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Stanford University School of Medicine

Malfunctioning glia – brain cells that aren’t nerve cells – may contribute big time to ALS and other neurological disorders

The field of neurology - or neurobiology, or neuroscience, take your pick - is named in honor of a talented tenth of the cells in the human brain, which respectable scientists call neurons and the rest of us call nerve cells. The other nine-tenths consist of three distinct types of cells collectively lumped together under the term "glia," after the Greek word for glue.

You can infer from that monicker that those "other" brain cells haven't been held in overly high regard. As I once wrote in a Stanford Medicine article called "The Brain's Silent Majority:"

Unlike their flashier electronic cousins [the neurons], glia speak in chemical whispers. Learning their language has been tougher. As a result, glial cells were long seen as inert nerve cement: just so many packing peanuts whose raison d’être is to keep our neurons from jiggling when we jog.

But pioneering Stanford gliologist (I just made up that term) Ben Barres, MD, PhD - who trained as a practicing neurologist before circling back for his PhD - couldn't help noticing, in autopsies, that the brains of people with "neurological" disorders invariably showed obvious signs of glial disarray. So he resolved to devote his career to the study of glial cells, which have now emerged as major players in, among other things, the formation and pruning of the all-important neuron-to-neuron contacts called synapses.

In the strictly material sense, "you" aren't much more or less than the sum total of all your synapses - about 100 trillion of them. That would (again, strictly materially speaking) elevate glia to a godlike status, wouldn't it?

But on Earth, at least, power is a double-edged sword. Barres and others have amassed a growing pile of implications about the kinds of damage - from neurodegenerative disorders like Alzheimer's to neurodevelopmental ones like autism and Rett syndrome - that can result when glia go wrong.

Barres and a postdoc in his lab, Steven Sloan, PhD, have penned a commmentary in a just-published issue of Proceedings of the National Academy of Sciences, to accompany a study by other researchers fingering glial-cell malfunction in yet another scourge: amyotrophic lateral sclerosis (ALS). The most frequent form of motor-neuron degenerative disease, ALS is informally known as Lou Gehrig's disease in memory of a baseball star of yesteryear who, slowly and very publicly, died too young.

Write Barres and Sloan:

For many years, a neuron-centric mentality has dominated this field of research... But this strict attention on neuronal pathology is beginning to broaden... [The new study] shows that glial cells unexpectedly can play a much more fundamental, even primary, role in driving neurodegenerative disease.

Has brain science, unlike the proverbial drunk who kept on looking for his car keys under the lamppost not because he dropped them there but because the light is better, managed to stop looking for defects in all the wrong places?

Previously: Using video and a white board to describe complicated research, Neuroinflammation, microglia, and the brain in the balance, Unsung brain-cell population implicated in variety of autism and Surprise! Warrior immune proteins help heal injured nerves
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