ライフサイエンスコーパス: nonfibrillar

1 hese conditions, Abeta42 was aggregated, but nonfibrillar.

2 Both fibrillar and nonfibrillar Abeta (diffuse) deposits were visible in th

3 duce Abeta fibrils at the cost of augmenting nonfibrillar Abeta assemblies could be harmful.

4 ibrillization but decreased the abundance of nonfibrillar Abeta assemblies, compared with wild-type A

5 reduced the relative abundance of a specific nonfibrillar Abeta assembly (Abeta*56).

6 Also, at 3 months of age, we observed nonfibrillar Abeta deposition within the olfactory bulb-

7 sities were absent in areas where there were nonfibrillar Abeta deposits.

8 ent with distinct localization, and identify nonfibrillar Abeta oligomer-positive aggregates as track

9 ansgenic mouse models suggests that soluble, nonfibrillar Abeta oligomers may induce synaptic failure

10 Dot blot analysis demonstrated that nonfibrillar Abeta oligomers were highly soluble and ext

11 operties: heparin binds to fibrillar but not nonfibrillar Abeta.

12 er of Abeta, and mediates cell attachment to nonfibrillar Abeta.

13 Globular and nonfibrillar AbetaPs are continuously released during no

14 Globular and nonfibrillar AbetaPs are continuously released during no

15 Globular and nonfibrillar AbetaPs are released continually during nor

16 Soluble nonfibrillar ABri oligomers were observed prior to the a

17 the formation pathways of beta-oligomers and nonfibrillar aggregates from wild-type full-length recom

18 creases the overall solubility, destabilizes nonfibrillar aggregates, and accelerates fibril formatio

19 the amyloid peptide, possibly in the form of nonfibrillar aggregates, could play a central role.

20 of two proline residues resulted in soluble, nonfibrillar aggregates, which did not mature into insol

21 beta fibrils and induces the accumulation of nonfibrillar aggregates.

22 -crystallin also prevented the unfolding and nonfibrillar aggregation of R3Abeta2m.

23 rkinsonian movement disorder concurrent with nonfibrillar alpha-synuclein inclusions and the loss of

24 ween these trends suggested the existence of nonfibrillar alpha-synuclein oligomers, some of which we

25 l-specific antibody showed drusen to contain nonfibrillar amyloid structures.

26 the incorporation of soluble PrPC into both nonfibrillar and fibrillar PrP-res deposits in TSE-infec

27 ither fibrillar as in light chain amyloid or nonfibrillar as in light chain deposition disease.

28 The nonfibrillar beta-sheet region is at intermediate temper

29 r beta-sheets, random coils/fibrils, fibrils/nonfibrillar beta-sheets, and alpha-helices/nonfibrillar

30 ingle-phase regions: alpha-helices, fibrils, nonfibrillar beta-sheets, and random coils; and four two

31 ls; and four two-phase regions: random coils/nonfibrillar beta-sheets, random coils/fibrils, fibrils/

32 /nonfibrillar beta-sheets, and alpha-helices/nonfibrillar beta-sheets.

33 isassembly, resulting in a variable shell of nonfibrillar, but still immobile, aggregates at the surf

34 Type VI collagen is a nonfibrillar collagen expressed in many connective tissu

35 To date, a specific role for this nonfibrillar collagen has not been explored in the setti

36 neurons, but show for the first time that a nonfibrillar collagen is necessary for the formation of

37 ional program that includes a subunit of the nonfibrillar collagen VI.

38 e discovered that col19a1, the gene encoding nonfibrillar collagen XIX, is expressed by subsets of hi

39 residue in the amino acid sequence, yet all nonfibrillar collagens contain sites where this repeatin

40 We previously discovered a family of nonfibrillar collagens that organize synaptic differenti

41 NE can digest elastin, fibrillar and nonfibrillar collagens, and other ECM components in addi

42 with the high thermal stability reported for nonfibrillar collagens.

43 hortly after the divergence of fibrillar and nonfibrillar collagens.

44 Fibrillar and nonfibrillar components of ECM can limit and facilitate

45 nontoxic if they are washed free of adsorbed nonfibrillar components.

