𝔖 Bobbio Scriptorium
✦   LIBER   ✦

A compensatory subpopulation of motor neurons in a mouse model of amyotrophic lateral sclerosis

✍ Scribed by Anneliese M. Schaefer; Joshua R. Sanes; Jeff W. Lichtman

Publisher
John Wiley and Sons
Year
2005
Tongue
English
Weight
916 KB
Volume
490
Category
Article
ISSN
0021-9967

No coin nor oath required. For personal study only.

πŸ“œ SIMILAR VOLUMES

Progressive motor neuron impairment in a
Progressive motor neuron impairment in an animal model of familial amyotrophic lateral sclerosis
✍ Mimoun Azzouz; Nathalie Leclerc; Mark Gurney; Jean-Marie Warter; Philippe Poindr πŸ“‚ Article πŸ“… 1997 πŸ› John Wiley and Sons 🌐 English βš– 114 KB πŸ‘ 2 views

Mutations of Cu,Zn superoxide dismutase cause an autosomal dominant form of familial amyotrophic lateral sclerosis. An animal model of the disease has been produced by expressing mutant human SOD1 in transgenic mice (G93A). In order to quantify the dysfunction of the motor unit in transgenic mice, e

Regular exercise is beneficial to a mous
Regular exercise is beneficial to a mouse model of amyotrophic lateral sclerosis
✍ Ilias G. Kirkinezos; Dayami Hernandez; Walter G. Bradley; Carlos T. Moraes πŸ“‚ Article πŸ“… 2003 πŸ› John Wiley and Sons 🌐 English βš– 138 KB

## Abstract We tested whether a regular exercise regimen was associated with a change in the life span of G93A‐SOD1 transgenic mice, a model of familial ALS. Regular treadmill running for 10 weeks led to a significant increase in the life span of G93A‐SOD1 mice. The effect was stronger in male mice

Effect of rosmarinic acid in motor dysfu
Effect of rosmarinic acid in motor dysfunction and life span in a mouse model of familial amyotrophic lateral sclerosis
✍ Yosuke Shimojo; Kunio Kosaka; Yoshihiro Noda; Takahiko Shimizu; Takuji Shirasawa πŸ“‚ Article πŸ“… 2009 πŸ› John Wiley and Sons 🌐 English βš– 385 KB

## Abstract Amyotrophic lateral sclerosis (ALS) is a late‐onset progressive neurodegenerative disease affecting motor neurons. About 2% of patients with the disease are associated with mutations in the gene encoding Cu/Zn superoxide dismutase (SOD1). The purpose of this study is to assess the effec