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1 identified: prion mutations cause Gerstmann Straussler syndrome and hereditary Creuzfeldt-Jakob dise
6 tal familial insomnia (FFI) n = 9, Gerstmann-Straussler-Scheinker syndrome (GSS)) n = 4), patients wi
10 Stop PrP variant associated with a Gerstmann-Straussler-Scheinker-like prion disease) spontaneously f
12 reutzfeldt-Jakob disease (CJD) and Gerstmann-Straussler-Scheinker F198S disease brains all have an in
13 reutzfeldt-Jakob disease (CJD) and Gerstmann-Straussler-Scheinker syndrome have been attributed to pa
17 , Creutzfeldt-Jakob disease (CJD), Gerstmann-Straussler-Scheinker syndrome, and fatal familial insomn
18 ensitivity limited to variant CJD, Gerstmann-Straussler-Scheinker syndrome and fatal familial insomni
19 e been classified as familial CJD, Gerstmann-Straussler-Scheinker syndrome, or fatal familial insomni
20 While many present with classical Gerstmann-Straussler-Scheinker syndrome, a slowly progressive cere
21 with neuropathologically confirmed Gerstmann-Straussler-Scheinker disease displaying a somewhat unusu
24 e Kuru, Creutzfeldt-Jakob disease, Gerstmann-Straussler-Scheinker syndrome (GSS), and fatal familial
26 prion disease P102L, historically Gerstmann-Straussler-Scheinker syndrome, originates from central E
30 opathological profile of a case of Gerstmann-Straussler-Scheinker disease associated with a novel pri
35 h various mutations causing CJD or Gerstmann-Straussler-Scheinker syndrome, 6 had positive and 2 had
37 herited prion disease [also termed Gerstmann-Straussler-Scheinker (GSS) syndrome] with unusual featur
39 ), classically associated with the Gerstmann-Straussler-Scheinker (GSS) phenotype, also shows marked
40 inicopathological phenotype of the Gerstmann-Straussler-Scheinker disease (GSS) variant linked to the
42 ding behavior was observed for the Gerstmann-Straussler-Scheinker disease-associated F198S mutant, in
43 d neuronal loss, by expressing the Gerstmann-Straussler-Scheinker haplotype Q217R-129V in human neuro
44 lic aliphatic residues such as the Gerstmann-Straussler-Scheinker-linked leucines can promote the in
45 mice overexpressing PrP linked to Gerstmann-Straussler Scheinker syndrome, and the failure of gene-t
46 g point mutations corresponding to Gerstmann-Straussler-Scheinker disease (P102L), Creutzfeld-Jakob d
47 he human PrP gene, associated with Gerstmann-Straussler syndrome (GSS), has been introduced into the
48 mutation A116V is associated with Gerstmann-Straussler-Scheinker syndrome, but no accumulation of Pr
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