๐”– Bobbio Scriptorium
โœฆ   LIBER   โœฆ

Hdac6 deletion delays disease progression in the SOD1G93A mouse model of ALS

โœ Scribed by Taes, I.; Timmers, M.; Hersmus, N.; Bento-Abreu, A.; Van Den Bosch, L.; Van Damme, P.; Auwerx, J.; Robberecht, W.


Book ID
121717519
Publisher
Oxford University Press
Year
2013
Tongue
English
Weight
229 KB
Volume
22
Category
Article
ISSN
0964-6906

No coin nor oath required. For personal study only.


๐Ÿ“œ SIMILAR VOLUMES


Disease progression of human SOD1 (G93A)
โœ Arifumi Matsumoto; Yohei Okada; Masanori Nakamichi; Masaya Nakamura; Yoshiaki To ๐Ÿ“‚ Article ๐Ÿ“… 2006 ๐Ÿ› John Wiley and Sons ๐ŸŒ English โš– 832 KB

The recent development of a rat model of amyotrophic lateral sclerosis (ALS) in which the rats harbor a mutated human SOD1 (G93A) gene has greatly expanded the range of potential experiments, because the rats' large size permits biochemical analyses and therapeutic trials, such as the intrathecal in

Antisense peptide nucleic acid targeting
โœ Alan Rembach; Bradley J. Turner; Stephen Bruce; Irwin K. Cheah; Rachel L. Scott; ๐Ÿ“‚ Article ๐Ÿ“… 2004 ๐Ÿ› John Wiley and Sons ๐ŸŒ English โš– 344 KB

## Abstract Glutamate excitotoxicity is strongly implicated as a major contributing factor in motor neuron degeneration in amyotrophic lateral sclerosis (ALS). Excitotoxicity results from elevated intracellular calcium ion (Ca^2+^) levels, which in turn recruit cell death signaling pathways. Recent