Overexpression of wild-type human amyloid precursor protein alters GABAergic transmission.
Journal
Scientific reports
ISSN: 2045-2322
Titre abrégé: Sci Rep
Pays: England
ID NLM: 101563288
Informations de publication
Date de publication:
02 09 2021
02 09 2021
Historique:
received:
05
05
2021
accepted:
13
08
2021
entrez:
3
9
2021
pubmed:
4
9
2021
medline:
16
11
2021
Statut:
epublish
Résumé
The function of the amyloid precursor protein (APP) is not fully understood, but its cleavage product amyloid beta (Aβ) together with neurofibrillary tangles constitute the hallmarks of Alzheimer's disease (AD). Yet, imbalance of excitatory and inhibitory neurotransmission accompanied by loss of synaptic functions, has been reported much earlier and independent of any detectable pathological markers. Recently, soluble APP fragments have been shown to bind to presynaptic GABA
Identifiants
pubmed: 34475508
doi: 10.1038/s41598-021-97144-3
pii: 10.1038/s41598-021-97144-3
pmc: PMC8413381
doi:
Substances chimiques
APP protein, human
0
Amyloid beta-Protein Precursor
0
Receptors, Glutamate
0
gamma-Aminobutyric Acid
56-12-2
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
17600Informations de copyright
© 2021. The Author(s).
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