| [1] Yang ZH, Li XB, Yuan Y, Huang SX, Liu L, Tang BS, Zhang RX. The progress of treatment in transthyretin related familial amyloid polyneuropathies[J]. Zhonghua Shen Jing Ke Za Zhi, 2018, 51:227-232.[杨紫晗, 李小波, 袁毅, 黄顺祥, 刘蕾, 唐北沙, 张如旭. 转甲状腺素蛋白相关家族性淀粉样多发性神经病的治疗进展[J]. 中华神经科杂志, 2018, 51:227-232.]
[2] Liu G, Ni W, Wang H, Li H, Zhang Y, Wang N, Wu Z. Clinical features of familial amyloid polyneuropathy carrying transthyretin mutations in four Chinese kindreds[J]. J Peripher Nerv Syst, 2017, 22:19-26.
[3] Andrade C. A peculiar form of peripheral neuropathy; familiar atypical generalized amyloidosis with special involvement of the peripheral nerves[J]. Brain, 1952, 75:408-427.
[4] Mariani LL, Lozeron P, Théaudin M, Mincheva Z, Signate A, Ducot B, Algalarrondo V, Denier C, Adam C, Nicolas G, Samuel D, Slama MS, Lacroix C, Misrahi M, Adams D; French Familial Amyloid Polyneuropathies Network (CORNAMYL) Study Group. Genotype-phenotype correlation and course of transthyretin familial amyloid polyneuropathies in France[J]. Ann Neurol, 2015, 78:901-916.
[5] Ueda M, Yamashita T, Misumi Y, Masuda T, Ando Y. Origin of sporadic late-onset hereditary ATTR Val30Met amyloidosis in Japan[J]. Amyloid, 2018, 25:143-147.
[6] Liu L, Li XB, Hu ZM, Huang SX, Tang BS, Zhang RX. Clinical and genetic features of transthyretin-related familial amyloid polyneuropathy in China[J]. Chin Med J (Engl), 2020, 133:2616-2618.
[7] Yuan SJ, Zheng M, Yuan Y. Research progress of disease burden in transthyretin amyloid polyneuropathy[J]. Xian Dai Yu Fang Yi Xue, 2021, 48:1331-1334.[袁淑娟, 郑铭, 袁云. 转甲状腺素蛋白淀粉样变性多发性神经病的疾病负担研究进展[J]. 现代预防医学, 2021, 48:1331-1334.]
[8] Ebenezer GJ, Liu Y, Judge DP, Cunningham K, Truelove S, Carter ND, Sebastian B, Byrnes K, Polydefkis M. Cutaneous nerve biomarkers in transthyretin familial amyloid polyneuropathy[J]. Ann Neurol, 2017, 82:44-56.
[9] Liang XZ, Chen YJ. Research progress of nervous system damage caused by TTR gene mutation[J]. Zhong Nan Yi Xue Ke Xue Za Zhi, 2020, 48:565-568.[梁修梓, 陈勇军. TTR基因突变致神经系统损害的研究进展[J]. 中南医学科学杂志, 2020, 48:565-568.]
[10] Adams D, Samuel D, Goulon-Goeau C, Nakazato M, Costa PM, Feray C, Planté V, Ducot B, Ichai P, Lacroix C, Metral S, Bismuth H, Said G. The course and prognostic factors of familial amyloid polyneuropathy after liver transplantation[J]. Brain, 2000, 123:1495-1504.
[11] Merlini G, Bellotti V. Molecular mechanisms of amyloidosis[J]. N Engl J Med, 2003, 349:583-596.
[12] Hendren NS, Roth LR, Grodin JL. Disease-specific biomarkers in transthyretin cardiac amyloidosis[J]. Curr Heart Fail Rep, 2020, 17:77-83.
[13] Adams D, Suhr OB, Hund E, Obici L, Tournev I, Campistol JM, Slama MS, Hazenberg BP, Coelho T; European Network for TTR-FAP (ATTReuNET). First European consensus for diagnosis, management, and treatment of transthyretin familial amyloid polyneuropathy[J]. Curr Opin Neurol, 2016, 29 Suppl 1:14-26.
[14] Nativi-Nicolau JN, Karam C, Khella S, Maurer MS. Screening for ATTR amyloidosis in the clinic:overlapping disorders, misdiagnosis, and multiorgan awareness[J]. Heart Fail Rev, 2021.[Epub ahead of print]
[15] Adams D, Koike H, Slama M, Coelho T. Hereditary transthyretin amyloidosis:a model of medical progress for a fatal disease[J]. Nat Rev Neurol, 2019, 15:387-404.
