A decade ago, glia were the neglected stepchildren of neuroscience. Although glia outnumber neurons by about ten to 1 in the adult human brain, providing support for neurons has traditionally been viewed as their primary function. Glial biology has come into its own recently, as researchers have shown that glia are critical for the development of the nervous system and have key roles in various neurodegenerative disorders. Glia regulate brain vasculature and the blood-brain barrier, modulating ischemia and migraines. Moreover, they are important in the repair of neurons after injury and also contribute to neuropathology in neurodegenerative diseases. In this issue, we present a focus on glia and disease, which highlights recent efforts in some of these areas and discusses how advances in understanding glial biology may lead to new treatments.
Multiple sclerosis is caused by the malfunction of glia, specifically by the failure of remyelination by oligodendrocytes. In their perspective, Robert Miller and Sha Mi discuss the molecular mechanisms of demyelination and remyelination. They describe how successful repair after demyelination recapitulates the cell-cell interactions that control myelination during development. By examining the mechanisms that reduce myelination in adult animals, such as glial scarring and the expression of myelination-inhibiting molecules, they identify a variety of therapeutic targets that might allow researchers to intervene at critical stages to reverse demyelination in disease.
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