{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,11]],"date-time":"2026-10-11T03:40:06Z","timestamp":1791690006613,"version":"4.3.4"},"reference-count":141,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2024,6,24]],"date-time":"2024-06-24T00:00:00Z","timestamp":1719187200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Annals of Neurology"],"published-print":{"date-parts":[[2024,9]]},"abstract":"<jats:p>\n                    Amyloid neuropathy is caused by deposition of insoluble \u03b2\u2010pleated amyloid sheets in the peripheral nervous system. It is most common in: (1) light\u2010chain amyloidosis, a clonal non\u2010proliferative plasma cell disorder in which fragments of immunoglobulin, light or heavy chain, deposit in tissues, and (2) hereditary transthyretin (ATTRv) amyloidosis, a disorder caused by autosomal dominant mutations in the\n                    <jats:italic>TTR<\/jats:italic>\n                    gene resulting in mutated protein that has a higher tendency to misfold. Amyloid fibrils deposit in the endoneurium of peripheral nerves, often extensive in the dorsal root ganglia and sympathetic ganglia, leading to atrophy of Schwann cells in proximity to amyloid fibrils and blood\u2013nerve barrier disruption. Clinically, amyloid neuropathy is manifested as a length\u2010dependent sensory predominant neuropathy associated with generalized autonomic failure. Small unmyelinated nerves are involved early and prominently in early\u2010onset Val30Met ATTRv, whereas other ATTRv and light\u2010chain amyloidosis often present with large\u2010 and small\u2010fiber involvement. Nerve conduction studies, quantitative sudomotor axon testing, and intraepidermal nerve fiber density are useful tools to evaluate denervation. Amyloid deposition can be demonstrated by tissue biopsy of the affected organ or surrogate site, as well as bone\u2010avid radiotracer cardiac imaging. Treatment of light\u2010chain amyloidosis has been revolutionized by monoclonal antibodies and stem cell transplantation with improved 5\u2010year survival up to 77%. Novel gene therapy and transthyretin stabilizers have revolutionized treatment of ATTRv, improving the course of neuropathy (less change in the modified Neuropathy Impairment Score\u2009+\u20097 from baseline) and quality of life. With great progress in amyloidosis therapies, early diagnosis and presymptomatic testing for ATTRv family members has become paramount. 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