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1 tations of TTR such as L55P (associated with familial amyloid polyneuropathy).
2 00 mutations in the TTR gene are involved in familial amyloid polyneuropathy.
3 as Alzheimer's and Parkinson's diseases and familial amyloid polyneuropathy.
4 a useful prognostic marker in transthyretin familial amyloid polyneuropathy.
5 on detected by MIBG imaging in transthyretin familial amyloid polyneuropathy.
6 ly the only medication approved to treat TTR familial amyloid polyneuropathy.
7 ing, while several TTR mutants are linked to familial amyloid polyneuropathy.
8 tively cause senile systemic amyloidosis and familial amyloid polyneuropathy.
9 the course of senile systemic amyloidosis or familial amyloid polyneuropathy.
10 the diseases senile systemic amyloidosis and familial amyloid polyneuropathy.
11 nsidered part of the syndrome of TTR-related familial amyloid polyneuropathy.
12 ibits the amyloidogenesis of the most common familial amyloid polyneuropathy and familial amyloid car
13 ween TTR amyloid deposition and the onset of familial amyloid polyneuropathy and senile systemic amyl
14 fibril formation is observed systemically in familial amyloid polyneuropathy and senile systemic amyl
15 e, transthyretin V30M mutant associated with familial amyloid polyneuropathy, and Abeta42 associated
16 yloid diseases: senile systemic amyloidosis, familial amyloid polyneuropathy, and familial amyloid ca
17 associated with senile systemic amyloidosis, familial amyloid polyneuropathy, and familial amyloid ca
18 oid diseases, including Alzheimer's disease, familial amyloid polyneuropathy, and senile systemic amy
19 opic hepatic transplantation is effective in familial amyloid polyneuropathy associated with variant
21 eripheral nervous system which characterizes familial amyloid polyneuropathy caused by variant TTR.
24 Autonomic neuropathy is a major component of familial amyloid polyneuropathy (FAP) due to mutated tra
28 ino liver transplant in which a patient with familial amyloid polyneuropathy (FAP) received an orthot
29 utonomic symptoms are early presentations of familial amyloid polyneuropathy (FAP) with transthyretin
31 he clinical status of patients with V30M TTR familial amyloid polyneuropathy (FAP), we quantified pla
32 ansthyretin (senile systemic amyloidosis and familial amyloid polyneuropathy), immunoglobulin light c
33 TTR mutation is the most prevalent cause of familial amyloid polyneuropathy in heterozygotes, wherea
35 at tolcapone, already in clinical trials for familial amyloid polyneuropathy, is a strong candidate f
40 Secondary end points included changes in the familial amyloid polyneuropathy stage, polyneuropathy di
41 an Medicines Agency for the treatment of TTR familial amyloid polyneuropathy, the most common familia
42 elay neurologic progression of transthyretin familial amyloid polyneuropathy, there are no approved p
43 ials for the treatment of Transthyretin Type Familial Amyloid Polyneuropathy (TTR-FAP) and demonstrat
46 presentations of the disease: transthyretin familial amyloid polyneuropathy, which primarily affects
47 ATTR patients after LTx, as reported to the Familial Amyloid Polyneuropathy World Transplant Registr