Beta-Amyloid (Aβ
Alzheimer’s disease
GABA
KCC2
NKCC1
beta amyloid
bumetanide
Journal
Molecules (Basel, Switzerland)
ISSN: 1420-3049
Titre abrégé: Molecules
Pays: Switzerland
ID NLM: 100964009
Informations de publication
Date de publication:
10 Apr 2022
10 Apr 2022
Historique:
received:
10
02
2022
revised:
22
03
2022
accepted:
06
04
2022
entrez:
23
4
2022
pubmed:
24
4
2022
medline:
27
4
2022
Statut:
epublish
Résumé
Alzheimer's disease (AD) is a neurodegenerative disorder with an increasing need for developing disease-modifying treatments as current therapies only provide marginal symptomatic relief. Recent evidence suggests the γ-aminobutyric acid (GABA) neurotransmitter system undergoes remodeling in AD, disrupting the excitatory/inhibitory (E/I) balance in the brain. Altered expression levels of K-Cl-2 (KCC2) and N-K-Cl-1 (NKCC1), which are cation-chloride cotransporters (CCCs), have been implicated in disrupting GABAergic activity by regulating GABA
Identifiants
pubmed: 35458638
pii: molecules27082440
doi: 10.3390/molecules27082440
pmc: PMC9027496
pii:
doi:
Substances chimiques
Amyloid beta-Peptides
0
Chlorides
0
Peptide Fragments
0
Slc12a2 protein, mouse
0
Solute Carrier Family 12, Member 2
0
Symporters
0
amyloid beta-protein (1-42)
0
Bumetanide
0Y2S3XUQ5H
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : Alzheimers New Zealand
ID : 3718869
Organisme : Freemasons New Zealand
ID : 3719321
Organisme : Alzheimers New Zealand Charitable Trust
ID : 3720863
Organisme : Health Research Council of New Zealand
ID : 3627373
Organisme : Neurological Foundation of New Zealand
ID : 3723991
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