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1                                              Gerstmann-Straussler-Scheinker (GSS) disease is a domina
2                                              Gerstmann-Straussler-Scheinker disease (GSS) is an inher
3                                              Gerstmann-Straussler-Scheinker disease (GSS) is characte
4                                              Gerstmann-Straussler-Scheinker syndrome (GSS) is a genet
5                                              Gerstmann-Straussler-Scheinker syndrome (GSS) with the P
6 n = 17, fatal familial insomnia (FFI) n = 9, Gerstmann-Straussler-Scheinker syndrome (GSS)) n = 4), p
7                               Importantly, a Gerstmann-Straussler-Scheinker mutation carrier in the a
8                   This mutation results in a Gerstmann-Straussler-Scheinker-like disease with extensi
9                                    Whereas a Gerstmann-Straussler-Scheinker disease version of PrP wi
10 o the Y145Stop PrP variant associated with a Gerstmann-Straussler-Scheinker-like prion disease) spont
11 rP cerebral amyloid angiopathy (PrP-CAA) and Gerstmann-Straussler-Scheinker (GSS) syndrome.
12 sporadic Creutzfeldt-Jakob disease (CJD) and Gerstmann-Straussler-Scheinker F198S disease brains all
13 disease, Creutzfeldt-Jakob disease (CJD) and Gerstmann-Straussler-Scheinker syndrome have been attrib
14 seases such as Creutzfeldt-Jakob disease and Gerstmann-Straussler-Scheinker syndrome.
15 enetic Creutzfeldt-Jakob disease (gCJD), and Gerstmann-Straussler-Scheinker (GSS) syndrome are neurod
16 akob disease and related conditions, such as Gerstmann-Straussler-Scheinker disease.
17  have been identified: prion mutations cause Gerstmann Straussler syndrome and hereditary Creuzfeldt-
18 tions create anchorless molecules that cause Gerstmann-Straussler-Scheinker (GSS) disease.
19 on disease, Creutzfeldt-Jakob disease (CJD), Gerstmann-Straussler-Scheinker syndrome, and fatal famil
20 onally have been classified as familial CJD, Gerstmann-Straussler-Scheinker syndrome, or fatal famili
21 nd a low sensitivity limited to variant CJD, Gerstmann-Straussler-Scheinker syndrome and fatal famili
22            While many present with classical Gerstmann-Straussler-Scheinker syndrome, a slowly progre
23 ssociated with neuropathologically confirmed Gerstmann-Straussler-Scheinker disease displaying a some
24                    The genetic prion disease Gerstmann-Straussler-Scheinker syndrome can arise from p
25 ly distinct forms of familial prion disease (Gerstmann-Straussler-Scheinker P102L).
26 hat include Kuru, Creutzfeldt-Jakob disease, Gerstmann-Straussler-Scheinker syndrome (GSS), and fatal
27  in genetic Creutzfeldt-Jakob disease-E200K, Gerstmann-Straussler-Scheinker-P102L and fatal familial
28  (Phe(198) --> Ser) associated with familial Gerstmann-Straussler-Scheinker disease.
29  inherited prion disease P102L, historically Gerstmann-Straussler-Scheinker syndrome, originates from
30 y exhibit several hallmark features of human Gerstmann-Straussler-Scheinker (GSS) syndrome.
31 on, sensory symptoms and loss of reflexes in Gerstmann-Straussler-Scheinker syndrome can be explained
32  symptoms and loss of lower limb reflexes in Gerstmann-Straussler-Scheinker syndrome is due to pathol
33 sing inherited prion disease (IPD) including Gerstmann-Straussler-Scheinker (GSS) disease phenotypes
34 n presentation of inherited prion disease is Gerstmann-Straussler-Scheinker syndrome, typically prese
35                 Our Tg(PrP-A116V) mice model Gerstmann-Straussler-Scheinker disease (GSS), a genetic
36 nt of an inherited human prion disease named Gerstmann-Straussler-Scheinker syndrome.
37 cular-neuropathological profile of a case of Gerstmann-Straussler-Scheinker disease associated with a
38  asymptomatic woman with a family history of Gerstmann-Straussler-Sheinker syndrome (GSS).
39                 We developed a cell model of Gerstmann-Straussler-Scheinker disease, a neurodegenerat
40 histologic changes that are pathognomonic of Gerstmann-Straussler-Scheinker disease.
41 (specifically mutated PrP(A116V)) plaques of Gerstmann-Straussler-Scheinker disease (GSS) and compare
42 seases, and perhaps more akin to subtypes of Gerstmann-Straussler-Scheinker disease.
43 tients with various mutations causing CJD or Gerstmann-Straussler-Scheinker syndrome, 6 had positive
44                                     Shorter, Gerstmann-Straussler-Scheinker-like PrP(res) fragments a
45 with an inherited prion disease [also termed Gerstmann-Straussler-Scheinker (GSS) syndrome] with unus
46  to noncyclic aliphatic residues such as the Gerstmann-Straussler-Scheinker-linked leucines can promo
47 re model and in the human brain carrying the Gerstmann-Straussler-Scheinker disease Q217R mutation.
48 eposits and neuronal loss, by expressing the Gerstmann-Straussler-Scheinker haplotype Q217R-129V in h
49 -state folding behavior was observed for the Gerstmann-Straussler-Scheinker disease-associated F198S
50 ude the hydrophobic domain implicated in the Gerstmann-Straussler-Scheinker (GSS) mutation (P102L).
51     The clinicopathological phenotype of the Gerstmann-Straussler-Scheinker disease (GSS) variant lin
52 102 (P102L), classically associated with the Gerstmann-Straussler-Scheinker (GSS) phenotype, also sho
53  containing point mutations corresponding to Gerstmann-Straussler-Scheinker disease (P102L), Creutzfe
54 genic (Tg) mice overexpressing PrP linked to Gerstmann-Straussler Scheinker syndrome, and the failure
55 P102L in the human PrP gene, associated with Gerstmann-Straussler syndrome (GSS), has been introduced
56 y was observed for mutations associated with Gerstmann-Straussler-Scheinker syndrome and fatal famili
57 pathogenic mutation A116V is associated with Gerstmann-Straussler-Scheinker syndrome, but no accumula