A few posts ago I wrote about the life-long importance of the environment on early development in the human brain. Early experiences affect the way a neural network forms, a process that occurs all the way into a person’s late teens or early twenties. Our brains start with a giant jumbled mess of billions of synaptic connections. But as we grow and learn, only certain connections are strengthened while others are pruned away. While some ability to change (neural plasticity) remains throughout life, early infancy and childhood – at least in some real tangible ways – affects the way we’re wired throughout our lives.
But it’s not just the people we interact with or the things we see and hear. Other life forms other than humans can have a profound impact as well. Take, for example, some common pathogens.
Several previous studies have linked early infancy infections with changes to neural pathways later in life. Even mild bouts with sicknesses can lead to attention deficit disorders and trouble with motor functions. But while science had made some of these small connections, the physiological mechanisms behind them remained unclear.
Now, researchers at the Ohio State University have reported at least one of the reasons why this can happen. Some of these neural affects can be attributed to a lack of iron.
Early in a person’s development, neural cells called oligodendrocytes require a decent amount of iron so that they can pump out the white matter that wraps around the business end of neurons, a protective coating that project from the main body of a brain cell and is pretty damned important for their general effective functioning. When a brain begins fighting an infection, however, neurons hang on to most of their iron, leaving little left for the production of white matter.
In their study, scientists gave a mild E. coli infection to 3-day-old mice, which roughly translates to the last three months of prenatal development in humans. This caused a transient inflammatory response in their brains that was resolved within 72 hours. This brain inflammation, though fleeting, interfered with storage and release of iron, temporarily resulting in reduced iron availability in the brain. When the iron was needed most, it was unavailable.
What’s more, those mice that were infected early in their lives also showed a small – but statistically significant – predisposition toward motor control issues and hallmarks of attention disorders later in life – roughly during a person’s young adulthood years. The brains of these same mice contained lower levels of white matter and fewer oligodendrocytes, suggesting that brief reductions in brain-iron availability during early development have long-lasting effects on brain development.
Though other researchers have observed links between newborn infections and effects on white matter and behavior, scientists had not figured out why those associations exist. Ohio State’s group focused on understanding how immune system activation can trigger unexpected interactions between the central nervous system and other parts of the body.
“We’re not the first to show early inflammatory events can change the brain and behavior, but we’re the first to propose a detailed mechanism connecting neonatal inflammation to physiological changes in the central nervous system,” said Daniel McKim, a lead author on the paper and a student in Ohio State’s Neuroscience Graduate Studies Program.
Just another reason for overprotective parents to freak out at the slightest hint of trouble, fever, redness, or crying. You’re welcome, world.
The study, “Neonatal E. Coli Infection Causes Neuro-Behavioral Deficits Associated with Hypomyelination and Neuronal Sequestration of Iron,” was published in The Journal of Neuroscience by McKim, laboratory director Jonathan Godbout, associate professor of neuroscience, and a whole host of other researchers. Check out the link if you want to know who. I’m far too lazy.