All Relations between Polyneuropathies and ttr

Publication Sentence Publish Date Extraction Date Species
A Martinho, I Gonçalves, M Costa, C R Santo. Stress and glucocorticoids increase transthyretin expression in rat choroid plexus via mineralocorticoid and glucocorticoid receptors. Journal of molecular neuroscience : MN. vol 48. issue 1. 2013-01-09. PMID:22371232. several mutated forms of ttr cause familial amyloidotic polyneuropathy, an inheritable lethal disease. 2013-01-09 2023-08-12 rat
Lior Leibou, Jacob Frand, Menachem Sadeh, Alexander Lossos, Eyal Kremer, Avi Livneh, David Yarnitsky, Oscar Herman, Ron Dabb. Clinical and genetic findings in eight Israeli patients with transthyretin-associated familial amyloid polyneuropathy. The Israel Medical Association journal : IMAJ. vol 14. issue 11. 2013-01-08. PMID:23240369. transthyretin (ttr)-associated familial amyloid polyneuropathy (fap) is an autosomal dominant multisystem disease with neurological and extra-neurological manifestations. 2013-01-08 2023-08-12 Not clear
Yuya Hayashi, Yoshimasa Mori, Shogo Yamashita, Keiichi Motoyama, Taishi Higashi, Hirofumi Jono, Yukio Ando, Hidetoshi Arim. Potential use of lactosylated dendrimer (G3)/α-cyclodextrin conjugates as hepatocyte-specific siRNA carriers for the treatment of familial amyloidotic polyneuropathy. Molecular pharmaceutics. vol 9. issue 6. 2012-12-28. PMID:22510029. to reveal the potential use of lactosylated-dendrimer (g3) conjugates with α-cyclodextrin (lac-α-cde (g3)) as novel hepatocyte-specific sirna carriers in order to treat transthyretin (ttr)-related familial amyloidotic polyneuropathy (fap), we evaluated the rnai effect of sirna complexes with lac-α-cde (g3) both in vitro and in vivo. 2012-12-28 2023-08-12 mouse
S K Palaninatha. Nearly 200 X-ray crystal structures of transthyretin: what do they tell us about this protein and the design of drugs for TTR amyloidoses? Current medicinal chemistry. vol 19. issue 15. 2012-10-26. PMID:22471981. single point mutations enhance the amyloidogenicity of ttr, causing familial amyloid cardiomyopathy, familial amyloid polyneuropathy, and central nervous system selective amyloidosis. 2012-10-26 2023-08-12 human
G Arsequell, A Plana. Methods to evaluate the inhibition of TTR fibrillogenesis induced by small ligands. Current medicinal chemistry. vol 19. issue 15. 2012-10-26. PMID:22471983. transthyretin is an amyloidogenic protein associated with several amyloidosis, namely familial amyloidotic polyneuropathy, familial amyloidotic cardiomyopathy, and central nervous system selective amyloidosis, familial rare diseases caused by single point mutants, and senile systemic amyloidosis associated with wild-type ttr. 2012-10-26 2023-08-12 Not clear
Steven M Johnson, Stephen Connelly, Colleen Fearns, Evan T Powers, Jeffery W Kell. The transthyretin amyloidoses: from delineating the molecular mechanism of aggregation linked to pathology to a regulatory-agency-approved drug. Journal of molecular biology. vol 421. issue 2-3. 2012-09-25. PMID:22244854. this strategy afforded the drug tafamidis which was recently approved by the european medicines agency for the treatment of ttr familial amyloid polyneuropathy, the most common familial ttr amyloid disease. 2012-09-25 2023-08-12 Not clear
Steven M Johnson, Stephen Connelly, Colleen Fearns, Evan T Powers, Jeffery W Kell. The transthyretin amyloidoses: from delineating the molecular mechanism of aggregation linked to pathology to a regulatory-agency-approved drug. Journal of molecular biology. vol 421. issue 2-3. 2012-09-25. PMID:22244854. tafamidis is the first and currently the only medication approved to treat ttr familial amyloid polyneuropathy. 2012-09-25 2023-08-12 Not clear
