Fig. 6: Possible phase transition in the progression of neurodegenerative disease.
From: Mechanism of amyloid fibril formation triggered by breakdown of supersaturation
a Schematic model of amyloid fibril (PDB ID, 6GK3) formation from monomeric β2m (PDB ID, 2D4F) in the presence of serum albumin (PDB ID, 1AO6). Amyloid formation is prevented by a barrier of supersaturation, and the HANABI system is important for identifying innate factors that maintain healthy proteostasis. Molecular diagrams were created using PyMOL Molecular Graphics. The figures were modified under the terms of the Creative Commons Attribution CC BY license from Nakajima et al.49. b From a physicochemical perspective, amyloid formation is a phase transition from soluble to solid states that is limited by supersaturation in the model of dynamic biomarkers of the Alzheimer’s disease pathological cascade95. Therapeutic strategies that reduce the degree of supersaturation by measuring the risk of amyloid “ignition” may be more effective than “extinguishing” amyloid elongation49.
