Synapses are the electrochemical contact junctions that allow nerve cells, or neurons, to transmit impulses to one another. It’s the strength, position and electrochemical predisposition of those synapses — hundreds of millions of them in a healthy adult human’s brain — that, in sum, give us our identity: Their firing patterns are behind our every thought, emotion, action, and recollection.
In the living brain, synapses are formed and eliminated throughout life. Somehow, some mysterious guiding force sculpts the brain’s architecture by determining which of these connections should be created and where, and which should be eliminated and when.
For all their synaptic flash, neurons constitute a mere tenth of all the cells in a human brain. But until not so long ago, the job descriptions of the vast bulk of brain cells — called glial cells or, collectively, glia — were written in invisible ink. In fact, their very name (“glia” is the Greek word for glue) testifies to the shoulder-shrugging with which neuroscientists have traditionally viewed these cells.
Ben Barres, MD, PhD, felt differently. He devoted his entire career to studying this unsung population’s activities, which I outlined some years ago in an article called “The Brain’s Silent Majority” for our magazine, Stanford Medicine. Glia, it turns out, play a huge, previously unimagined role in determining just which synapses should be born, and where and when; and which should die, and when.
Since then, progress in the Barres’ lab and in those of his many trainees who’ve moved on to prestigious positions elsewhere has been unremitting. But Barres died on Dec. 27, at the age of 63, some 20 months after being diagnosed with pancreatic cancer.
Up to that very point in time, Barres never veered from his original and lifelong goal, which, as per his just-published obituary, was:
…to figure out the molecular and cellular causes of the brain tissue degeneration seen in Alzheimer’s, Parkinson’s and Huntington’s diseases; multiple sclerosis; amyotrophic lateral sclerosis, or Lou Gehrig’s disease; and glaucoma, an optic-nerve degenerative disease. Research in Barres’ lab has strongly implicated inflamed or ‘reactive’ astrocytes and microglia [two classes of glial cells] as drivers in all of these neurodegenerative disorders — most recently, in a 2017 Nature paper [see this news release] describing how certain reactive astrocytes secrete something that kills stressed or injured neurons.
Barres’ life and career defied categories. Again, from his obituary:
Barres was incontestably visionary yet, ironically, face-blind — he … relied on voices or visual cues such as hats and hairstyles to identify even people he knew well. … [L]acking a romantic partner or children, he treated his trainees as his family … He especially championed the cause of women in academia, with whom he empathized; he was transgender … [and] an outspoken champion of marginalized minorities in academia and society, not infrequently digressing for a few minutes during his scientific talks to point out the differences he’d personally experienced in how other scientists treated him when they perceived him as a woman versus as a man.
Scientist, visionary, personage, mensch. I regret the passing of this human comet. They don’t come around every day.
Previously: Long-term, 3-D culture method lets slow-developing brain cells mature in a dish, Jekyll & Hyde tale unfolding within the human brain may explain neurodegenerative disease and Alzheimer’s puzzle pieces are coming together