyloidogenesis | Mechanistic overlap | Background |
| PMID 36362302 | Fibrinaloid microclots in POTS / Long COVID | Documents microclot presence in PASC subsets | Patient-cohort evidence |
These are preserved from the original version of this page because they carry provenance value for the topic. Most document researcher communications or reference slides; none are primary data.
Images:
/media/amyloid/kevin-jihad-science.jpg - stylised avatar associated with
Kevin McCairn PhD. Retained for historical provenance; this page no longer
treats McCairn as the central node of the topic (see the main review for
the current framing)./media/amyloid/mccairn-broadcast.jpg - locally archived frame from a
McCairn stream (permission granted by the source).Video:
Papers (canonical sources only):
Archived commentary (not peer-reviewed):
Archived streams (commentary, not primary data):
