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M.B. Pepys

and P.N. Hawkins


February 27, 2014: This chapter has been re-evaluated and remains up-to-date. No changes have been necessary.


Key aspects of AL, AA, ATTR, Aβ‎2m and ALECT2 amyloidosis, including both molecular mechanisms and treatment. Update on cerebral amyloid angiopathy (CAA).

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date: 24 September 2021

Amyloidosis is the clinical condition caused by extracellular deposition of amyloid in the tissues. Amyloid deposits are composed of amyloid fibrils, abnormal insoluble protein fibres formed by misfolding of their normally soluble precursors. About 30 different proteins can form clinically or pathologically significant amyloid fibrils in vivo as a result of either acquired or hereditary abnormalities. Small, focal, clinically silent amyloid deposits in the brain, heart, seminal vesicles, and joints are a universal accompaniment of ageing. However, clinically important amyloid deposits usually accumulate progressively, disrupting the structure and function of affected tissues and lead inexorably to organ failure and death. No treatment yet exists which can specifically clear amyloid deposits, but intervention which reduces the availability of the amyloid fibril precursor proteins may lead to amyloid regression with clinical benefit....

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