Augmented Cuprizone Model of Neuroprotection
Axonal transection or loss is a notable pathology of MS as a consequence of demyelination of axons in the brain. Protecting demyelinated axons is critical to maintain neural integrity as transection/loss of axons is the major cause of neurological decline in MS patients. Renovo’s cuprizone mouse model can evaluate neuroprotection potential of pharmaceutical compounds and biologics by analyzing the swollen and transected axons that are reminiscent of neuronal damage. Animals undergo demyelination through a combination of cuprizone-laced chow and injections of rapamycin, with concurrent therapeutic dosing of client compounds. In addition, Renovo’s 3D-EM capabilities allow comprehensive analysis of the neuroprotective effect by studying neuronal ultrastructural changes.
Experimental End Points:
- Quantification of axonal degeneration (identified by axonal ovoids)
- Myelinated axons in corpus callosum
- Additional histological quantification (OPCs, oligodendrocytes, microglia, astrocytes etc.)
- 3D-EM evaluation of myelin and axonal parameters
- 3D-EM evaluation of mitochondrial integrity and volumetrics