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Unsung brain-cell population implicated in variety of autism

Like the late Rodney Dangerfield, and as I once wrote in Stanford Medicine, glial cells "don't get no respect." Combined, the three glial cell types - astrocytes, oligodendricytes, and microglia - constitute a good 90 percent of all the cells in the brain. Yet the remaining 10 percent - the neurons - are so celebrated they've lent their name to brain science: neurobiology.

Stanford's Ben Barres, MD, PhD, a lonely voice in the wilderness, has long advocated paying more attention to glial cells. His experience as a young neurologist in the 1980s convinced him that they're involved in all sorts of brain pathology.

And, belatedly, glial cells are getting some grudging respect, in appreciation of their increasingly well-characterized roles in everything from directing blood vessels to increase their diameters in the vicinity of busy nerve circuits to determining which synapses will live and which will die.

In a new study just published in Nature Neuroscience, a genetic deficiency known to be responsible for Rett syndrome, the most physically disabling of the autistic disorders, has been shown to wreak many of its damaging effects via astrocytes. These gorgeous star-shaped glial cells, alone, account for almost half of all cells in the human brain (although by volume not so much, as they're smaller than neurons).

In the study, investigators at Oregon Health and Science University employed a mouse model of Rett's syndrome in which the condition's defining gene defect was present in every cell of every mouse. When the investigators restored that defective gene to the mice's astrocytes - and only their astrocytes - many of the signature symptoms of the disease cleared up.

Rett Syndrome was once assumed to be exclusively a function of damaged neurons. This latest finding, like many others over the past decade, goes to show that glial cells aren't just a bunch of packing peanuts whose main job is to keep our neurons from jiggling when we jog.

Photo by Ibtrav

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