Turning Down Gene Expression Promotes Nerve Cell Maintenance

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Turning Down Gene Expression Promotes Nerve Cell Maintenance

http://www.medicalnewstoday.com/articles/137455.php

Anyone with a sweet tooth knows that too much of a good thing can

lead to negative consequences. The same can be said about the signals

that help maintain nerve cells, as demonstrated in a new study of

myelin, a protein key to efficient neuronal transmission.

Normal nerve cells have a myelin sheath, which, much like the

insulation on a cable, allows for rapid and efficient signal

conduction. However, in several diseases - the most well-known being

multiple sclerosis - demyelination processes cause the breakdown of

this " insulation " , and lead to deficits in perception, movement,

cognition, etc. Thus, in order to help patients of demyelinating

disease, researchers are studying the pathways that control myelin

formation and maintenance.

A new study by University of California scientists examines the role

of a structural protein, called lamin, in maintaining myelin. They

found that, while lamin is necessary in the initial stages of myelin

formation, too much lamin promotes myelin breakdown. Further

investigation led the researchers to the discovery of a signal that

fine-tunes lamin expression. This signal, a microRNA called miR-23,

can turn down lamin gene expression, and thereby prevent

demyelination due to lamin overexpression.

This new work reported in Disease Models & Mechanisms (DMM),

dmm.biologists.org, adds another piece to the puzzle that is

understanding myelin formation and maintenance. Additionally, the

identification of miR-23 as a myelin regulator introduces a new

potential drug target in developing treatments for demyelinating

illness.