Purpurin modulates Tau-derived VQIVYK fibrillization and ameliorates Alzheimer's disease-like symptoms in animal model.
Alzheimer Disease
/ drug therapy
Amyloid beta-Peptides
/ drug effects
Animals
Animals, Genetically Modified
/ genetics
Anthraquinones
/ pharmacology
Blood-Brain Barrier
/ drug effects
Disease Models, Animal
Drosophila melanogaster
/ genetics
Humans
Hydrophobic and Hydrophilic Interactions
Oligopeptides
/ genetics
Peptide Fragments
/ antagonists & inhibitors
Phosphorylation
/ drug effects
Protein Aggregates
/ drug effects
Protein Conformation, beta-Strand
/ drug effects
Repressor Proteins
/ antagonists & inhibitors
tau Proteins
/ genetics
Aggregation
Amyloid
Inhibitor
PHF6 peptide
Purpurin
Tau protein
Journal
Cellular and molecular life sciences : CMLS
ISSN: 1420-9071
Titre abrégé: Cell Mol Life Sci
Pays: Switzerland
ID NLM: 9705402
Informations de publication
Date de publication:
Jul 2020
Jul 2020
Historique:
received:
10
03
2019
accepted:
19
09
2019
revised:
11
08
2019
pubmed:
29
9
2019
medline:
11
7
2020
entrez:
29
9
2019
Statut:
ppublish
Résumé
Neurofibrillary tangles of the Tau protein and plaques of the amyloid β peptide are hallmarks of Alzheimer's disease (AD), which is characterized by the conversion of monomeric proteins/peptides into misfolded β-sheet rich fibrils. Halting the fibrillation process and disrupting the existing aggregates are key challenges for AD drug development. Previously, we performed in vitro high-throughput screening for the identification of potent inhibitors of Tau aggregation using a proxy model, a highly aggregation-prone hexapeptide fragment
Identifiants
pubmed: 31562564
doi: 10.1007/s00018-019-03312-0
pii: 10.1007/s00018-019-03312-0
doi:
Substances chimiques
Amyloid beta-Peptides
0
Anthraquinones
0
Oligopeptides
0
Peptide Fragments
0
Protein Aggregates
0
Repressor Proteins
0
tau Proteins
0
tau hexapeptide PHF6
0
purpurin anthraquinone
L1GT81LS6N
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM