A new study indicates that male DNA, left over from pregnancy with a male fetus, can persist in a woman’s brain throughout the rest of her life. Although the exact biological impact of the DNA is yet unclear, the study found that women with more male DNA in their brains were less likely to suffer from Alzheimer’s disease, suggesting that male DNA could help protect mothers from this disease.
Researchers published their findings in the journal PLoS ONE. During pregnancy, mammal mothers and fetuses exchange DNA as well as cells. Previous work has shown that fetal cells can linger in a mother’s blood and bone for decades. This is called fetal microchimerism. This lingering fetal DNA could benefit the mother’s health, by promoting tissue repair and improving the immune system, but it may also cause adverse effects, such as autoimmune reactions.
Scientists had previously shown that fetal microchimerism occurs in mouse brains, but had not yet discovered it in humans. A team of researchers, led by autoimmunity specialist and rheumatologist J. Lee Nelson, of the Fred Hutchinson Cancer Research Center in Seattle, Washington, took samples from autopsied brains of 59 women who died between the ages of 32 and 101.
They found evidence of male DNA in the brains of 63% of the women. The DNA was scattered across multiple brain regions. The team also examined the brains for signs of Alzheimer’s in order to correlate between the disease and the observed microchimerism. 33 had AD, but the women with AD had significantly less male DNA in their brains that the ones who didn’t have it.
It remains unclear whether that correlation implies that fetal male DNA helps protect women against AD and it’s difficult to reach any firm conclusions between microchimerism and AD because the team had little information about the pregnancies of the women in their study.
Reference: “Male Microchimerism in the Human Female Brain” by William F. N. Chan, Cécile Gurnot, Thomas J. Montine, Joshua A. Sonnen, Katherine A. Guthrie and J. Lee Nels, 26 September 2012, PLoS ONE.