46 rmation but ultimately appeared to stabilize nonfibrillar conformations, including oligomer-like asse

47 In contrast, on nonfibrillar (denatured) collagen, the cells enter the c

48 Nonfibrillar deposits were mainly composed of intact ADa

49 selective NSAID were restricted primarily to nonfibrillar deposits.

50 inflammatory events are not prevalent in the nonfibrillar "diffuse" plaques often seen in age-matched

51 can, a small leucine-rich proteoglycan, is a nonfibrillar extracellular matrix component with functio

52 Results suggest that accumulation of a nonfibrillar form of mutant htt in the cytoplasm contrib

53 ssion promoted the appearance of this novel, nonfibrillar form of the prion aggregate.

54 fibrillin into the extracellular matrix in a nonfibrillar form.

55 t react with these molecules in their native nonfibrillar forms.

56 her PN-2/AbetaPP nor its KPI domain bound to nonfibrillar HCHWA-D Abeta.

57 These studies describe a unique mechanism of nonfibrillar homogeneous self-assembly and suggest a gen

58 7 and C38 act synergistically to destabilize nonfibrillar intermediates (N17 effect) and lower the dr

59 ibrillizes without an appreciable buildup of nonfibrillar intermediates, in contrast to the well-stud

60 ccelerates fibril formation and destabilizes nonfibrillar intermediates.

61 on, we are able to show that EGCG stabilizes nonfibrillar large aggregates during fibrillogenesis.

62 charged membranes, and show that binding of nonfibrillar, low molecular mass oligomers of Abeta40 to

63 mino acid sequence analysis of the extracted nonfibrillar MCM kappa-light chain reveals that it belon

64 I to XIX represent the structurally diverse, nonfibrillar members.

65 monomers and nontoxic soluble assemblies of nonfibrillar morphology.

66 expressing either nonamyloidogenic mIAPP or nonfibrillar mutant hIAPP.

67 ause systemic amyloidosis always contain the nonfibrillar normal plasma protein, serum amyloid P comp

68 Amyloid fibril formation involves nonfibrillar oligomeric intermediates, which are importa

69 e demonstrate both in vitro and in vivo that nonfibrillar, oligomeric forms of Abeta are able to inte

70 The resulting nonfibrillar oligomers displayed significantly reduced b

71 two steps (step one being the appearance of nonfibrillar oligomers in the solution and step two bein

72 In this study, we tested the hypothesis that nonfibrillar oligomers may be a common link in amyloid d

73 s been hypothesized that the accumulation of nonfibrillar oligomers of alpha-synuclein, which serve a

74 The presence of nonfibrillar oligomers was verified using the M204 antib

75 appears to be correlated with the amount of nonfibrillar oligomers.

76 M204, a monoclonal antibody that recognizes nonfibrillar oligomers; OC, a polyclonal antibody that r

77 TR sensitizes human neurons to extracellular nonfibrillar or fibrillar Abeta1-42 cytotoxicity.

78 In addition, antibodies raised to four nonfibrillar peptides corresponding to internal Abeta se

79 in parenchyma accumulates numerous, diffuse, nonfibrillar plaques, whereas the thalamic microvessels

80 fibrillization leads to the accumulation of nonfibrillar, potentially toxic oligomers.

81 o in the turn, formed only a small amount of nonfibrillar precipitate after prolonged incubation.

82 gregation of polyQ molecules at the level of nonfibrillar species, acting as a cap that destabilizes

83 formation of heterogeneous distributions of nonfibrillar species.

84 k dysfunction, suggesting the involvement of nonfibrillar species.

85 lar endothelial and smooth muscle cells with nonfibrillar structures of both variants and wild-type A

86 g plaques are only of the diffuse type, with nonfibrillar, thioflavin S-, and Congo red-negative amyl

87 antibody, we came to observe the presence of nonfibrillar, toxic oligomers in drusen.

88 Moreover, when preventing nonfibrillar transthyretin deposition with anakinra or t

89 e amyloid are Congo red-negative and largely nonfibrillar ultrastructurally.

90 Therefore, nonfibrillar, versus fibrillar, Abeta-related mechanisms