Amyloid-β
Health sciences
Molecular neuroscience
Neuroscience
Pathophysiology
Journal
iScience
ISSN: 2589-0042
Titre abrégé: iScience
Pays: United States
ID NLM: 101724038
Informations de publication
Date de publication:
15 Dec 2023
15 Dec 2023
Historique:
received:
16
05
2023
revised:
13
09
2023
accepted:
03
11
2023
medline:
6
12
2023
pubmed:
6
12
2023
entrez:
6
12
2023
Statut:
epublish
Résumé
Synaptic weakening and loss are well-correlated with the pathology of Alzheimer's disease (AD). Oligomeric amyloid beta (oAβ) is considered a major synaptotoxic trigger for AD. Recent studies have implicated hyperactivation of the complement cascade as the driving force for loss of synapses caused by oAβ. However, the initial synaptic cues that trigger pathological complement activity remain elusive. Here, we examined a form of synaptic long-term depression (LTD) mediated by metabotropic glutamate receptors (mGluRs) that is disrupted in rodent models of AD. Exogenous application of oAβ (1-42) to mouse hippocampal slices enhanced the magnitude of mGlu subtype 5 receptor (mGlu
Identifiants
pubmed: 38053635
doi: 10.1016/j.isci.2023.108412
pii: S2589-0042(23)02489-6
pmc: PMC10694656
doi:
Types de publication
Journal Article
Langues
eng
Pagination
108412Informations de copyright
© 2023 The Authors.
Déclaration de conflit d'intérêts
The authors declare no competing interests.
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