What do newborn brains with hypoxic injury and MS brains share?  AXIN2.  A potential target for remyelination.

 White matter brain injuries in infants occur when birth takes place prematurely and before lung development is complete. The lack of oxygen creates a disruption in the nerve cells ability to create myelin, or the protective coating found on nerves. Without this myelin, the brain cells die and can lead to cerebral palsy.

The researchers have also discovered this gene in patients with multiple sclerosis.

Nature Neuroscience (2011) doi:10.1038/nn.2855

Abstract

Permanent damage to white matter tracts, comprising axons and myelinating oligodendrocytes, is an important component of brain injuries of the newborn that cause cerebral palsy and cognitive disabilities, as well as multiple sclerosis in adults. However, regulatory factors relevant in human developmental myelin disorders and in myelin regeneration are unclear. We found that AXIN2 was expressed in immature oligodendrocyte progenitor cells (OLPs) in white matter lesions of human newborns with neonatal hypoxic-ischemic and gliotic brain damage, as well as in active multiple sclerosis lesions in adults.

Axin2 is a target of Wnt transcriptional activation that negatively feeds back on the pathway, promoting ß-catenin degradation. We found that Axin2 function was essential for normal kinetics of remyelination. The small molecule inhibitor XAV939, which targets the enzymatic activity of tankyrase, acted to stabilize Axin2 levels in OLPs from brain and spinal cord and accelerated their differentiation and myelination after hypoxic and demyelinating injury. Together, these findings indicate that Axin2 is an essential regulator of remyelination and that it might serve as a pharmacological checkpoint in this process.

http://excitonic.com/2011/06/27/hope-for-infant-brain-injuries-like-cerebral-palsy-as-well-as-multiple-sclerosis/

My question is...with more evidence mounting daily that MS looks like a disease of hypoxic injury....how can neurologists and researchers continue to refute the connection to CCSVI?  And how can they continue to cling to the EAE mouse model?  

Joan