In a new study, researchers found that too much of a certain amino acid in utero could cause schizophrenia in mice despite the quality of postpartum caregiving—and the study suggests that the same would be true with humans.
They plan to use the findings to develop better treatments for—and possibly avert—schizophrenia and other psychiatric disorders.
The research was conducted by a team at the University of California, Irvine.
The study is the most recent of three showing how mice that receive extra methionine, an amino acid essential to metabolism, experience genetic and behavioral changes that mark schizophrenia in humans.
The first found that giving extra methionine to adult mice caused them to exhibit symptoms of schizophrenia, such as social withdrawal and impaired communication, memory, and reasoning skills.
The second showed that mice that received excess methionine during the brain development stage of pregnancy had offspring whose genes and behavior indicate schizophrenia in people.
The third study answers the question. The researchers switched the offspring at birth so that the pups with extra methionine were fostered by mothers without it and vice versa.
It made no difference: The pups with excess methionine showed signs of schizophrenia, and those without it did not.
This means nurture was unable to rescue the former from developing schizophrenic behaviors. Nor did it engender the disorder in offspring without the extra amino acid.
In the study, the team analyzed the pups’ brain chemistry, genes, and activity. They found that about 800 genes were affected by the excess methionine and that within 24 hours of birth, these genes had altered the pups’ brains.
The results match schizophrenia in humans, and the researchers are confident that the changes the mice experienced would occur in people as well.
Because they were able to detect the differences so early in life, scientists believe that a drug could be developed to stop these changes from happening.’
The goal is to create pharmaceuticals to treat, cure or—ideally—prevent schizophrenia. Currently, medications can only address a few symptoms, such as hallucinations.
And schizophrenia patients may not be the only ones to benefit.
One gene that showed a particularly large change is already associated with epilepsy, autism, and Alzheimer’s, suggesting at least one common thread between these diseases and schizophrenia.
Future work may examine whether autism, schizophrenia, and Alzheimer’s are actually the same disease presenting itself differently in childhood, adolescence, and old age, respectively.
One author of the study is Amal Alachkar.
The study is published in Communications Biology.
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