在Crouzon综合征小鼠模型中,大脑中FGFR3过度激活是导致记忆障碍的原因

Maxence Cornille, Stéphanie Moriceau, R. Khonsari, Y. Heuzé, L. Loisay, Valérie Boitez, A. Morice, Éric Arnaud, C. Collet, M. Bensidhoum, N. Kaci, N. Boddaert, G. Paternoster, T. Rauschendorfer, Sabine Werner, S. Mansour, F. Di Rocco, F. Oury, L. Legeai-Mallet
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引用次数: 1

摘要

FGFR3功能获得突变可独立于颅骨异常导致学习和记忆障碍。Cornille等人认为FGFR3信号通路的调节可能对治疗颅缝闭闭中观察到的神经和认知障碍有价值。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
FGFR3 overactivation in the brain is responsible for memory impairments in Crouzon syndrome mouse model
FGFR3 gain-of-function mutation leads to learning and memory impairments independently of skull abnormalities. Cornille et al. suggest that modulation of the FGFR3 signaling pathway might be of value for treating the neurological and cognitive impairments observed in craniosynostosis.
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