If there wasn’t enough reason to be concerned about children suffering psychological and physical neglect—by their family, in foster homes, or from war or weather catastrophes—we now have three good lines of evidence that neglect harms a child’s developing brain.
But there’s also hope that some of this harm can be undone if caught in time.
The first evidence comes from cognitive studies done in Romania, where the Bucharest Early Intervention Project (BEIP) has transferred some children reared in its infamous orphanages, selected at random, into quality foster care homes. In 2007, Charles Nelson, PhD, and colleagues documented cognitive impairment in institutionalized children, but also showed improvement when children were placed in good foster homes, especially when they were placed before age 2.
Gray and white
Sheridan, Nelson and colleagues obtained brain MRIs from three groups of 8- to 11-year old children: 29 had been reared in an institution, 25 had left the institution for a high-quality foster home (where they spent 6 to 9 years), and 20 typically developing children who were never institutionalized served as controls.
The findings were mixed:
- Children who had spent their entire lives in an institution had significantly lower volumes of white matter—necessary for making connections in the brain—in the cortex of the brain than did the controls. But if they were transferred into foster care, their white matter volume became indistinguishable from that in controls.
- Children spending any amount of time in an institution—even if later placed in foster care—had significantly smaller gray matter volumes in the cortex.
“White matter, which forms the ‘information superhighway’ of the brain, shows some evidence of ‘catch up,’” says Sheridan.
Why did white matter bounce back, but not gray matter? Sheridan and Nelson speculate that white matter grows more slowly over time, possibly making it more amenable to intervention, whereas gray matter growth peaks during specific “sensitive” times in early childhood when social experience may wield a greater, more lasting influence.
And here’s the third salvo: Earlier this month, the journal Science reported findings from the Boston Children’s Hospital lab of Gabriel Corfas, PhD, showing how neglect and social isolation lead to cognitive impairment at the cellular level.
The team, led by Corfas and postdoctoral fellow Manabu Makinodan, MD, PhD, simulated neglect in mice by placing them in isolation early in life.
The results were striking. Cells that make up the brain’s white matter, known as oligodendrocytes, failed to mature, and failed to produce proper amounts of myelin, the fatty “insulation” on nerve fibers that boosts the speed and efficiency of communication between different areas of the brain. This was especially true in the prefrontal cortex. The mice, for their part, showed reduced sociability and deficits in working memory.
Confirming the earlier research, Corfas’s team showed that the effects of social isolation are timing-dependent. If mice were isolated during a specific period in their development, they failed to recover sociability and memory function even when they were put back in a social environment. Conversely, if they were isolated after this so-called critical period, they remained normal.
Drilling down further, the investigators found that the brains of socially isolated mice had less neuregulin-1 (NRG1), a protein essential to the development of the nervous system. When they eliminated a receptor for NRG1 found on oligodendrocytes, known as ErbB3, the effect was the same as being in isolation. Even when the mice were in a stimulating, social environment, their myelination and behavior were abnormal.
“These observations indicate that the mechanisms we found are necessary for the brain to ‘benefit’ from early social experience,” says Corfas.
Can this child be saved?
Could this molecular knowledge help children recover from the effects of neglect and social deprivation—say, a child who’s been adopted from an institution overseas?
Perhaps. The Corfas lab is now investigating drugs that might stimulate myelin growth by targeting NRG1, ErbB3 or related pathways.
But it won’t be simple. First, the stress of early adversity may affect more than the brain—another BEIP study shows it may actually “age” children’s DNA. And tinkering with myelination in the brain isn’t something you want to do lightly.
“Having both too much and too little myelination is bad,” Corfas cautions. “This is a pathway that requires very careful regulation.”
There are, of course, other ways to help these children—expedited adoptions, better disaster planning, more social services. But sadly, some interventions will mean changing the world first.