Cargando…
N-terminal Domain of Amyloid-β Impacts Fibrillation and Neurotoxicity
[Image: see text] Alzheimer’s disease is characterized by the presence of distinct amyloid-β peptide (Aβ) assemblies with diverse sizes, shapes, and toxicity. However, the primary determinants of Aβ aggregation and neurotoxicity remain unknown. Here, the N-terminal amino acid residues of Aβ42 that d...
Autores principales: | Shi, Jing-Ming, Li, Hai-Yun, Liu, Hang, Zhu, Li, Guo, Yi-Bo, Pei, Jie, An, Hao, Li, Yan-Song, Li, Sha-Di, Zhang, Ze-Yu, Zheng, Yi |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
American Chemical Society
2022
|
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9631750/ https://www.ncbi.nlm.nih.gov/pubmed/36340079 http://dx.doi.org/10.1021/acsomega.2c04583 |
Ejemplares similares
-
An N-terminal antibody promotes the transformation of amyloid fibrils into oligomers and enhances the neurotoxicity of amyloid-beta: the dust-raising effect
por: Liu, Yu-Hui, et al.
Publicado: (2015) -
Alzheimer’s amyloid-β A2T variant and its N-terminal peptides inhibit amyloid-β fibrillization and rescue the induced cytotoxicity
por: Lin, Tien-Wei, et al.
Publicado: (2017) -
An N-terminal Fragment of the Prion Protein Binds to Amyloid-β Oligomers and Inhibits Their Neurotoxicity in Vivo
por: Fluharty, Brian R., et al.
Publicado: (2013) -
Structural conversion of neurotoxic amyloid-β(1–42) oligomers to fibrils
por: Ahmed, Mahiuddin, et al.
Publicado: (2010) -
Chitosan Oligosaccharides Inhibit/Disaggregate Fibrils and Attenuate Amyloid β-Mediated Neurotoxicity
por: Dai, Xueling, et al.
Publicado: (2015)