Use of IL4i1 to Promote Re-myelination and Reduce Inflammation
Categories: “Neurological Disorders“
Reference #: 2014-009
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Georgetown researchers propose generating an IL4i1 peptide or small molecule mimic that can suppress inflammation and promote oligodendrocyte progenitor cell differentiation necessary for brain lesion repair. Further, the researchers propose a method of diagnosing a subject as having a predisposition to a condition marked by impairment of myelin regeneration in the central nervous system.
- Prevent progression of neurodegenerative disorders such as multiple sclerosis (MS) by promoting re-myelination and thereby improving nerve conduction, acceleration, metabolic isolation etc.
- Regulate inflammation in the central nervous system to create conditions necessary for regeneration
- Potential biomarker to assess MS disease progression
- neuro-inflammatory disorder causing impairment of myelin regeneration and/or axonal loss causes demyelination.
- Other conditions marked by an impairment of myelin regeneration in the central nervous system (CNS)
- Promotes body’s own regenerative capabilities
- Reduced probability of adverse reaction in humans with native protein
- Possible application to other neurodegenerative diseases
The cause of multiple sclerosis is unknown, however recent technological advances have elucidated some of the complications by which the disease can progress, equipped with this knowledge Georgetown researchers were able to uncover the role of IL4i1 in assuaging the disorder. The researchers found that IL4i1 is expressed during brain injury in a manner that correlated with tissue repair. The findings suggest that not only does IL4i1 suppress inflammation, but it also leads to the oligodendrocyte progenitor cell differentiation necessary for regeneration. Naturally the researchers seek to enhance the effect of IL4i1 by developing ways in which to administer it to afflicted persons in therapeutically effective amounts.
STAGE OF DEVELOPMENT
Target validation in murine models.
EPO Allowed – 15840643.9
Germany, UK, France
Jeffrey Huang, Ph.D.