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1 gen occurs in two major forms: fibrillar and non-fibrillar.
2                 Evidence suggests that these non-fibrillar Abeta assemblies are implicated in synapti
3      Our results suggest that the ability of non-fibrillar Abeta oligomers to interact with and disru
4                           This suggests that non-fibrillar Abeta or early stage plaque depostion migh
5 haracterize in postmortem human brain tissue non-fibrillar Abeta structures in amyloid plaques of cas
6 r's plaque peptide Abeta(1-40), as well as a non-fibrillar aggregate induced by Zn(2+).
7 en the autophagy receptor p62/SQSTM1 and the non-fibrillar aggregate surface.
8 on to TMEM106B fibrils, we detected abundant non-fibrillar aggregated TDP-43 by immunogold labelling.
9 f the monomer and the hairpin assembles into non-fibrillar aggregates, demonstrating that the hairpin
10 associate with themselves to form larger but non-fibrillar aggregates.
11 to be the arrest of aggregation in an early, non-fibrillar aggregation stage.
12  but also rescues proteins from irreversible non-fibrillar aggregation.
13           This study suggests that the small non-fibrillar alpha-synuclein aggregates are the critica
14              These data suggest that soluble non-fibrillar amyloid may contribute to the pathogenesis
15       Recently it has been demonstrated that non-fibrillar assemblies of A beta possess electrophysio
16     It is increasingly recognized that small non-fibrillar beta-sheet-rich oligomers of PrP may be of
17            Collagen XV (COLXV) is a secreted non-fibrillar collagen found within basement membrane (B
18 e amino acid sequence of type VI collagen, a non-fibrillar collagen that forms antiparallel dimers.
19 which encodes the alpha chain of an atypical non-fibrillar collagen with a single transmembrane domai
20  that while DDR1b clusters co-localized with non-fibrillar collagen, DDR1b/DDR2 filamentous structure
21                                              Non-fibrillar collagens are structurally more variable a
22 are found in the triple-helix domains of all non-fibrillar collagens, and perturbations to the triple
23 ound normally in the triple helix domains of non-fibrillar collagens, such as type IV collagen in bas
24  in the -Gly-X-Y- repeating pattern found in non-fibrillar collagens.
25 nts may be common aggregation motifs for the non-fibrillar collagens.
26 analyzed alleles of candidate genes encoding non-fibrillar components of TTR amyloid deposits and a m
27 FBD brains has shown the presence of ABri as non-fibrillar deposits as well as amyloid fibrils.
28 y into amyloid structures while MHP1 forms a non-fibrillar film.
29     Growing evidence suggests water-soluble, non-fibrillar forms of amyloid-beta protein (Abeta) have
30        Using immunogold electron microscopy, non-fibrillar forms of PrP(d) were shown to accumulate m
31         Serum amyloid P component (SAP) is a non-fibrillar glycoprotein belonging to the pentraxin fa
32 that the cellular fibrillation also involves non-fibrillar intermediate species, and the microtubule-
33 choring directs the assembly of Sup35NM into non-fibrillar, membrane-bound aggregates that resemble P
34 infected hosts, PrPSc usually accumulates as non-fibrillar, membrane-bound aggregates.
35 uctural analyses indicate that despite their non-fibrillar morphology, the metastable Zn(2+)-Abeta40
36         These findings provide evidence that non-fibrillar oligomeric species are likely to play a cr
37  Moreover, we report the novel findings that non-fibrillar oligomeric species of ABri are more toxic
38 es suggest that increased propensity to form non-fibrillar oligomers is the shared property of these
39               Recent studies have implicated non-fibrillar oligomers of the amyloid beta (Abeta) pept
40 nsists of mineralized collagen fibrils and a non-fibrillar organic matrix, which acts as a 'glue' tha
41                   These results suggest that non-fibrillar particles, with masses equivalent to 14-28
42 are either absent or present only as diffuse non-fibrillar plaques in the brain parenchyma.
43 er, all amyloid deposits contain the normal, non-fibrillar plasma glycoprotein, serum amyloid P compo
44  symmetry, which are efficient inhibitors of non-fibrillar protein aggregation.
45 yloidogenic light chain) and ultrastructural non-fibrillar punctate deposits.
46  partitioning to a faster pathway leading to non-fibrillar self-associated aggregates at higher prote
47                                              Non-fibrillar soluble oligomeric forms of amyloid-beta p
48 s both the small aggregate fractions contain non-fibrillar spherical aggregates with distinct size di
49 he increased size, the protofibrils remained non-fibrillar, suggesting that the deposition of the pro