Are we born with specific behavioral characteristics, or is the brain influenced by environmental factors during its early development? According to research conducted by the National Institute of Mental Health (NIMH), it might just be a little of both.
A new study claims that genes linked to schizophrenia and autism belong to a “select club” in which regulatory activity peaks during a critical and “environmentally sensitive” period in development.
Researchers tracked the activity across the lifespan of an environmentally responsive regulatory mechanism called DNA methylation, which abruptly turns on within the brain's prefrontal cortex during a pivotal transition from fetal to postnatal life.
Epigenetic mechanisms like methylation leave chemical “instructions” that tell genes what kind of tissue to produce or what functions to activate. And while the instructions are inherited (though not part of human DNA), they are also can be influenced by environmental factors.
According to Barbara Lipska, PhD, an NIMH scientist and lead author of the study, developmental brain disorders may be traceable to altered methylation of genes early in life. For example, genes that code for the enzymes that carry out methylation have been implicated in schizophrenia.
“In the prenatal brain, these genes help to shape developing circuitry for learning, memory and other executive functions which become disturbed in the disorders,” says Lipska. "Our study reveals that methylation in a family of those genes changes dramatically during the transition from fetal to postnatal life."
While the process is believed to be influenced by methylation and genetic variability, the study shows that regulation of these genes could also be sensitive to environmental influences during this critical early life period.
NIMH director Tom Insel, MD, also commented on the study, saying it reminds the field that genetic sequence is "only part of the story of development."
"Epigenetics links nurture and nature," Insel said, "showing us when and where the environment can influence how the genetic sequence is read."
The study seems to have important implications for understanding how conditions like autism and schizophrenia might begin, but how should the field use this information? Will it be helpful in prevention efforts, or can knowing the cause potentially improve how treatment is approached?