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A vast group of rare systemic diseases characterized by the presence of insoluble fibrillar protein deposits in tissues. Amyloidoses are classified according to biochemical type of amyloid protein involved.
Doxycycline disrupts amyloid fibril ฮฒ-sheet structure through direct binding while inhibiting MMP-9 and MMP-2 matrix degradation. Curcumin enhances this effect via RAGE receptor antagonism and advanced glycation end-product reduction, creating synergistic anti-fibrillogenic and anti-inflammatory effects
Metformin activates AMPK-dependent pathways enhancing HSP70 and HSP90 chaperone expression while promoting proteasomal degradation through FOXO3a transcriptional activity. Additionally modulates serum amyloid P component (SAP) binding to amyloid fibrils and complement cascade activation
Heparanase inhibition prevents degradation of basement membrane heparan sulfate proteoglycans that normally sequester amyloidogenic proteins. SST0001 preserves HSPG2 (perlecan) and SDC1 (syndecan-1) function, reducing amyloid fibril nucleation and maintaining tissue architecture integrity
Ayurvedic Rasayana compounds (Withanoside IV from Withania somnifera, Bacosides from Bacopa monnieri) enhance lysosomal biogenesis through TFEB nuclear translocation and mTORC1 inhibition, promoting autophagic clearance of misfolded amyloid proteins via LC3-II upregulation and SQSTM1/p62-mediated selective autophagy
Traditional Kampo formula Orengedokuto (containing berberine, baicalein, geniposide) inhibits NLRP3 inflammasome assembly and caspase-1 activation, preventing IL-1ฮฒ and IL-18 release and gasdermin D-mediated pyroptotic cell death that perpetuates amyloid fiber formation and tissue damage
PCSK9 inhibition increases LDLR expression enhancing hepatic clearance of circulating amyloidogenic proteins. Additionally disrupts apolipoprotein-amyloid fibril co-deposition and reduces oxidized lipid-mediated amyloid aggregation acceleration through improved lipid homeostasis and reduced APOE4-amyloid interactions