But it would be good to get more support on 2-73 and remyelination. We've notably put that on the back burner for now. Reason unknown. (And it's not being 'researched in secret to burn the shorts'.)
Shortly after that article was posted, the NIH published this article that shows the importance of chromatin to "induce myelin repair for treatment of demyelinating diseases such as multiple sclerosis."
(You'll recall that the University of California San Diego discovered that changes in the structure of chromatin, the tightly coiled form of DNA, trigger neurons to lose their specialized function and revert to an earlier cell state. This results in the loss of synaptic connections, an effect associated with memory loss and dementia.)
Chromatin remodeling and epigenetic regulation of oligodendrocyte myelination and myelin repair
Elijah Koreman 1 , Xiaowei Sun 1 , Q Richard Lu 2 Affiliations expand PMID: 29254827 PMCID: PMC5828965 DOI: 10.1016/j.mcn.2017.11.010 Free PMC article Abstract
Oligodendrocytes are essential for the development, function, and health of the vertebrate central nervous system. These cells maintain axon myelination to ensure saltatory propagation of action potentials. Oligodendrocyte develops from neural progenitor cells, in a step-wise process that involves oligodendrocyte precursor specification, proliferation, and differentiation. The lineage progression requires coordination of transcriptional and epigenetic circuits to mediate the stage-specific intricacies of oligodendrocyte development. Epigenetic mechanisms involve DNA methylation, histone modifications, ATP-dependent chromatin remodeling, and non-coding RNA modulation that regulate the chromatin state over regulatory genes, which must be expressed or repressed to establish oligodendrocyte identity and lineage progression. In this review, we will focus on epigenetic programming associated with histone modification enzymes, chromatin remodeling, and non-coding RNAs that regulate oligodendrocyte lineage progression, and discuss how these mechanisms might be harnessed to induce myelin repair for treatment of demyelinating diseases such as multiple sclerosis.
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