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Kim, Jae-Ick
Neural Circuit and Neurodegenerative Disease Lab.
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Reelin and APP Cooperatively Modulate Dendritic Spine Formation In Vitro and In Vivo

Author(s)
Lee, Hyun-juPark, Jin-HeeTrotter, Justin H.Maher, James N.Keenoy, Kathleen E.Jang, You MiLee, YoungeunKim, Jae-IckWeeber, Edwin J.Hoe, Hyang-Sook
Issued Date
2023-03
DOI
10.5607/en22044
URI
https://scholarworks.unist.ac.kr/handle/201301/62470
Citation
EXPERIMENTAL NEUROBIOLOGY, v.32, no.1, pp.42 - 55
Abstract
Amyloid precursor protein (APP) plays an important role in the pathogenesis of Alzheimer’s disease (AD), but the normal function of APP at synapses is poorly understood. We and others have found that APP interacts with Reelin and that each protein is individually important for dendritic spine formation, which is associated with learning and memory, in vitro. However, whether Reelin acts through APP to modulate dendritic spine formation or synaptic function remains unknown. In the present study, we found that Reelin treatment significantly increased dendritic spine density and PSD-95 puncta number in primary hippocampal neurons. An examination of the molecular mechanisms by which Reelin regulates dendritic spinogenesis revealed that Reelin enhanced hippocampal dendritic spine formation in a Ras/ERK/CREB signaling-dependent manner. Interestingly, Reelin did not increase dendritic spine number in primary hippocampal neurons when APP expression was reduced or in vivo in APP knockout (KO) mice. Taken together, our data are the first to demonstrate that Reelin acts cooperatively with APP to modulate dendritic spine formation and suggest that normal APP function is critical for Reelin-mediated dendritic spinogenesis at synapses.
Publisher
한국뇌신경과학회
ISSN
1226-2560
Keyword (Author)
APPReelinDendritic spineAlzheimer?s diseaseRas signaling
Keyword
AMYLOID-PRECURSOR-PROTEINSYNAPTIC PLASTICITYCOFILIN PHOSPHORYLATIONMOUSE MODELRECEPTORNMDARASNEURONSENHANCEMENTDISRUPTION

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