Pyk2 overexpression in postsynaptic neurons blocks amyloid β
Alzheimer’s disease
amyloid β
co-culture
microfluidics
synapses
Journal
Brain communications
ISSN: 2632-1297
Titre abrégé: Brain Commun
Pays: England
ID NLM: 101755125
Informations de publication
Date de publication:
2020
2020
Historique:
received:
16
04
2020
revised:
12
07
2020
accepted:
03
08
2020
entrez:
15
3
2021
pubmed:
16
3
2021
medline:
16
3
2021
Statut:
epublish
Résumé
Recent meta-analyses of genome-wide association studies identified a number of genetic risk factors of Alzheimer's disease; however, little is known about the mechanisms by which they contribute to the pathological process. As synapse loss is observed at the earliest stage of Alzheimer's disease, deciphering the impact of Alzheimer's risk genes on synapse formation and maintenance is of great interest. In this article, we report a microfluidic co-culture device that physically isolates synapses from pre- and postsynaptic neurons and chronically exposes them to toxic amyloid β peptides secreted by model cell lines overexpressing wild-type or mutated (V717I) amyloid precursor protein. Co-culture with cells overexpressing mutated amyloid precursor protein exposed the synapses of primary hippocampal neurons to amyloid β
Identifiants
pubmed: 33718872
doi: 10.1093/braincomms/fcaa139
pii: fcaa139
pmc: PMC7941669
doi:
Types de publication
Journal Article
Langues
eng
Pagination
fcaa139Informations de copyright
© The Author(s) (2020). Published by Oxford University Press on behalf of the Guarantors of Brain.
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