For years, changes in the brain –whether from learning to ridea bike, taking a Prozac, or sinking into Alzheimer’s disease – have been attributedto the activity of neurons and the small chemical junctions between them,called synapses. Targeting synapses is like fiddling with the connections ateither end or calling the cable company. But ignoring the wiring in between maybe a mistake.
“All ideas about communication and plasticity in thenervous system were focused on the synapse,” says Douglas Fields at the NationalInstitutes of Health in Bethesda, Maryland. That’s starting to change, as he and other neuroscientists realise that neurons alone are not enough to explain our brain’s plasticity – its ability to learn, adapt, and form new memories.
“All ideas about communication and plasticity in the nervous system were focused on the synapse,” says Douglas Fields at the National Institutes of Health in Bethesda, Maryland. That’s starting to change, as he and other neuroscientists realise that neurons alone are not enough to explain our brain’s plasticity – its ability to learn, adapt, and form new memories. What it comes down to is myelin, the fatty sheath that envelops most neurons. We are used to thinking of it like insulation along a cable – allowing electrical impulses to zip along faster. But we are learning that this fatty layer is not like a wire’s insulation, installed uniformly and left unattended. Instead, it is dynamic and autonomous, customising itself to match the brain’s demands. The cells that produce it respond in real time to our cognitive needs: new insulation is laid down to help the brain master a skill; a frayed section can be replaced. What’s more, these additions and renovations continue well into adulthood.
This new kind of plasticity has come as a shock to many researchers. Bill Rebeck at Georgetown University in Washington DC has been a professor of neuroscience for over a decade, but when he heard about it last year, he was gobsmacked. “Wait, really?” was all he could mutter. And plasticity is just the start. Because they are not nerve cells, which are notoriously hard to tinker with, we might be able to tweak them manually to give the brain an extra boost when needed, or to help mend the damage behind conditions such as multiple sclerosis. It turns out a most vital part of our cognitive potential has been hiding in plain sight.
To better understand why myelin is so important, you need to look at how information travels around the brain. A neuron sends electrical impulses zipping down long projections called axons to the synapse, a small gap that chemicals called neurotransmitters travel across. These relay the signal to neighbouring neurons. Myelin keeps the information tightly confined within the axon, allowing a speedy trip.
The substance is thought to have evolved to allow animals to react quickly. But myelin does more than just speed up our reflexes, it is also crucial to learning, development and behaviour. “Ultimately it allows us to have clever brains,” says William Richardson, who studies neuronal plasticity at University College London.
Hints about the role of myelination in cognitive abilities come from the way it is produced during our lifetime. A small amount is made as we develop in the womb, but after birth it takes off, and we see surges as infants learn to crawl, walk and talk. By about age 4, the rate of myelination slows, and teenagers still have the prefrontal cortex left to myelinate – an area crucial for planning and consideration of consequences. Until then, processing in the prefrontal cortex is slow and inefficient and teens remain precariously impulsive. The finer circuitry is complete by the time we reach our 40s, but from the 60s onwards the coverings start to fray and degenerate, which fits with the common experience of cognitive decline as we age. As myelin degenerates, the signals get fuzzier.
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