New technologies are allowing us to explore the brain as never before. We are entering a new era in neuroscience where our knowledge of the brain is beginning to match the urgent need to prevent and treat diseases of the brain.




Brain Guardians Remove Dying Neurons

By adolescence, your brain already contains most of the neurons that you’ll have for the rest of your life. But a few regions continue to grow new nerve cells— and require the services of cellular sentinels, specialized immune cells that keep the brain safe by getting rid of dead or dysfunctional cells.

Greg Lemke’s lab described the surprising extent to which both dying and dead neurons are cleared away April 2016 in Nature.

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Cell Reports

Brain Mapping Tool 20 Times More Powerful Than Previous Version

Edward Callaway’s lab has developed a new reagent to map the brain’s complex network of connections that is 20 times more efficient than their previous version. This tool, detailed by first author Euiseok Kim in Cell Reports in April 2016, improves upon a technique called rabies virus tracing, which was originally developed by Callaway and is commonly used to map neural connections.

This dramatic improvement will help researchers illuminate aspects of brain disorders where connectivity and global processing goes awry, such as in autism, schizophrenia and some motor and neurodevelopmental diseases.

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Nature Comm.

Tiny Microscopes Reveal Hidden Role Of Nervous System Cells

A microscope about the size of a penny is giving scientists a new window into the everyday activity of cells within the spinal cord. The new miniaturized imaging methods, described on April 28, 2016 in Nature Communications, reveal more about nervous system function and could lead to pain treatments for spinal cord injuries, chronic itch and diseases such as amyotrophic lateral sclerosis (ALS).

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Tamping Down Neurons’ Energy Use Could Treat Neurodegeneration

Salk Institute scientists showed how an FDA-approved drug boosts the health of brain cells by limiting their energy use. Like removing unnecessary lighting from a financially strapped household to save on electricity bills, the drug—called rapamycin—prolongs the survival of diseased neurons by forcing them to reduce protein production to conserve cellular energy.

Rapamycin has been shown to extend lifespan and reduce symptoms in a broad range of diseases and, at the cellular level, is known to slow down the rate at which proteins are made.

But the new Salk research, led by Salk Professor Tony Hunter and published in the journal eLife, suggests that rapamycin could also target the neural damage associated with Leigh syndrome, a rare genetic disease, and potentially other forms of neurodegeneration as well.

Previous studies on rapamycin, which blocks an energy sensor in cells, suggested that the drug prevents neurodegeneration by encouraging cells to degrade damaged components. But recent data hinted that rapamycin might also affect mitochondria, organelles that produce energy in the form of adenosine triphosphate (ATP).

Hunter, Salk Professor Rusty Gage, first author Xinde Zheng and colleagues reprogrammed skin cells from patients with Leigh syndrome into brain cells in a dish. The Leigh syndrome neurons decayed and showed clear signs of energy depletion. Meanwhile, Leigh syndrome neurons exposed to rapamycin had more ATP and showed less degeneration. By turning down the dial on protein production, the diseased neurons were able to survive longer.

The teams are continuing to investigate how rapamycin’s effect on reducing protein synthesis could be harnessed into a treatment for mitochondria-related neurodegenerative diseases.

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Nature Neuroscience

Adult Brain Prunes Branched Connections Of New Neurons

When tweaking its architecture, the adult brain works like a sculptor— starting with more than it needs so it can carve away the excess to achieve an ideal design. That’s the conclusion of a new study that tracked developing cells in an adult mouse brain in real time.

New brain cells began with a period of overgrowth before the brain pruned back its connections. The observation, described May 2016 in Nature Neuroscience, suggests that novel cells in the adult brain have more in common with those in the embryonic brain than scientists previously thought.

While most of the brain’s billions of cells are formed before birth, Salk Professor Rusty Gage and others previously showed that in a few select areas of the mammalian brain, stem cells develop into new neurons during adulthood. In this study, his group focused on cells in the dentate gyrus, an area thought to be responsible for the formation of memories.

Over a period of about a month, the Salk team kept track of each new neural branch, called a dendrite, on growing neurons, as well as each dendrite that was pruned away. Here, the branches of one cell are shown—new dendrites are in green, those pruned away are orange, and dendrites that both developed and were pruned away since the last snapshot are in pink.

Gage and first author Tiago Gonçalves followed—on a daily basis—the growth of neurons over several weeks. When mice were housed in environments with lots of stimuli, the new cells grew quickly, sending out dozens of branches called dendrites which receive electrical signals from surrounding neurons. When kept in empty housing, new neurons grew slightly slower and sent out less dendrites. But, in both cases, the new dendrites began to be pruned back.

Defects in the dendrites of neurons have been linked to brain disorders like schizophrenia, Alzheimer’s, epilepsy and autism. Charting how the brain shapes these branches—both during embryonic development and in adulthood—may be the key to understanding mental health.

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