[16] Du K, Li F, Wang H, Miao Y, Lv H, Zhang W, Wang Z, Yuan Y, Meng L. Hereditary transthyretin amyloidosis in mainland China:a unicentric retrospective study[J]. Ann Clin Transl Neurol, 2021, 8:831-841.
[17] Yamashita T, Ueda M, Misumi Y, Masuda T, Nomura T, Tasaki M, Takamatsu K, Sasada K, Obayashi K, Matsui H, Ando Y. Genetic and clinical characteristics of hereditary transthyretin amyloidosis in endemic and non-endemic areas:experience from a single-referral center in Japan[J]. J Neurol, 2018, 265:134-140.
[18] Adams D, Lozeron P, Theaudin M, Mincheva Z, Cauquil C, Adam C, Signate A, Vial C, Maisonobe T, Delmont E, Franques J, Vallat JM, Sole G, Pereon Y, Lacour A, Echaniz-Laguna A, Misrahi M, Lacroix C; French Network for FAP. Regional difference and similarity of familial amyloidosis with polyneuropathy in France[J]. Amyloid, 2012, 19 Suppl 1:61-64.
[19] Luigetti M, Romano A, Di Paolantonio A, Bisogni G, Sabatelli M. Diagnosis and treatment of hereditary transthyretin amyloidosis (hATTR) polyneuropathy:current perspectives on improving patient care[J]. Ther Clin Risk Manag, 2020, 16:109-123.
[20] Adams D, Ando Y, Beirão JM, Coelho T, Gertz MA, Gillmore JD, Hawkins PN, Lousada I, Suhr OB, Merlini G. Expert consensus recommendations to improve diagnosis of ATTR amyloidosis with polyneuropathy[J]. J Neurol, 2020.[Epub ahead of print]
[21] Tojo K, Tsuchiya-Suzuki A, Sekijima Y, Morita H, Sumita N, Ikeda S. Upper limb neuropathy such as carpal tunnel syndrome as an initial manifestation of ATTR Val30Met familial amyloid polyneuropathy[J]. Amyloid, 2010, 17:32-35.
[22] Conceição I, González-Duarte A, Obici L, Schmidt HH, Simoneau D, Ong ML, Amass L. "Red-flag" symptom clusters in transthyretin familial amyloid polyneuropathy[J]. J Peripher Nerv Syst, 2016, 21:5-9.
[23] Reynolds MM, Veverka KK, Gertz MA, Dispenzieri A, Zeldenrust SR, Leung N, Pulido JS. Ocular manifestations of familial transthyretin amyloidosis[J]. Am J Ophthalmol, 2017, 183:156-162.
[24] Lobato L, Rocha A. Transthyretin amyloidosis and the kidney[J]. Clin J Am Soc Nephrol, 2012, 7:1337-1346.
[25] Briemberg HR, Amato AA. Transthyretin amyloidosis presenting with multifocal demyelinating mononeuropathies[J]. Muscle Nerve, 2004, 29:318-322.
[26] Lozeron P, Mariani LL, Dodet P, Beaudonnet G, Théaudin M, Adam C, Arnulf B, Adams D. Transthyretin amyloid polyneuropathies mimicking a demyelinating polyneuropathy[J]. Neurology, 2018, 91:e143-152.
[27] Huang X, Zi XH. Quantitative nerve sensory testing and its clinical application[J]. Lin Chuang Shen Jing Dian Sheng Li Xue Za Zhi, 2001, 10:184-186.[黄献, 资晓宏. 神经定量感觉检查及临床应用[J]. 临床神经电生理学杂志, 2001, 10:184-186.]
[28] Planté-Bordeneuve V, Said G. Familial amyloid polyneuropathy[J]. Lancet Neurol, 2011, 10:1086-1097.
[29] Rousseau A, Cauquil C, Dupas B, Labbé A, Baudouin C, Barreau E, Théaudin M, Lacroix C, Guiochon-Mantel A, Benmalek A, Labetoulle M, Adams D. Potential role of in vivo confocal microscopy for imaging corneal nerves in transthyretin familial amyloid polyneuropathy[J]. JAMA Ophthalmol, 2016, 134:983-989.
