All Relations between Polyneuropathies and ttr

Publication Sentence Publish Date Extraction Date Species
Joel N Buxbau. Evaluation of tafamidis as first-line therapeutic agent for transthyretin familial amyloidotic polyneuropathy. Degenerative neurological and neuromuscular disease. vol 2. 2020-10-01. PMID:30890886. almost 100 mutations in the human transthyretin (ttr) gene cause the autosomal dominant disorders of familial amyloidotic polyneuropathy (fap) and familial amyloidotic cardiomyopathy. 2020-10-01 2023-08-13 human
Joel N Buxbau. Evaluation of tafamidis as first-line therapeutic agent for transthyretin familial amyloidotic polyneuropathy. Degenerative neurological and neuromuscular disease. vol 2. 2020-10-01. PMID:30890886. deposition of amyloid derived from a kinetically or thermodynamically unstable mutant ttr precursor produces an ascending sensorimotor polyneuropathy with marked autonomic involvement. 2020-10-01 2023-08-13 human
Philippe Kerschen, Violaine Planté-Bordeneuv. Current and Future Treatment Approaches in Transthyretin Familial Amyloid Polyneuropathy. Current treatment options in neurology. vol 18. issue 12. 2020-09-30. PMID:27873215. treatment of transthyretin familial amyloid polyneuropathy (ttr fap) must be tailored to disease stage. 2020-09-30 2023-08-13 Not clear
Nelson Ferreira, Alda Pereira-Henriques, Maria Rosário Almeid. Transthyretin chemical chaperoning by flavonoids: Structure-activity insights towards the design of potent amyloidosis inhibitors. Biochemistry and biophysics reports. vol 3. 2020-09-30. PMID:29124175. to investigate structure-activity relationships relevant for the interaction of flavonoids with transthyretin (ttr), the protein associated with familial amyloid polyneuropathy (fap), we compared the effects of major tea catechins and their larger polymers theaflavins, side-by-side, on ttr amyloid formation process. 2020-09-30 2023-08-13 Not clear
Meenakshi Verma, Amandeep Girdhar, Basant Patel, Nirmal K Ganguly, Ritushree Kukreti, Vibha Tanej. Q-Rich Yeast Prion [ Frontiers in molecular neuroscience. vol 11. 2020-09-30. PMID:29593496. evidences suggest that transthyretin (ttr), a plasma protein associated with transthyretin amyloidosis or familial polyneuropathy (fap) interacts with heterologous amyloid proteins including amyloid beta and islet amyloid polypeptide. 2020-09-30 2023-08-13 Not clear
Daniel Serrano, Christopher B Atzinger, Marc F Bottema. Understanding the Disease Course and Therapeutic Benefit of Tafamidis Across Real-World Studies of Hereditary Transthyretin Amyloidosis with Polyneuropathy: A Proof of Concept for Integrative Data Analytic Approaches. Neurology and therapy. vol 7. issue 1. 2020-09-30. PMID:29611130. hereditary transthyretin (ttr) amyloidosis with polyneuropathy (hattr-pn) is a rare, autosomal dominant amyloidosis characterized primarily by progressive ascending sensorimotor neuropathy often associated with  autonomic involvement. 2020-09-30 2023-08-13 Not clear
Arman Çakar, Hacer Durmuş-Tekçe, Yeşim Parma. Familial Amyloid Polyneuropathy. Noro psikiyatri arsivi. vol 56. issue 2. 2020-09-29. PMID:31223250. transthyretin-related familial amyloid polyneuropathy (ttr-fap) is a life-threatening disease caused by the accumulation of amyloidogenic transthyretin (ttr) protein in tissues. 2020-09-29 2023-08-13 Not clear
Yo-Tsen Liu, Yueh-Jung Yen, Frans Ricardo, Yu Chang, Pei-Hao Wu, Shing-Jong Huang, Kon-Ping Lin, Tsyr-Yan Y. Biophysical characterization and modulation of Transthyretin Ala97Ser. Annals of clinical and translational neurology. vol 6. issue 10. 2020-09-07. PMID:31502419. ala97ser (a97s) is the major transthyretin (ttr) mutation in taiwanese patients of familial amyloid polyneuropathy (fap), characterized by a late-onset but rapidly deteriorated neuropathy. 2020-09-07 2023-08-13 Not clear
Francesca Magrinelli, Gian Maria Fabrizi, Lucio Santoro, Fiore Manganelli, Giampietro Zanette, Tiziana Cavallaro, Stefano Tamburi. Pharmacological treatment for familial amyloid polyneuropathy. The Cochrane database of systematic reviews. vol 4. 2020-08-20. PMID:32311072. disease-modifying pharmacological agents for transthyretin (ttr)-related familial amyloid polyneuropathy (fap) have become available in the last decade, but evidence on their efficacy and safety is limited. 2020-08-20 2023-08-13 Not clear
Laura Pont, Gemma Marin, María Vergara-Barberán, Leonardo G Gagliardi, Victoria Sanz-Nebot, José M Herrero-Martínez, Fernando Benavent. Polymeric monolithic microcartridges with gold nanoparticles for the analysis of protein biomarkers by on-line solid-phase extraction capillary electrophoresis-mass spectrometry. Journal of chromatography. A. vol 1622. 2020-07-24. PMID:32381302. the performance of these novel microcartridges was evaluated with human transthyretin (ttr), which is a protein related to different types of familial amyloidotic polyneuropathies (fap). 2020-07-24 2023-08-13 human
