P-glycoprotein: a role in the export of amyloid-β in Alzheimer's disease?
ATP Binding Cassette Transporter, Subfamily B
/ genetics
Alzheimer Disease
/ genetics
Amyloid beta-Peptides
/ genetics
Animals
Blood-Brain Barrier
/ metabolism
Brain
/ metabolism
Disease Models, Animal
Gene Expression Regulation
Humans
Neurons
/ metabolism
Peptide Fragments
/ genetics
Presenilin-1
/ genetics
Presenilin-2
/ genetics
Protein Aggregates
Protein Transport
Proteolysis
Signal Transduction
ABCB1
Alzheimer's disease
P-glycoprotein
amyloid beta
blood-brain barrier
Journal
The FEBS journal
ISSN: 1742-4658
Titre abrégé: FEBS J
Pays: England
ID NLM: 101229646
Informations de publication
Date de publication:
02 2020
02 2020
Historique:
received:
24
06
2019
revised:
09
10
2019
accepted:
19
11
2019
pubmed:
22
11
2019
medline:
21
10
2020
entrez:
22
11
2019
Statut:
ppublish
Résumé
The accumulation of amyloid-β (Aβ) peptides is a key histopathological feature of the Alzheimer's brain. Defective clearance mechanisms result in toxic levels of soluble Aβ
Substances chimiques
ABCB1 protein, human
0
ATP Binding Cassette Transporter, Subfamily B
0
Amyloid beta-Peptides
0
PSEN1 protein, human
0
PSEN2 protein, human
0
Peptide Fragments
0
Presenilin-1
0
Presenilin-2
0
Protein Aggregates
0
amyloid beta-protein (1-40)
0
amyloid beta-protein (1-42)
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
612-625Informations de copyright
© 2019 Federation of European Biochemical Societies.
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