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1 hese conditions, Abeta42 was aggregated, but nonfibrillar.
2 copy and dynamic light scattering identified nonfibrillar ~20-nm oligomers, while at high concentrati
3  the relative contributions of fibrillar and nonfibrillar AB components to the in vivo AB PET signal
4               Results: Neither fibrillar nor nonfibrillar AB content alone sufficed to explain the AB
5 - and genotype-matched sets of fibrillar and nonfibrillar AB data (predictors) and AB PET results (ou
6  derives from the composite of fibrillar and nonfibrillar AB plaque components.
7 PET tracer binding, the greater abundance of nonfibrillar AB plaque in AD-model mice contributes impo
8 undance of nonfibrillar AB, we estimate that nonfibrillar AB produced 79% 25% of the net in vivo AB P
9 , a regression model compiling fibrillar and nonfibrillar AB together with the estimate of individual
10 r, given the relatively greater abundance of nonfibrillar AB, we estimate that nonfibrillar AB produc
11 igher contribution to the AB PET signal than nonfibrillar AB.
12                           Both fibrillar and nonfibrillar Abeta (diffuse) deposits were visible in th
13 duce Abeta fibrils at the cost of augmenting nonfibrillar Abeta assemblies could be harmful.
14 ibrillization but decreased the abundance of nonfibrillar Abeta assemblies, compared with wild-type A
15 reduced the relative abundance of a specific nonfibrillar Abeta assembly (Abeta*56).
16  the relative contributions of fibrillar and nonfibrillar Abeta components to the in vivo Abeta PET s
17               Results: Neither fibrillar nor nonfibrillar Abeta content alone sufficed to explain the
18 - and genotype-matched sets of fibrillar and nonfibrillar Abeta data (predictors) and Abeta PET resul
19        Also, at 3 months of age, we observed nonfibrillar Abeta deposition within the olfactory bulb-
20 sities were absent in areas where there were nonfibrillar Abeta deposits.
21 ent with distinct localization, and identify nonfibrillar Abeta oligomer-positive aggregates as track
22 ansgenic mouse models suggests that soluble, nonfibrillar Abeta oligomers may induce synaptic failure
23          Dot blot analysis demonstrated that nonfibrillar Abeta oligomers were highly soluble and ext
24  derives from the composite of fibrillar and nonfibrillar Abeta plaque components.
25 PET tracer binding, the greater abundance of nonfibrillar Abeta plaque in AD-model mice contributes i
26 ance of nonfibrillar Abeta, we estimate that nonfibrillar Abeta produced 79% +/- 25% of the net in vi
27 , a regression model compiling fibrillar and nonfibrillar Abeta together with the estimate of individ
28 r, given the relatively greater abundance of nonfibrillar Abeta, we estimate that nonfibrillar Abeta
29 er contribution to the Abeta PET signal than nonfibrillar Abeta.
30 operties: heparin binds to fibrillar but not nonfibrillar Abeta.
31 er of Abeta, and mediates cell attachment to nonfibrillar Abeta.
32                                 Globular and nonfibrillar AbetaPs are continuously released during no
33                                 Globular and nonfibrillar AbetaPs are continuously released during no
34                                 Globular and nonfibrillar AbetaPs are released continually during nor
35                                      Soluble nonfibrillar ABri oligomers were observed prior to the a
36  B-sheet nanofibers and one forming a stable nonfibrillar aggregate.
37 the formation pathways of beta-oligomers and nonfibrillar aggregates from wild-type full-length recom
38 creases the overall solubility, destabilizes nonfibrillar aggregates, and accelerates fibril formatio
39 the amyloid peptide, possibly in the form of nonfibrillar aggregates, could play a central role.
40 of two proline residues resulted in soluble, nonfibrillar aggregates, which did not mature into insol
41 beta fibrils and induces the accumulation of nonfibrillar aggregates.
42 -crystallin also prevented the unfolding and nonfibrillar aggregation of R3Abeta2m.
43 rkinsonian movement disorder concurrent with nonfibrillar alpha-synuclein inclusions and the loss of
44 ween these trends suggested the existence of nonfibrillar alpha-synuclein oligomers, some of which we
45 l-specific antibody showed drusen to contain nonfibrillar amyloid structures.
46  the incorporation of soluble PrPC into both nonfibrillar and fibrillar PrP-res deposits in TSE-infec
47 ither fibrillar as in light chain amyloid or nonfibrillar as in light chain deposition disease.
48                                          The nonfibrillar beta-sheet region is at intermediate temper
49 r beta-sheets, random coils/fibrils, fibrils/nonfibrillar beta-sheets, and alpha-helices/nonfibrillar
50 ingle-phase regions: alpha-helices, fibrils, nonfibrillar beta-sheets, and random coils; and four two
51 ls; and four two-phase regions: random coils/nonfibrillar beta-sheets, random coils/fibrils, fibrils/
52 /nonfibrillar beta-sheets, and alpha-helices/nonfibrillar beta-sheets.
53 isassembly, resulting in a variable shell of nonfibrillar, but still immobile, aggregates at the surf
54                        Type VI collagen is a nonfibrillar collagen expressed in many connective tissu
55            To date, a specific role for this nonfibrillar collagen has not been explored in the setti
56  neurons, but show for the first time that a nonfibrillar collagen is necessary for the formation of
57                       Collagen Q (ColQ) is a nonfibrillar collagen that plays a crucial role at the v
58 ional program that includes a subunit of the nonfibrillar collagen VI.
59 e discovered that col19a1, the gene encoding nonfibrillar collagen XIX, is expressed by subsets of hi
60  residue in the amino acid sequence, yet all nonfibrillar collagens contain sites where this repeatin
61         We previously discovered a family of nonfibrillar collagens that organize synaptic differenti
62 ructural ECM proteins (such as fibrillar and nonfibrillar collagens), and specialized injury-associat
63         NE can digest elastin, fibrillar and nonfibrillar collagens, and other ECM components in addi
64 with the high thermal stability reported for nonfibrillar collagens.
65 hortly after the divergence of fibrillar and nonfibrillar collagens.
66                                Fibrillar and nonfibrillar components of ECM can limit and facilitate
67 nontoxic if they are washed free of adsorbed nonfibrillar components.
68 rmation but ultimately appeared to stabilize nonfibrillar conformations, including oligomer-like asse
69                              In contrast, on nonfibrillar (denatured) collagen, the cells enter the c
70                                              Nonfibrillar deposits were mainly composed of intact ADa
71 selective NSAID were restricted primarily to nonfibrillar deposits.
72 inflammatory events are not prevalent in the nonfibrillar "diffuse" plaques often seen in age-matched
73 can, a small leucine-rich proteoglycan, is a nonfibrillar extracellular matrix component with functio
74 ulation, there are also alterations in other nonfibrillar extracellular matrix components, such as fi
75       Results suggest that accumulation of a nonfibrillar form of mutant htt in the cytoplasm contrib
76 ssion promoted the appearance of this novel, nonfibrillar form of the prion aggregate.
77 fibrillin into the extracellular matrix in a nonfibrillar form.
78 t react with these molecules in their native nonfibrillar forms.
79 her PN-2/AbetaPP nor its KPI domain bound to nonfibrillar HCHWA-D Abeta.
80 These studies describe a unique mechanism of nonfibrillar homogeneous self-assembly and suggest a gen
81 7 and C38 act synergistically to destabilize nonfibrillar intermediates (N17 effect) and lower the dr
82 ibrillizes without an appreciable buildup of nonfibrillar intermediates, in contrast to the well-stud
83 ccelerates fibril formation and destabilizes nonfibrillar intermediates.
84 on, we are able to show that EGCG stabilizes nonfibrillar large aggregates during fibrillogenesis.
85  charged membranes, and show that binding of nonfibrillar, low molecular mass oligomers of Abeta40 to
86 mino acid sequence analysis of the extracted nonfibrillar MCM kappa-light chain reveals that it belon
87 I to XIX represent the structurally diverse, nonfibrillar members.
88  monomers and nontoxic soluble assemblies of nonfibrillar morphology.
89  expressing either nonamyloidogenic mIAPP or nonfibrillar mutant hIAPP.
90 ause systemic amyloidosis always contain the nonfibrillar normal plasma protein, serum amyloid P comp
91            Amyloid fibril formation involves nonfibrillar oligomeric intermediates, which are importa
92 e demonstrate both in vitro and in vivo that nonfibrillar, oligomeric forms of Abeta are able to inte
93                                The resulting nonfibrillar oligomers displayed significantly reduced b
94  two steps (step one being the appearance of nonfibrillar oligomers in the solution and step two bein
95 In this study, we tested the hypothesis that nonfibrillar oligomers may be a common link in amyloid d
96 s been hypothesized that the accumulation of nonfibrillar oligomers of alpha-synuclein, which serve a
97                              The presence of nonfibrillar oligomers was verified using the M204 antib
98 gation; and a reversible off-pathway to form nonfibrillar oligomers, unreactive to ThT and too large
99  appears to be correlated with the amount of nonfibrillar oligomers.
100  M204, a monoclonal antibody that recognizes nonfibrillar oligomers; OC, a polyclonal antibody that r
101 TR sensitizes human neurons to extracellular nonfibrillar or fibrillar Abeta1-42 cytotoxicity.
102       In addition, antibodies raised to four nonfibrillar peptides corresponding to internal Abeta se
103 in parenchyma accumulates numerous, diffuse, nonfibrillar plaques, whereas the thalamic microvessels
104  fibrillization leads to the accumulation of nonfibrillar, potentially toxic oligomers.
105 o in the turn, formed only a small amount of nonfibrillar precipitate after prolonged incubation.
106 gregation of polyQ molecules at the level of nonfibrillar species, acting as a cap that destabilizes
107  formation of heterogeneous distributions of nonfibrillar species.
108 k dysfunction, suggesting the involvement of nonfibrillar species.
109 lar endothelial and smooth muscle cells with nonfibrillar structures of both variants and wild-type A
110 g plaques are only of the diffuse type, with nonfibrillar, thioflavin S-, and Congo red-negative amyl
111 antibody, we came to observe the presence of nonfibrillar, toxic oligomers in drusen.
112                    Moreover, when preventing nonfibrillar transthyretin deposition with anakinra or t
113 e amyloid are Congo red-negative and largely nonfibrillar ultrastructurally.
114                                   Therefore, nonfibrillar, versus fibrillar, Abeta-related mechanisms

 
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