[30] Zhang SB, Wu HB, Dai DW, Dai YM. The research progression of sympathetic skin response in clinical application[J]. Heilongjiang Yi Xue, 2016, 40:392-394.[张士保, 吴宏波, 代大伟, 代亚美. 交感神经皮肤反应临床应用研究进展[J]. 黑龙江医学, 2016, 40:392-394.]
[31] Guy CD, Jones CK. Abdominal fat pad aspiration biopsy for tissue confirmation of systemic amyloidosis:specificity, positive predictive value, and diagnostic pitfalls[J]. Diagn Cytopathol, 2001, 24:181-185.
[32] Do Amaral B, Coelho T, Sousa A, Guimarães A. Usefulness of labial salivary gland biopsy in familial amyloid polyneuropathy Portuguese type[J]. Amyloid, 2009, 16:232-238.
[33] Haagsma EB, Van Gameren II, Bijzet J, Posthumus MD, Hazenberg BP. Familial amyloidotic polyneuropathy:long-term follow-up of abdominal fat tissue aspirate in patients with and without liver transplantation[J]. Amyloid, 2007, 14:221-226.
[34] Guan HZ, Liu Q, Chen L, Qian M, Liu Z, Guan YZ, Ren HT, Zhao YH, Chen W. Clinical, neuropathological and genetic findings in patients with transthyretin-associated familial amyloid polyneuropathy[J]. Zhonghua Shen Jing Ke Za Zhi, 2015, 48:7-12.[关鸿志, 柳青, 陈琳, 钱敏, 刘智, 管宇宙, 任海涛, 赵燕环,陈未. 转甲蛋白相关家族性淀粉样周围神经病的临床、病理与遗传学研究[J]. 中华神经科杂志, 2015, 48:7-12.]
[35] Meng LC, Lyu H, Zhang W, Liu J, Wang ZX, Yuan Y. Hereditary transthyretin amyloidosis in eight Chinese families[J]. Chin Med J (Engl), 2015, 128:2902-2905.
[36] Chen X, Graham J, Dabbah MA, Petropoulos IN, Ponirakis G, Asghar O, Alam U, Marshall A, Fadavi H, Ferdousi M, Azmi S, Tavakoli M, Efron N, Jeziorska M, Malik RA. Small nerve fiber quantification in the diagnosis of diabetic sensorimotor polyneuropathy:comparing corneal confocal microscopy with intraepidermal nerve fiber density[J]. Diabetes Care, 2015, 38:1138-1144.
[37] Zhang Y, Liu Z, Zhang Y, Wang H, Liu X, Zhang S, Liu X, Fan D. Corneal sub-basal whorl-like nerve plexus:a landmark for early and follow-up evaluation in transthyretin familial amyloid polyneuropathy[J]. Eur J Neurol, 2021, 28:630-638.
[38] Magrinelli F, Fabrizi GM, Santoro L, Manganelli F, Zanette G, Cavallaro T, Tamburin S. Pharmacological treatment for familial amyloid polyneuropathy[J]. Cochrane Database Syst Rev, 2020, 4:CD012395.
[39] Denier C, Ducot B, Husson H, Lozeron P, Adams D, Meyer L, Said G, Planté-Bordeneuve V. A brief compound test for assessment of autonomic and sensory-motor dysfunction in familial amyloid polyneuropathy[J]. J Neurol, 2007, 254:1684-1688.
[40] Suhr OB, Friman S, Ericzon BG. Early liver transplantation improves familial amyloidotic polyneuropathy patients' survival[J]. Amyloid, 2005, 12:233-238.
[41] Yamashita T, Ando Y, Okamoto S, Misumi Y, Hirahara T, Ueda M, Obayashi K, Nakamura M, Jono H, Shono M, Asonuma K, Inomata Y, Uchino M. Long-term survival after liver transplantation in patients with familial amyloid polyneuropathy[J]. Neurology, 2012, 78:637-643.
[42] Ohya Y, Okamoto S, Tasaki M, Ueda M, Jono H, Obayashi K, Takeda K, Okajima H, Asonuma K, Hara R, Tanihara H, Ando Y, Inomata Y. Manifestations of transthyretin-related familial amyloidotic polyneuropathy:long-term follow-up of Japanese patients after liver transplantation[J]. Surg Today, 2011, 41:1211-1218.
