Abstract
Amyloidosis is defined as the cascade of structural changes of proteins leading to the formation of insoluble fibril aggregates that accumulate in tissue as amyloid plaques. All types of amyloidosis are structurally characterized by the cross β-pleated sheet conformation of the fibrils irrespective of their biochemical composition (reviewed by Glenner, 1980). This common structural feature of fibril aggregates is the basis of their insolubility and relative resistance to proteolytic digestion (Jarrett and Lansbury, 1993; Nordstedt et al., 1994). Amyloid plaque formation and deposition is believed to be the key event in nerve cell death in chronic and incurable neurodegenerative diseases such as Alzheimer’s Disease (AD) (reviewed by Scikoe, 1996) and Creutzfeldt-Jakob Disease (CJD) (reviewed by Prusiner, 1996). One of the major therapeutic approaches to arrest, or at least slow down the progression of these devastating diseases, is to stop proteins from aggregating into amyloid fibrils.
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Post, C. et al. (1998). Anthracyclines and Amyloidosis. In: Fisher, A., Hanin, I., Yoshida, M. (eds) Progress in Alzheimer’s and Parkinson’s Diseases. Advances in Behavioral Biology, vol 49. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-5337-3_29
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DOI: https://doi.org/10.1007/978-1-4615-5337-3_29
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