Isabel Conceiçã. Clinical features of TTR-FAP in Portugal. Amyloid : the international journal of experimental and clinical investigation : the official journal of the International Society of Amyloidosis. vol 19 Suppl 1. 2012-09-21. PMID:22480206. familial amyloid polyneuropathy (fap) is an autosomal dominant disorder characterized by the extracellular deposition of transthyretin (ttr) fibrils in several tissues, particularly in the peripheral nervous system. 2012-09-21 2023-08-12 Not clear
Yu Su, Hirofumi Jono, Masaharu Torikai, Akihiko Hosoi, Kenji Soejima, Jianying Guo, Masayoshi Tasaki, Yohei Misumi, Mitsuharu Ueda, Satoru Shinriki, Makoto Shono, Konen Obayashi, Toshihiro Nakashima, Keishin Sugawara, Yukio And. Antibody therapy for familial amyloidotic polyneuropathy. Amyloid : the international journal of experimental and clinical investigation : the official journal of the International Society of Amyloidosis. vol 19 Suppl 1. 2012-09-21. PMID:22506915. in this study, to establish the antibody therapy for familial amyloidotic polyneuropathy (fap), we generated a monoclonal anti-ttr antibody, which specifically reacts with surface epitopes of ttr (mab attr) and evaluated its binding affinity and specificity for ttr amyloid fibrils. 2012-09-21 2023-08-12 Not clear
Haruki Koike, Gen Sobu. Late-onset familial amyloid polyneuropathy in Japan. Amyloid : the international journal of experimental and clinical investigation : the official journal of the International Society of Amyloidosis. vol 19 Suppl 1. 2012-09-21. PMID:22506939. transthyretin (ttr) val30met-associated familial amyloid polyneuropathy (fap attr val30met) is the most common form of fap. 2012-09-21 2023-08-12 Not clear
Yuya Hayashi, Yoshimasa Mori, Taishi Higashi, Keiichi Motoyama, Hirofumi Jono, Dinah W Y Sah, Yukio Ando, Hidetoshi Arim. Systemic delivery of transthyretin siRNA mediated by lactosylated dendrimer/α-cyclodextrin conjugates into hepatocyte for familial amyloidotic polyneuropathy therapy. Amyloid : the international journal of experimental and clinical investigation : the official journal of the International Society of Amyloidosis. vol 19 Suppl 1. 2012-09-21. PMID:22519861. in particular, when considering the sirna therapeutics for familial amyloidotic polyneuropathy (fap) caused by the deposition of variant transthyretin (ttr) in various organs, hepatocyte-selective sirna delivery is desired because ttr is predominantly synthesized by hepatocytes. 2012-09-21 2023-08-12 Not clear
Hirofumi Jono, Takayuki Anno, Keiichi Motoyama, Yohei Misumi, Masayoshi Tasaki, Toshinori Oshima, Yoshimasa Mori, Mineyuki Mizuguchi, Mitsuharu Ueda, Satoru Shinriki, Makoto Shono, Konen Obayashi, Hidetoshi Arima, Yukio And. Potential use of glucuronylglucosyl-β-cyclodextrin as a novel therapeutic tool for familial amyloidotic polyneuropathy. Amyloid : the international journal of experimental and clinical investigation : the official journal of the International Society of Amyloidosis. vol 19 Suppl 1. 2012-09-21. PMID:22620966. transthyretin (ttr)-related familial amyloidotic polyneuropathy, which is induced by amyloidogenic transthyretin (attr), is characterized by systemic accumulation of amyloid fibrils. 2012-09-21 2023-08-12 human
David Adams, Pierre Lozeron, Marie Theaudin, Zoia Mincheva, Cecile Cauquil, Clovis Adam, Aissatou Signate, Christophe Vial, Thierry Maisonobe, Emilien Delmont, Jerome Franques, Jean-Michel Vallat, Guilhem Sole, Yann Pereon, Arnaud Lacour, Andoni Echaniz-Laguna, Micheline Misrahi, Catherine Lacroi. Regional difference and similarity of familial amyloidosis with polyneuropathy in France. Amyloid : the international journal of experimental and clinical investigation : the official journal of the International Society of Amyloidosis. vol 19 Suppl 1. 2012-09-21. PMID:22620968. familial amyloidosis with polyneuropathy (fap) in france have a large genetic heterogeneity with 29 transthyretin (ttr) gene mutations; met30-ttr is the most frequent one (62%); followed by tyr77-ttr (11.8%) and phe77-ttr (6.2%). 2012-09-21 2023-08-12 Not clear
