Cargando…
In situ fibrillizing amyloid-beta 1-42 induces neurite degeneration and apoptosis of differentiated SH-SY5Y cells
The progression of Alzheimer’s disease is causatively linked to the accumulation of amyloid-β aggregates in the brain, however, it is not clear how the amyloid aggregates initiate the death of neuronal cells. The in vitro toxic effects of amyloid peptides are most commonly examined using the human n...
Autores principales: | Krishtal, Jekaterina, Bragina, Olga, Metsla, Kristel, Palumaa, Peep, Tõugu, Vello |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Public Library of Science
2017
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5655426/ https://www.ncbi.nlm.nih.gov/pubmed/29065138 http://dx.doi.org/10.1371/journal.pone.0186636 |
Ejemplares similares
-
Toxicity of amyloid beta 1-40 and 1-42 on SH-SY5Y cell line
por: Krishtal, Jekaterina, et al.
Publicado: (2015) -
Copper(II) partially protects three histidine residues and the N‐terminus of amyloid‐β peptide from diethyl pyrocarbonate (DEPC) modification
por: Friedemann, Merlin, et al.
Publicado: (2020) -
Effect of methionine-35 oxidation on the aggregation of amyloid-β peptide
por: Friedemann, Merlin, et al.
Publicado: (2015) -
Oxidation of Methionine-35 in Alzheimer’s amyloid-beta peptide and the aggregation of the oxidized peptide
por: Friedemann, Merlin, et al.
Publicado: (2015) -
Copper(I)-binding properties of de-coppering drugs for the treatment of Wilson disease. α-Lipoic acid as a potential anti-copper agent
por: Smirnova, Julia, et al.
Publicado: (2018)