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1 xpressing PrP linked to Gerstmann-Straussler Scheinker syndrome, and the failure of gene-targeted mic
2                         Gerstmann-Straussler-Scheinker (GSS) disease is a dominantly inherited, human
3 disease (IPD) including Gerstmann-Straussler-Scheinker (GSS) disease phenotypes in humans.
4 ss molecules that cause Gerstmann-Straussler-Scheinker (GSS) disease.
5 omain implicated in the Gerstmann-Straussler-Scheinker (GSS) mutation (P102L).
6 lly associated with the Gerstmann-Straussler-Scheinker (GSS) phenotype, also shows marked clinical an
7 kob disease (gCJD), and Gerstmann-Straussler-Scheinker (GSS) syndrome are neurodegenerative disorders
8 ngiopathy (PrP-CAA) and Gerstmann-Straussler-Scheinker (GSS) syndrome.
9 lmark features of human Gerstmann-Straussler-Scheinker (GSS) syndrome.
10 on disease [also termed Gerstmann-Straussler-Scheinker (GSS) syndrome] with unusual features such as
11  PrP(A116V)) plaques of Gerstmann-Straussler-Scheinker disease (GSS) and compared plaque-related feat
12                         Gerstmann-Straussler-Scheinker disease (GSS) is an inherited neurodegenerativ
13                         Gerstmann-Straussler-Scheinker disease (GSS) is characterized by the accumula
14 ogical phenotype of the Gerstmann-Straussler-Scheinker disease (GSS) variant linked to the codon 102
15 g(PrP-A116V) mice model Gerstmann-Straussler-Scheinker disease (GSS), a genetic prion disease charact
16 ations corresponding to Gerstmann-Straussler-Scheinker disease (P102L), Creutzfeld-Jakob disease (E20
17 al profile of a case of Gerstmann-Straussler-Scheinker disease associated with a novel prion protein
18 athologically confirmed Gerstmann-Straussler-Scheinker disease displaying a somewhat unusual constell
19 uman brain carrying the Gerstmann-Straussler-Scheinker disease Q217R mutation.
20               Whereas a Gerstmann-Straussler-Scheinker disease version of PrP with eight extra octare
21 veloped a cell model of Gerstmann-Straussler-Scheinker disease, a neurodegenerative condition charact
22 or was observed for the Gerstmann-Straussler-Scheinker disease-associated F198S mutant, in which case
23 ore akin to subtypes of Gerstmann-Straussler-Scheinker disease.
24 ted conditions, such as Gerstmann-Straussler-Scheinker disease.
25 ssociated with familial Gerstmann-Straussler-Scheinker disease.
26 at are pathognomonic of Gerstmann-Straussler-Scheinker disease.
27 Jakob disease (CJD) and Gerstmann-Straussler-Scheinker F198S disease brains all have an intact C1 cle
28 loss, by expressing the Gerstmann-Straussler-Scheinker haplotype Q217R-129V in human neuroblastoma ce
29          Importantly, a Gerstmann-Straussler-Scheinker mutation carrier in the asymptomatic phase and
30 familial prion disease (Gerstmann-Straussler-Scheinker P102L).
31                         Gerstmann-Straussler-Scheinker syndrome (GSS) is a genetic prion disease typi
32                         Gerstmann-Straussler-Scheinker syndrome (GSS) with the P102L mutation is a ra
33 l insomnia (FFI) n = 9, Gerstmann-Straussler-Scheinker syndrome (GSS)) n = 4), patients with Alzheime
34 utzfeldt-Jakob disease, Gerstmann-Straussler-Scheinker syndrome (GSS), and fatal familial insomnia.
35 tations associated with Gerstmann-Straussler-Scheinker syndrome and fatal familial insomnia.
36 limited to variant CJD, Gerstmann-Straussler-Scheinker syndrome and fatal familial insomnia.
37 e genetic prion disease Gerstmann-Straussler-Scheinker syndrome can arise from point mutations of pro
38 and loss of reflexes in Gerstmann-Straussler-Scheinker syndrome can be explained by neuropathological
39 Jakob disease (CJD) and Gerstmann-Straussler-Scheinker syndrome have been attributed to particular in
40  lower limb reflexes in Gerstmann-Straussler-Scheinker syndrome is due to pathology in the caudal spi
41 utations causing CJD or Gerstmann-Straussler-Scheinker syndrome, 6 had positive and 2 had negative RT
42  present with classical Gerstmann-Straussler-Scheinker syndrome, a slowly progressive cerebellar atax
43 dt-Jakob disease (CJD), Gerstmann-Straussler-Scheinker syndrome, and fatal familial insomnia (FFI) wh
44 116V is associated with Gerstmann-Straussler-Scheinker syndrome, but no accumulation of PrP(Sc) is de
45 sified as familial CJD, Gerstmann-Straussler-Scheinker syndrome, or fatal familial insomnia.
46 ase P102L, historically Gerstmann-Straussler-Scheinker syndrome, originates from central England, wit
47 erited prion disease is Gerstmann-Straussler-Scheinker syndrome, typically presenting with gait ataxi
48 feldt-Jakob disease and Gerstmann-Straussler-Scheinker syndrome.
49 man prion disease named Gerstmann-Straussler-Scheinker syndrome.
50 s mutation results in a Gerstmann-Straussler-Scheinker-like disease with extensive PrP amyloid deposi
51 riant associated with a Gerstmann-Straussler-Scheinker-like prion disease) spontaneously forms amyloi
52                Shorter, Gerstmann-Straussler-Scheinker-like PrP(res) fragments are also present.
53 ic residues such as the Gerstmann-Straussler-Scheinker-linked leucines can promote the in vitro forma
54 dt-Jakob disease-E200K, Gerstmann-Straussler-Scheinker-P102L and fatal familial insomnia was highly d