[43] Sakashita N, Ando Y, Haraoka K, Terazaki H, Yamashita T, Nakamura M, Takeya M. Severe congestive heart failure with cardiac liver cirrhosis 10 years after orthotopic liver transplantation for familial amyloidotic polyneuropathy[J]. Pathol Int, 2006, 56:408-412.
[44] Okamoto S, Hörnsten R, Obayashi K, Wijayatunga P, Suhr OB. Continuous development of arrhythmia is observed in Swedish transplant patients with familial amyloidotic polyneuropathy (amyloidogenic transthyretin Val30Met variant)[J]. Liver Transpl, 2011, 17:122-128.
[45] Munar-Qués M, Salva-Ladaria L, Mulet -Perera P, Solé M, López-Andreu FR, Saraiva MJ. Vitreous amyloidosis after liver transplantation in patients with familial amyloid polyneuropathy:ocular synthesis of mutant transthyretin[J]. Amyloid, 2000, 7:266-269.
[46] Bulawa CE, Connelly S, Devit M, Wang L, Weigel C, Fleming JA, Packman J, Powers ET, Wiseman RL, Foss TR, Wilson IA, Kelly JW, Labaudinière R. Tafamidis, a potent and selective transthyretin kinetic stabilizer that inhibits the amyloid cascade[J]. Proc Natl Acad Sci USA, 2012, 109:9629-9634.
[47] Coelho T, Maia LF, Martins da Silva A, Waddington Cruz M, Planté-Bordeneuve V, Lozeron P, Suhr OB, Campistol JM, Conceição IM, Schmidt HH, Trigo P, Kelly JW, Labaudinière R, Chan J, Packman J, Wilson A, Grogan DR. Tafamidis for transthyretin familial amyloid polyneuropathy:a randomized, controlled trial[J]. Neurology, 2012, 79:785-792.
[48] Coelho T, Maia LF, da Silva AM, Cruz MW, Planté-Bordeneuve V, Suhr OB, Conceiçao I, Schmidt HH, Trigo P, Kelly JW, Labaudinière R, Chan J, Packman J, Grogan DR. Long-term effects of tafamidis for the treatment of transthyretin familial amyloid polyneuropathy[J]. J Neurol, 2013, 260:2802-2814.
[49] Planté-Bordeneuve V, Gorram F, Salhi H, Nordine T, Ayache SS, Le Corvoisier P, Azoulay D, Feray C, Damy T, Lefaucheur JP. Long-term treatment of transthyretin familial amyloid polyneuropathy with tafamidis:a clinical and neurophysiological study[J]. J Neurol, 2017, 264:268-276.
[50] Barroso FA, Judge DP, Ebede B, Li H, Stewart M, Amass L, Sultan MB. Long-term safety and efficacy of tafamidis for the treatment of hereditary transthyretin amyloid polyneuropathy:results up to 6 years[J]. Amyloid, 2017, 24:194-204.
[51] Berk JL, Suhr OB, Obici L, Sekijima Y, Zeldenrust SR, Yamashita T, Heneghan MA, Gorevic PD, Litchy WJ, Wiesman JF, Nordh E, Corato M, Lozza A, Cortese A, Robinson-Papp J, Colton T, Rybin DV, Bisbee AB, Ando Y, Ikeda S, Seldin DC, Merlini G, Skinner M, Kelly JW, Dyck PJ; Diflunisal Trial Consortium. Repurposing diflunisal for familial amyloid polyneuropathy:a randomized clinical trial[J]. JAMA, 2013, 310:2658-2667.
[52] Berk JL, Suhr OB, Sekijima Y, Yamashita T, Heneghan M, Zeldenrust SR, Ando Y, Ikeda S, Gorevic P, Merlini G, Kelly JW, Skinner M, Bisbee AB, Dyck PJ, Obici L; Familial Amyloidosis Consortium. The Diflunisal Trial:study accrual and drug tolerance[J]. Amyloid, 2012, 19 Suppl 1:37-38.
[53] Sekijima Y, Tojo K, Morita H, Koyama J, Ikeda S. Safety and efficacy of long-term diflunisal administration in hereditary transthyretin (ATTR) amyloidosis[J]. Amyloid, 2015, 22:79-83.
[54] Reddy KS, Roy A. Cardiovascular risk of NSAIDs:time to translate knowledge into practice[J]. PLoS Med, 2013, 10:e1001389.
[55] Pinheiro F, Varejão N, Esperante S, Santos J, Velázquez-Campoy A, Reverter D, Pallarès I, Ventura S. Tolcapone, a potent aggregation inhibitor for the treatment of familial leptomeningeal amyloidosis[J]. FEBS J, 2021, 288:310-324.
