Ben Barres
Ben Barres
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Ben Barres

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Ben Barres

Benjamin Barres (September 13, 1954 – December 27, 2017) was an American neurobiologist at Stanford University. His research focused on the interaction between neurons and glial cells in the nervous system. Beginning in 2008, he was chair of the Neurobiology Department at Stanford University School of Medicine. He transitioned to male in 1997, and became the first openly transgender scientist in the National Academy of Sciences in 2013. Barres is also known for his pioneering activism for equal opportunity in science, often citing his experiences as both a male and female scientist.

Barres was born on September 13, 1954, in West Orange, New Jersey, and was assigned female at birth. As a child, his salesman father and homemaker mother saw him as a tomboy. He later recalled: "Internally I felt strongly that I was a boy. This was evident in everything about my behavior." Attending a West Orange school, Barres excelled in mathematics and science.

At the age of 17, he learned that he had been born with Müllerian agenesis, for which he received surgical correction. He obtained a Bachelor of Science in Biology from Massachusetts Institute of Technology (1976), a medical degree (MD) from Dartmouth Medical School (1979), and a residency in neurology at Weill Cornell Medicine. During his residency, Barres noted the lack of knowledge about the causes or cures of neurodegeneration. In studying pathology reports, he noticed a correlation between neural degeneration and irregular patterns of glial cells in the brain and, intrigued, resigned his residency to pursue research in neuroscience at Harvard Medical School. He completed a PhD in neurobiology there in 1990, then did postdoctoral training at University College London under Martin Raff. In 1993, Barres joined the faculty of Neurobiology at the Stanford School of Medicine. After transitioning to male in 1997, Barres published on sexism in the sciences. In 2008, he was appointed to the Chair of Neurobiology at Stanford.

Barres authored or co-authored papers in journals such as Nature Neuroscience, Neuron, Science, and Cell. His research involved study of mammalian glial cells of the central nervous system (CNS), including the exploration of their function and development. Much of his early work was published under his deadname.

His first major discovery was how developing neurons provide signals to the myelinating glial cells called the oligodendrocytes that provide insulation on the axons. Some of his earliest works focussed on vertebrate nervous system development, including how and why many neurons fail to survive shortly after forming connections with their targets. These studies investigated how this programmed cell death, apoptosis, occurred in such a tremendous scale. Additionally, he studied processes such as the prerequisites for and consequences of axon myelination, and the interactions of various signaling molecules such as thyroid-hormone and retinoic acid within the formation of glial cells including oligodendrocytes.

Early in his time at Stanford, Barres discovered the importance of glial cells in the formation, development, maturation, and regeneration of neurons. His lab also discovered and developed methods for the purification and culturing of retinal ganglion cells and the glial cells with which they interact, including the oligodendrocytes and astrocytes of the optic nerve.

Near the turn of the 21st century he continued his study of glial cells and the mechanisms behind their ability to generate new neurons. He studied control of synapses by glia, and the differentiation of astrocytes by endothelial cells. He investigated the role of the protein Id2 in the control of oligodendrocyte development and established that removing this protein led to premature oligodendrocyte maturation.

In the 2010s Barres's research focused on using techniques such as immunopanning, immunohistochemistry, tissue culturing, and patch clamping to: 1) understand the cell-to-cell interactions in the developmental regulation of nodes of Ranvier and myelin sheaths; 2) determine to what extent glial cells play a role in synapse formation and function of synapses; 3) identify the signals that promote retinal ganglia growth and survival, and how such knowledge of these signals could be regenerated post-trauma; 4) identify the functions and developmental mechanisms of gray matter astrocytes. In these objectives, his lab discovered a number of novel glial signals for the induction of myelination, axonal sodium channel clustering, and synapse formation processes. Additionally, his lab characterized these processes and the exact identity of these novel signals.

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