BME 410 Lecture Notes - Lecture 10: Dipeptide, Motor Neuron, Fibroblast

• School: USC
• Department: Biomedical Engineering
• Course: BME 410
• Professor: Megan Mc Cain

Document Summary

Lecture 10: using scs and reprogramming to model disease. Als is largely monogenic, but genetically diverse. Als: the disease mechanism for sod1 als is different from most other forms of, the method of constructing the als mouse model (overexpression of mutant, mice are different from humans. Sod1) induces neurotoxic mechanisms that do not occur in patients (cid:1) (cid:1) (cid:1: als is caused by multiple cellular insults and treatment requires combinatorial drug therapy. Directed differentiation ipscs + 7tfs +hb9::rfp imns longitudinal tracking of neuronal degeneration. Excess glutamate receptors on c9-als imns are functional (cid:1) (cid:1) (cid:1) (cid:1) (cid:1) (cid:1) (cid:1) Reduced c9orf72 levels impair activity-dependent glutamate receptor endocytosis and degradation. Use reprogramming to generate rfp+ als patient motor neurons small molecule library track survival of motor neurons (cid:1) (cid:1) (cid:1) The next few years will see an improvement in engineering disease models and see if drug development.