Muscle specific kinase (MuSK) activation preserves neuromuscular junctions in the diaphragm but is not sufficient to provide a functional benefit in the SOD1G93A mouse model of ALS

Muscle specific kinase (MuSK) activation preserves neuromuscular junctions in the diaphragm but is not sufficient to provide a functional benefit in the SOD1G93A mouse model of ALS

Amyotrophic lateral sclerosis (ALS), a neurodegenerative disease affecting motor neurons, is characterized by rapid decline of motor function and ultimately respiratory failure. As motor neuron death occurs late in the disease, therapeutics that prevent the initial disassembly of the neuromuscular j...

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Bibliographic Details
Main Authors: Arundhati Sengupta-Ghosh, Sara L. Dominguez, Luke Xie, Kai H. Barck, Zhiyu Jiang, Timothy Earr, Jose Imperio, Lilian Phu, Hanna G. Budayeva, Donald S. Kirkpatrick, Hao Cai, Jeffrey Eastham-Anderson, Hai Ngu, Oded Foreman, Maj Hedehus, Michael Reichelt, Isidro Hotzel, Yonglei Shang, Richard A.D. Carano, Gai Ayalon, Amy Easton
Format: Article
Language:English
Published: Elsevier 2019-04-01
Series:Neurobiology of Disease
Subjects:
SOD1
Amyotrophic lateral sclerosis
Muscle specific kinase (MuSK)
Respiration
Diaphragm
Neuromuscular junction
Online Access:http://www.sciencedirect.com/science/article/pii/S0969996118303978

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http://www.sciencedirect.com/science/article/pii/S0969996118303978

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