Mice genetically manipulated to lack biglycan exhibit aberrant and unstable neuromuscular junctions (NMJs), the site where the nerve innervates the muscle (Ameye et al., 2002, Amenta et al., 2012). Biglycan is a leucine-rich extracellular matrix protein that is important for synaptic stabilization. At present, we are using biglycan null mice to better characterize the exhibited NMJ instability. Specifically, we are using immunofluorescence to search for denervation at these sites. These experiments are being carried out alongside a study investigating the potential of biglycan to reduce the symptoms of Amyotrophic Lateral Sclerosis (ALS) in a mouse model of ALS. ALS is a neurodegenerative disorder whereby the nerve dies back from the muscle it innervates, causing paralysis and eventual death. We hope that these studies will shed light on the potential of biglycan as a therapy for ALS and other similar disorders.
Slepian, Susannah,
"Characterizing instability of neuromuscular junctions in biglycan null mice"
(2014).
Summer Research Symposium.
Brown Digital Repository. Brown University Library.
https://doi.org/10.26300/73na-8p27
Each year, Brown University showcases the research of its undergraduates at the Summer Research Symposium. More than half of the student-researchers are UTRA recipients, while others receive funding from a variety of Brown-administered and national programs and fellowships and go …
