People born without a corpus callosum do not have a bridge between the two cerebral hemispheres. Neuroscientists from UNIGE have shown how the brain manages to adapt.

One in 4000 people is born without a corpus callosum, a brain structure consisting of neural fibers that are used to transfer information from one hemisphere to the other. A quarter of these individuals do not have any symptoms, while the remainder either have low intelligence quotients or suffer from severe cognitive disorders. In a study published in the journal Cerebral Cortex, neuroscientists from the University of Geneva (UNIGE) discovered that when the neuronal fibers that act as a bridge between the hemispheres are missing, the brain reorganizes itself and creates an impressive number of connections inside each hemisphere. These create more intra-hemispheric connections than in a healthy brain, indicating that plasticity mechanisms are involved. It is thought that these mechanisms enable the brain to compensate for the losses by recreating connections to other brain regions using alternative neural pathways.

The corpus callosum develops in utero between the tenth and twentieth week of gestation. Agenesis of the corpus callosum is a congenital brain malformation in which this brain structure fails to develop, resulting in one out of 4000 babies born without a corpus callosum. When it is missing, nothing replaces this structure measuring about ten centimeters, with the exception of cerebrospinal fluid. This means that the information transmitted from one hemisphere to the other can no longer be conveyed by the neuronal projections from the corpus callosum. “Their role in a healthy brain,” begins Vanessa Siffredi, a researcher in UNIGE’s Faculty of Medicine, “is to ensure the functioning of various cognitive and sensorimotor functions.” Surprisingly, 25% of people with this malformation have no visible signs; 50% have average intelligence quotients and learning difficulties; and the remaining 25% suffer from severe cognitive disorders.

Jason Asbahr.

Reese Jones

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New research suggests that electrophysiological brain signals associated with neural plasticity could help explain the rapid, antidepressant effects of the drug ketamine. The findings, European Neuropsychopharmacology, indicate that ketamine could reverse insensitivity to prediction error in depression.

In other words, the drug may help to alleviate depression by making it easier for patients to update their model of reality.

“Ketamine is exciting because of its potential to both treat, and better understand depression. This is largely because ketamine doesn’t work the way ordinary antidepressants do – its primary mechanism isn’t to increase monoamines in the brain like serotonin, and so ketamine gives us new insight into other potential mechanisms underlying depression,” said lead researcher Rachael Sumner, a postdoctoral research fellow at The University of Auckland School of Pharmacy.

A Stanford Medicine team used human stem cells to assemble a working nerve circuit connecting brain tissue to muscle tissue. The research could enable scientists to better understand neurological disorders that affect movement.

Poor sleep and other issues with circadian rhythm are common for people with Alzheimer’s disease. Now researchers may have a clue to why.

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“If your circadian clock is not quite right for years and years—you routinely suffer from disrupted sleep at night and napping during the day—the cumulative effect of chronic dysregulation could influence inflammatory pathways such that you accumulate more amyloid plaques,” says Erik Musiek. (Credit: Getty Images)

Fractured sleep, daytime sleepiness, and other signs of disturbance in one’s circadian rhythm are common complaints of people with Alzheimer’s disease, and the problems only get worse as the disease progresses.

Electricity is a key ingredient in living bodies. We know that voltage differences are important in biological systems; they drive the beating of the heart and allow neurons to communicate with one another. But for decades, it wasn’t possible to measure voltage differences between organelles—the membrane-wrapped structures inside the cell—and the rest of the cell.

A pioneering technology created by UChicago scientists, however, allows researchers to peer into cells to see how many different organelles use voltages to carry out functions.

“Scientists had noticed for a long time that charged dyes used for staining cells would get stuck in the mitochondria,” explained graduate student Anand Saminathan, the first author for the paper, which was published in Nature Nanotechnology. “But little work has been done to investigate the membrane potential of other organelles in live cells.”