
We tend to imagine ourselves as having one brain that is entirely our own, built from our own DNA. Yet tucked away within this landscape are cells from other people – our mothers and, for those who have been pregnant, our children.
During pregnancy, maternal cells cross the placenta, while fetal cells travel in the opposite direction. Some remain long after birth, a phenomenon called microchimerism. I’ve always found this bidirectional cellular legacy fascinating, particularly now we know that some of these cells settle in the brain. My children, born via donated eggs, didn’t inherit my DNA, but microchimerism means that some of my cells may nevertheless live within them, while theirs may live within me.
I’ve always wondered what influence they might have, and a recent study prompted me to investigate. Are these cells simply passengers, or do they help shape the brains we grow up with?
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In 2008, researchers first . Four years later, another team in women’s brains, probably acquired during pregnancies with male fetuses. Finding traces of another person is one thing. But establishing what those cells become, and whether they do anything useful, is another.
The new , published this month and not yet peer-reviewed, brings us closer to answering those questions. at Fred Hutchinson Cancer Center in Seattle and his colleagues detected maternal DNA in samples of brain tissue taken from children with epilepsy. They then examined RNA from these samples, alongside data from people without epilepsy. This cellular instruction manual revealed that the maternal cells had developed into a diverse cast that included neurons, immune cells, blood vessel cells and supporting cells called astrocytes.
“It was a surprise to see naturally occurring microchimerism detected in the human brain with such highly diverse neuronal, glial, immune and vascular identities, in both healthy and diseased cohorts,” says Kanaan.
The results suggest that cells from another person can acquire characteristics of the brain itself – although why we may need these maternal cells instead of just our own isn’t yet clear. But we have some clues from animals.
In 2022, researchers compared mice carrying reduced numbers of maternal cells with those carrying typical levels, recording their brain activity and behaviour. The results suggested that , preventing excessive pruning of connections between neurons.
Mice with fewer maternal cells had disrupted communication between the prefrontal cortex and the hippocampus, regions involved in planning and memory. These mice also performed worse on tasks that involved recalling previously learned information.
This points to maternal cells possibly playing a role by helping the fetal brain wire itself during early development. “Whether comparable mechanisms operate in humans remains an open question,” says Kanaan.
However, he’s happy to speculate. Kanaan says there is already evidence in humans that maternal cells can influence the developing immune system, and that it’s reasonable to expect that the same might be extended to the brain.
He also says cells travelling in the other direction might have : “In a mouse experiment, enhanced recruitment of fetal cells accompanied reduced brain injury and changes consistent with repair.”
The idea that fetal cells are key to repair has been suggested in humans, too. In the 2012 , there was a lower prevalence among those with Alzheimer’s. This could imply that fetal cells protect the brain. But the study couldn’t establish cause and effect, so we can’t rule out the possibility that the condition might have affected the persistence of these cells.
This is a common problem within the field. While microchimeric cells have been associated with , , and , in each case it’s challenging to distinguish whether they are contributing to the condition or have been recruited to repair injuries.
Evolution offers some intriguing possibilities for their role too. at Harvard University argues that mothers and their children have a , suggesting that natural selection may therefore tend to eliminate negative effects on health and favour beneficial effects of this cellular exchange.
However, Haig thinks their evolutionary “interests” don’t always align, particularly when it comes to how a mother’s resources are shared. “It is possible,” he says, “that offspring cells in a mother’s brain may promote care (and attachment) toward the offspring from whom the cells come, whereas maternal cells in offspring brains may favour cooperation toward the mother and with other siblings.”
For now, that remains a hypothesis. Still, all of these potential impacts on our health and behaviour raise a question. Why do some brains harbour more microchimeric cells than others? In Kanaan and his team’s study, for instance, despite maternal cells being found in the majority of samples, some had around 2.2 maternal cells per 100,000 cells, while others had up to 458.9 cells per 100,000. Do we know why?
“The answer is no, we do not know,” says Haig. He suspects there are genetic factors that contribute to this disparity.
For instance, cells carry proteins that help the immune system recognise whether a cell is “self” or “foreign”, but levels of recognition and tolerance vary, which may influence the number of microchimeric cells that survive.
Medical history may matter, too. For instance, pre-eclampsia, a dangerous condition characterised by high blood pressure in pregnancy, increases the permeability of the blood-brain barrier and may allow more fetal cells to cross into a mother’s brain.
Some differences may just be about sampling limitations – some brain regions can have more cells than another, meaning a negative sample doesn’t imply they aren’t present elsewhere.
Unfortunately, none of this allows us to say definitively that more microchimerism is better, or that we should be seeking ways to promote this cellular exchange to help protect brain health.
It may not be a satisfying conclusion, but it’s early days. The mere fact that the central nervous system can sustain, integrate and potentially benefit from genetically foreign cellular material at all . So, it may be a while before we truly get to grips with whether microchimeric cells contribute to resilience, vulnerability or repair – or all three in different contexts.
Until clearer answers emerge, I choose to take comfort in the possibility that some of my mum’s cells may remain within me. And although I can’t quite explain why (a genetic connection doesn’t define my concept of family), I also find something quietly moving about the possibility that my own cells have taken up residence in my children’s brains, potentially shaping their minds in unknown ways – and their cells possibly shaping mine in equal measure.