[56] Cotrina EY, Oliveira Â, Leite JP, Llop J, Gales L, Quintana J, Cardoso I, Arsequell G. Repurposing benzbromarone for familial amyloid polyneuropathy:a new transthyretin tetramer stabilizer[J]. Int J Mol Sci, 2020, 21:7166.
[57] Fox JC, Hellawell JL, Rao S, O'Reilly T, Lumpkin R, Jernelius J, Gretler D, Sinha U. First-in-Human study of AG10, a novel, oral, specific, selective, and potent transthyretin stabilizer for the treatment of transthyretin amyloidosis:a phase 1 safety, tolerability, pharmacokinetic, and pharmacodynamic study in healthy adult volunteers[J]. Clin Pharmacol Drug Dev, 2020, 9:115-129.
[58] Adams D, Gonzalez-Duarte A, O'Riordan WD, Yang CC, Ueda M, Kristen AV, Tournev I, Schmidt HH, Coelho T, Berk JL, Lin KP, Vita G, Attarian S, Planté-Bordeneuve V, Mezei MM, Campistol JM, Buades J, Brannagan TH 3rd, Kim BJ, Oh J, Parman Y, Sekijima Y, Hawkins PN, Solomon SD, Polydefkis M, Dyck PJ, Gandhi PJ, Goyal S, Chen J, Strahs AL, Nochur SV, Sweetser MT, Garg PP, Vaishnaw AK, Gollob JA, Suhr OB. Patisiran, an RNAi therapeutic, for hereditary transthyretin amyloidosis[J]. N Engl J Med, 2018, 379:11-21.
[59] Adams D, Suhr OB, Dyck PJ, Litchy WJ, Leahy RG, Chen J, Gollob J, Coelho T. Trial design and rationale for APOLLO, a Phase 3, placebo-controlled study of patisiran in patients with hereditary ATTR amyloidosis with polyneuropathy[J]. BMC Neurol, 2017, 17:181.
[60] Coelho T, Adams D, Conceição I, Waddington -Cruz M, Schmidt HH, Buades J, Campistol J, Berk JL, Polydefkis M, Wang JJ, Chen J, Sweetser MT, Gollob J, Suhr OB. A phase Ⅱ, open-label, extension study of long-term patisiran treatment in patients with hereditary transthyretin-mediated (hATTR) amyloidosis[J]. Orphanet J Rare Dis, 2020, 15:179.
[61] Solomon SD, Adams D, Kristen A, Grogan M, González-Duarte A, Maurer MS, Merlini G, Damy T, Slama MS, Brannagan TH 3rd, Dispenzieri A, Berk JL, Shah AM, Garg P, Vaishnaw A, Karsten V, Chen J, Gollob J, Vest J, Suhr O. Effects of patisiran, an RNA interference therapeutic, on cardiac parameters in patients with hereditary transthyretin-mediated amyloidosis[J]. Circulation, 2019, 139:431-443.
[62] Adams D, Polydefkis M, González-Duarte A, Wixner J, Kristen AV, Schmidt HH, Berk JL, Losada López IA, Dispenzieri A, Quan D, Conceição IM, Slama MS, Gillmore JD, Kyriakides T, Ajroud-Driss S, Waddington-Cruz M, Mezei MM, Planté -Bordeneuve V, Attarian S, Mauricio E, Brannagan TH 3rd, Ueda M, Aldinc E, Wang JJ, White MT, Vest J, Berber E, Sweetser MT, Coelho T; patisiran Global OLE study group. Long-term safety and efficacy of patisiran for hereditary transthyretin-mediated amyloidosis with polyneuropathy:12-month results of an open-label extension study[J]. Lancet Neurol, 2021, 20:49-59.
[63] Benson MD, Waddington-Cruz M, Berk JL, Polydefkis M, Dyck PJ, Wang AK, Planté-Bordeneuve V, Barroso FA, Merlini G, Obici L, Scheinberg M, Brannagan TH 3rd, Litchy WJ, Whelan C, Drachman BM, Adams D, Heitner SB, Conceição I, Schmidt HH, Vita G, Campistol JM, Gamez J, Gorevic PD, Gane E, Shah AM, Solomon SD, Monia BP, Hughes SG, Kwoh TJ, McEvoy BW, Jung SW, Baker BF, Ackermann EJ, Gertz MA, Coelho T. Inotersen treatment for patients with hereditary transthyretin amyloidosis[J]. N Engl J Med, 2018, 379:22-31.