Yukio And. [Effect of liver trasplantation on familial amyloidotic polyneuropathy (FAP) and its limt]. Rinsho shinkeigaku = Clinical neurology. vol 51. issue 11. 2012-09-18. PMID:22277510. familial amyloidotic polyneuropathy (fap) is a hereditary intractable disease induced by mutated transthyretin (ttr). 2012-09-18 2023-08-12 Not clear
Shu-Ichi Iked. [Metabolic turn over of amyloid fibrils and post-treatment regression of amyloid deposits in systemic amyloidosis with polyneuropathy]. Rinsho shinkeigaku = Clinical neurology. vol 51. issue 11. 2012-09-18. PMID:22277512. systemic amyloidosis that includes familial transthyretin (ttr)-related amyloid polyneuropathy (fap) and primary systemic immunoglobulin light chain (al)-derived amyloidosis was long considered to be an incurable disease, but effective therapeutic approaches developed during 20 years ago: liver transplantation for fap and high dose melphalan with autologous peripheral blood stem cell transplantation (auto-pbsct). 2012-09-18 2023-08-12 Not clear
Christine E Bulawa, Stephen Connelly, Michael Devit, Lan Wang, Charlotte Weigel, James A Fleming, Jeff Packman, Evan T Powers, R Luke Wiseman, Theodore R Foss, Ian A Wilson, Jeffery W Kelly, Richard Labaudinièr. Tafamidis, a potent and selective transthyretin kinetic stabilizer that inhibits the amyloid cascade. Proceedings of the National Academy of Sciences of the United States of America. vol 109. issue 24. 2012-08-28. PMID:22645360. one such compound, tafamidis meglumine (fx-1006a), has recently completed phase ii/iii trials for the treatment of transthyretin type familial amyloid polyneuropathy (ttr-fap) and demonstrated a slowing of disease progression in patients heterozygous for the v30m ttr mutation. 2012-08-28 2023-08-12 Not clear
Prayman T Sattianayagam, Angelika F Hahn, Carol J Whelan, Simon D J Gibbs, Jennifer H Pinney, Arie J Stangou, Dorota Rowczenio, Peter W Pflugfelder, Zoe Fox, Helen J Lachmann, Ashutosh D Wechalekar, Philip N Hawkins, Julian D Gillmor. Cardiac phenotype and clinical outcome of familial amyloid polyneuropathy associated with transthyretin alanine 60 variant. European heart journal. vol 33. issue 9. 2012-08-15. PMID:21992998. familial amyloid polyneuropathy (fap) is a dominantly inherited multi-system disease associated with transthyretin (ttr) mutations. 2012-08-15 2023-08-12 Not clear
Nelson Ferreira, Maria João Saraiva, Maria Rosário Almeid. Epigallocatechin-3-gallate as a potential therapeutic drug for TTR-related amyloidosis: "in vivo" evidence from FAP mice models. PloS one. vol 7. issue 1. 2012-05-29. PMID:22253829. familial amyloidotic polyneuropathy (fap) is a neurodegenerative disease caused by the extracellular deposition of mutant transthyretin (ttr), with special involvement of the peripheral nervous system (pns). 2012-05-29 2023-08-12 mouse
T Yamashita, Y Ando, S Okamoto, Y Misumi, T Hirahara, M Ueda, K Obayashi, M Nakamura, H Jono, M Shono, K Asonuma, Y Inomata, M Uchin. Long-term survival after liver transplantation in patients with familial amyloid polyneuropathy. Neurology. vol 78. issue 9. 2012-05-15. PMID:22345221. familial amyloid polyneuropathy (fap), which is a fatal disorder inherited in an autosomal dominant fashion, is characterized by systemic accumulation of polymerized transthyretin (ttr) in the peripheral nerves and systemic organs. 2012-05-15 2023-08-12 Not clear
Artur F Castro-Rodrigues, Luís Gales, Maria J Saraiva, Ana M Dama. Structural insights into a zinc-dependent pathway leading to Leu55Pro transthyretin amyloid fibrils. Acta crystallographica. Section D, Biological crystallography. vol 67. issue Pt 12. 2012-04-05. PMID:22120741. human transthyretin (ttr) is a homotetrameric protein that is responsible for the formation of amyloid in patients with familiar amyloidotic polyneuropathy (fap), familiar amyloidotic cardiomyopathy (fac) and senile systemic amyloidosis (ssa). 2012-04-05 2023-08-12 human