Virtual hypoxia and chronic necrosis of demyelinated axons in multiple sclerosis.

By B. Trapp, P. Stys. Lancet Neurology, 2009

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Oxidative damage in multiple sclerosis lesions (2011, background): “…may contribute to demye- lination and neurodegeneration in multiple sclerosis, it recently became clear that mitochondrial injury and subsequent energy failure is a major factor driving tissue injury (Lu et al., 2000; Dutta et al., 2006; Mahad et al., 2008; Trapp and Stys 2009; Witte et al., 2010).”
Multiple Sclerosis Pathology. (2018, background): “This appears to result in energy deficiency and subsequent ionic imbalance in oligodendrocytes, axons, and neurons, which can be amplified by age-related hypoxic tissue injury (Trapp and Stys 2009; Mahad et al. 2015).”
The pathobiology of vascular dementia (2013, positive): “Upregulation of VNa+1.2 channels increases the activity of the Na+/K+ ATPase, stressing further the energy budget of themarginally perfusedwhitematter (Trapp and Stys, 2009).”
Myelination and support of axonal integrity by glia (2010, background): “Once ATP is so low that the axonal membrane cannot be repolarized, a 'threshold' is reached that leads to abnormal calcium entry, proteolysis and axonal destructio”
Myelination and the trophic support of long axons (2010, background): “Nitric oxide readily diffuses into demyelinated axons and perturbs mitochondrial ATP generatio”