[64] Dasgupta NR, Rissing SM, Smith J, Jung J, Benson MD. Inotersen therapy of transthyretin amyloid cardiomyopathy[J]. Amyloid, 2020, 27:52-58.
[65] Benson MD, Kluve-Beckerman B, Zeldenrust SR, Siesky AM, Bodenmiller DM, Showalter AD, Sloop KW. Targeted suppression of an amyloidogenic transthyretin with antisense oligonucleotides[J]. Muscle Nerve, 2006, 33:609-618.
[66] Park GY, Jamerlan A, Shim KH, An SSA. Diagnostic and treatment approaches involving transthyretin in amyloidogenic diseases[J]. Int J Mol Sci, 2019, 20:2982.
[67] Habtemariam BA, Karsten V, Attarwala H, Goel V, Melch M, Clausen VA, Garg P, Vaishnaw AK, Sweetser MT, Robbie GJ, Vest J. Single-dose pharmacokinetics and pharmacodynamics of transthyretin targeting N-acetylgalactosamine-small interfering ribonucleic acid conjugate, vutrisiran, in healthy subjects[J]. Clin Pharmacol Ther, 2021, 109:372-382.
[68] Viney NJ, Guo S, Tai LJ, Baker BF, Aghajan M, Jung SW, Yu RZ, Booten S, Murray H, Machemer T, Burel S, Murray S, Buchele G, Tsimikas S, Schneider E, Geary RS, Benson MD, Monia BP. Ligand conjugated antisense oligonucleotide for the treatment of transthyretin amyloidosis:preclinical and phase 1 data[J]. ESC Heart Fail, 2021, 8:652-661.
[69] Cardoso I, Martins D, Ribeiro T, Merlini G, Saraiva MJ. Synergy of combined doxycycline/TUDCA treatment in lowering Transthyretin deposition and associated biomarkers:studies in FAP mouse models[J]. J Transl Med, 2010, 8:74.
[70] Obici L, Cortese A, Lozza A, Lucchetti J, Gobbi M, Palladini G, Perlini S, Saraiva MJ, Merlini G. Doxycycline plus tauroursodeoxycholic acid for transthyretin amyloidosis:a phase Ⅱ study[J]. Amyloid, 2012, 19 Suppl 1:34-36.
[71] aus dem Siepen F, Buss SJ, Andre F, Seitz S, Giannitsis E, Steen H, Katus HA, Kristen AV. Extracellular remodeling in patients with wild-type amyloidosis consuming epigallocatechin-3-gallate:preliminary results of T1 mapping by cardiac magnetic resonance imaging in a small single center study[J]. Clin Res Cardiol, 2015, 104:640-647.
[72] Ferreira N, Saraiva MJ, Almeida MR. Epigallocatechin-3-gallate as a potential therapeutic drug for TTR-related amyloidosis:"in vivo" evidence from FAP mice models[J]. PLoS One, 2012, 7:e29933.
[73] Goldsteins G, Persson H, Andersson K, Olofsson A, Dacklin I, Edvinsson A, Saraiva MJ, Lundgren E. Exposure of cryptic epitopes on transthyretin only in amyloid and in amyloidogenic mutants[J]. Proc Natl Acad Sci USA, 1999, 96:3108-3113.
[74] Higaki JN, Chakrabartty A, Galant NJ, Hadley KC, Hammerson B, Nijjar T, Torres R, Tapia JR, Salmans J, Barbour R, Tam SJ, Flanagan K, Zago W, Kinney GG. Novel conformation-specific monoclonal antibodies against amyloidogenic forms of transthyretin[J]. Amyloid, 2016, 23:86-97.
[75] Hosoi A, Su Y, Torikai M, Jono H, Ishikawa D, Soejima K, Higuchi H, Guo J, Ueda M, Suenaga G, Motokawa H, Ikeda T, Senju S, Nakashima T, Ando Y. Novel antibody for the treatment of transthyretin amyloidosis[J]. J Biol Chem, 2016, 291:25096-25105.
[76] Ando Y, Ueda M. Antibody therapy for transthyretin-related hereditary amyloid polyneuropathy:another therapeutic option[J]. Amyloid, 2017, 24(sup1):113-114. |