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Amyotrophic lateral sclerosis (ALS), also called Lou Gehrig’s disease, is centered around motor neuron deterioration. When these neurons die, muscles can’t function. Cholera toxin subunit B conjugated to Saporin (CTB-SAP) has a specificity towards motor neurons via GM1 ganglioside and has been used in different varieties to mimic complications in ALS.
Objective: To use the Cholera Toxin B-Saporin (CTB-SAP) mouse animal model of Amyotrophic lateral sclerosis (ALS) to determine the efficacy of mitochondrial division inhibitor 1 (Mdivi-1) for its potential neuroprotective effect.
Summary: Mdivi-1 reduced motor deficits in the ALS model. It also showed neuroprotective effects on motoneurons and promoted plasticity. This could represent a translational approach for motoneuron disorders.
Usage: To establish the model, mice received two injections of the retrogradely transported, ribosome-inactivating toxin, CTB-SAP (Cat. #IT-14) into the medial and lateral right gastrocnemius muscles, respectively, with a toxin dose of 6 μg/2 μL in PBS per injection.