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1  identified: prion mutations cause Gerstmann Straussler syndrome and hereditary Creuzfeldt-Jakob dise
2                                    Gerstmann-Straussler-Scheinker (GSS) disease is a dominantly inher
3                                    Gerstmann-Straussler-Scheinker disease (GSS) is an inherited neuro
4                                    Gerstmann-Straussler-Scheinker disease (GSS) is characterized by t
5                                    Gerstmann-Straussler-Scheinker syndrome (GSS) is a genetic prion d
6                                    Gerstmann-Straussler-Scheinker syndrome (GSS) with the P102L mutat
7 tal familial insomnia (FFI) n = 9, Gerstmann-Straussler-Scheinker syndrome (GSS)) n = 4), patients wi
8                          Whereas a Gerstmann-Straussler-Scheinker disease version of PrP with eight e
9                     Importantly, a Gerstmann-Straussler-Scheinker mutation carrier in the asymptomati
10         This mutation results in a Gerstmann-Straussler-Scheinker-like disease with extensive PrP amy
11 Stop PrP variant associated with a Gerstmann-Straussler-Scheinker-like prion disease) spontaneously f
12 utzfeldt-Jakob disease (gCJD), and Gerstmann-Straussler-Scheinker (GSS) syndrome are neurodegenerativ
13 l amyloid angiopathy (PrP-CAA) and Gerstmann-Straussler-Scheinker (GSS) syndrome.
14 reutzfeldt-Jakob disease (CJD) and Gerstmann-Straussler-Scheinker F198S disease brains all have an in
15 reutzfeldt-Jakob disease (CJD) and Gerstmann-Straussler-Scheinker syndrome have been attributed to pa
16 h as Creutzfeldt-Jakob disease and Gerstmann-Straussler-Scheinker syndrome.
17 se and related conditions, such as Gerstmann-Straussler-Scheinker disease.
18 te anchorless molecules that cause Gerstmann-Straussler-Scheinker (GSS) disease.
19 , Creutzfeldt-Jakob disease (CJD), Gerstmann-Straussler-Scheinker syndrome, and fatal familial insomn
20 ensitivity limited to variant CJD, Gerstmann-Straussler-Scheinker syndrome and fatal familial insomni
21 e been classified as familial CJD, Gerstmann-Straussler-Scheinker syndrome, or fatal familial insomni
22  While many present with classical Gerstmann-Straussler-Scheinker syndrome, a slowly progressive cere
23 with neuropathologically confirmed Gerstmann-Straussler-Scheinker disease displaying a somewhat unusu
24 t forms of familial prion disease (Gerstmann-Straussler-Scheinker P102L).
25          The genetic prion disease Gerstmann-Straussler-Scheinker syndrome can arise from point mutat
26 e Kuru, Creutzfeldt-Jakob disease, Gerstmann-Straussler-Scheinker syndrome (GSS), and fatal familial
27 c Creutzfeldt-Jakob disease-E200K, Gerstmann-Straussler-Scheinker-P102L and fatal familial insomnia w
28  --> Ser) associated with familial Gerstmann-Straussler-Scheinker disease.
29  prion disease P102L, historically Gerstmann-Straussler-Scheinker syndrome, originates from central E
30 several hallmark features of human Gerstmann-Straussler-Scheinker (GSS) syndrome.
31 y symptoms and loss of reflexes in Gerstmann-Straussler-Scheinker syndrome can be explained by neurop
32 and loss of lower limb reflexes in Gerstmann-Straussler-Scheinker syndrome is due to pathology in the
33 ited prion disease (IPD) including Gerstmann-Straussler-Scheinker (GSS) disease phenotypes in humans.
34 tion of inherited prion disease is Gerstmann-Straussler-Scheinker syndrome, typically presenting with
35       Our Tg(PrP-A116V) mice model Gerstmann-Straussler-Scheinker disease (GSS), a genetic prion dise
36 nherited human prion disease named Gerstmann-Straussler-Scheinker syndrome.
37 lly mutated PrP(A116V)) plaques of Gerstmann-Straussler-Scheinker disease (GSS) and compared plaque-r
38 opathological profile of a case of Gerstmann-Straussler-Scheinker disease associated with a novel pri
39       We developed a cell model of Gerstmann-Straussler-Scheinker disease, a neurodegenerative condit
40 d perhaps more akin to subtypes of Gerstmann-Straussler-Scheinker disease.
41  changes that are pathognomonic of Gerstmann-Straussler-Scheinker disease.
42 tic woman with a family history of Gerstmann-Straussler-Sheinker syndrome (GSS).
43 h various mutations causing CJD or Gerstmann-Straussler-Scheinker syndrome, 6 had positive and 2 had
44                           Shorter, Gerstmann-Straussler-Scheinker-like PrP(res) fragments are also pr
45 herited prion disease [also termed Gerstmann-Straussler-Scheinker (GSS) syndrome] with unusual featur
46 drophobic domain implicated in the Gerstmann-Straussler-Scheinker (GSS) mutation (P102L).
47 ), classically associated with the Gerstmann-Straussler-Scheinker (GSS) phenotype, also shows marked
48 inicopathological phenotype of the Gerstmann-Straussler-Scheinker disease (GSS) variant linked to the
49 nd in the human brain carrying the Gerstmann-Straussler-Scheinker disease Q217R mutation.
50 ding behavior was observed for the Gerstmann-Straussler-Scheinker disease-associated F198S mutant, in
51 d neuronal loss, by expressing the Gerstmann-Straussler-Scheinker haplotype Q217R-129V in human neuro
52 lic aliphatic residues such as the Gerstmann-Straussler-Scheinker-linked leucines can promote the in
53  mice overexpressing PrP linked to Gerstmann-Straussler Scheinker syndrome, and the failure of gene-t
54 g point mutations corresponding to Gerstmann-Straussler-Scheinker disease (P102L), Creutzfeld-Jakob d
55 he human PrP gene, associated with Gerstmann-Straussler syndrome (GSS), has been introduced into the
56 rved for mutations associated with Gerstmann-Straussler-Scheinker syndrome and fatal familial insomni
57  mutation A116V is associated with Gerstmann-Straussler-Scheinker syndrome, but no accumulation of Pr