Yun Jeong Lee, Jeeyoung Oh, Su-Kyeung Hwang, Eun Joo Lee, Dong Heon Yang, Yong-Jin Kim, Soonhak Kwon, Myung Chul Hyu. Extremely Early Onset Transthyretin Familial Amyloid Polyneuropathy with a Leu55Pro Mutation: A Pediatric Case Report and Literature Review. Neuropediatrics. vol 50. issue 5. 2020-06-09. PMID:31319424. transthyretin familial amyloid polyneuropathy (ttr-fap) is a life-threatening autosomal dominant disease caused by the deposition of amyloid fibrils composed of ttr proteins. 2020-06-09 2023-08-13 Not clear
Michelle Kaku, John L Ber. Neuropathy Associated with Systemic Amyloidosis. Seminars in neurology. vol 39. issue 5. 2020-06-03. PMID:31639841. the most common form of hereditary amyloidosis is caused by 1 of 140 mutations in the transthyretin (ttr) gene, which can lead to neuropathic hereditary transthyretin amyloidosis (hattr; previously referred to as transthyretin familial amyloid polyneuropathy), whereas acquired immunoglobulin light chain (al) amyloidosis is the most common acquired form. 2020-06-03 2023-08-13 Not clear
Andreia Dias, Diana Santos, Teresa Coelho, Miguel Alves-Ferreira, Jorge Sequeiros, Isabel Alonso, Alda Sousa, Carolina Lemo. Annals of clinical and translational neurology. vol 6. issue 4. 2020-02-18. PMID:31019999. transthyretin (ttr) familial amyloid polyneuropathy (fap) (omim 176300) shows a variable age-at-onset (ao), including within families. 2020-02-18 2023-08-13 Not clear
Chi-Chao Chao, Hsueh-Wen Hsueh, Hung-Wei Kan, Chun-Hua Liao, Hao-Hua Jiang, Hao Chiang, Whei-Min Lin, Ti-Yen Yeh, Yea-Huey Lin, Ya-Yin Cheng, Sung-Tsang Hsie. Skin nerve pathology: Biomarkers of premanifest and manifest amyloid neuropathy. Annals of neurology. vol 85. issue 4. 2020-02-13. PMID:30737830. small-fiber sensory and autonomic symptoms are early presentations of familial amyloid polyneuropathy (fap) with transthyretin (ttr) mutations. 2020-02-13 2023-08-13 Not clear
David Adams, Haruki Koike, Michel Slama, Teresa Coelh. Hereditary transthyretin amyloidosis: a model of medical progress for a fatal disease. Nature reviews. Neurology. vol 15. issue 7. 2020-01-23. PMID:31209302. hereditary amyloidogenic transthyretin (attrv) amyloidosis with polyneuropathy (also known as familial amyloid polyneuropathy) is a condition with adult onset caused by mutation of transthyretin (ttr) and characterized by extracellular deposition of amyloid and destruction of the somatic and autonomic pns, leading to loss of autonomy and death. 2020-01-23 2023-08-13 Not clear
Diana Santos, Teresa Coelho, Miguel Alves-Ferreira, Jorge Sequeiros, Denisa Mendonça, Isabel Alonso, Alda Sousa, Carolina Lemo. Large normal alleles of ATXN2 decrease age at onset in transthyretin familial amyloid polyneuropathy Val30Met patients. Annals of neurology. vol 85. issue 2. 2020-01-06. PMID:30615214. transthyretin (ttr)-related familial amyloid polyneuropathy (fap) is an autosomal dominant neurological disease, caused most frequently by a val30met (now classified as val50met) substitution in ttr. 2020-01-06 2023-08-13 Not clear
Sandeep Devarapalli, Daniel J Zhou, P James B Dyck, Ezequiel A Piccion. Transthyretin Amyloidosis Presenting With Upper-Extremity Neuropathy and Paucity of Autonomic Impairment. Journal of clinical neuromuscular disease. vol 20. issue 4. 2019-12-13. PMID:31135624. ttr familial amyloid polyneuropathy commonly presents as length-dependent sensorimotor polyneuropathy with marked and early autonomic involvement. 2019-12-13 2023-08-13 Not clear
Sandeep Devarapalli, Daniel J Zhou, P James B Dyck, Ezequiel A Piccion. Transthyretin Amyloidosis Presenting With Upper-Extremity Neuropathy and Paucity of Autonomic Impairment. Journal of clinical neuromuscular disease. vol 20. issue 4. 2019-12-13. PMID:31135624. multiple pathogenic mutations in ttr gene have been identified, of which val50met is commonly associated with ttr familial amyloid polyneuropathy, and val142ile is commonly associated with familial amyloid cardiomyopathy. 2019-12-13 2023-08-13 Not clear
Joel N Buxbau. Treatment of hereditary and acquired forms of transthyretin amyloidosis in the era of personalized medicine: the role of randomized controlled trials. Amyloid : the international journal of experimental and clinical investigation : the official journal of the International Society of Amyloidosis. vol 26. issue 2. 2019-12-06. PMID:30907141. there have now been randomized controlled trials of four different therapeutics for hereditary amyloid polyneuropathy related to transthyretin (ttr) deposition and one for amyloidotic cardiomyopathy of both genetic and sporadic origin. 2019-12-06 2023-08-13 Not clear
Tatsufumi Murakami, Yoshihide Sunad. Transthyretin Amyloid Neuropathy: The Schwann Cell Hypothesis. Advances in experimental medicine and biology. vol 1190. 2019-12-06. PMID:31760657. transthyretin (ttr)-familial amyloid polyneuropathy (fap) is a systemic amyloidosis caused by mutations in the ttr gene. 2019-12-06 2023-08-13 Not clear