Prenatal exposure to valproic acid increases miR-132 levels in the mouse embryonic brain.
Yuta Hara, Yukio Ago, Erika Takano and 5 others
PMID 28670439WHAT IT FOUND
Prenatal valproic acid raised mouse embryonic brain miR-132 at E12.5, not E14.5, and reduced MeCP2 and p250GAP.
This is an animal molecular finding, not evidence for human autism or therapy.
Key findings
01At E12.5, prenatal valproic acid increased miR-132 about 2.5-fold in male embryonic brain, while miR-9 and miR-124 did not change.
02At E14.5, prenatal valproic acid did not change miR-132 levels in male or female embryonic brain.
03Prenatal valproic acid at E12.5 reduced MeCP2 mRNA at 6 h and p250GAP mRNA at 24 h in embryonic brain, but not in P1 cortex.
STILL TO COME
How it was doneWhat they found
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What it does not show
This was an animal study in mice, not a study of human patients or therapy. The outcomes were embryonic brain RNA levels and mouse behaviour, not speech, motor, or occupational function. The supplied methods do not describe random allocation or blinding. The paper did not test whether changing miR-132 causes autism-like behaviour. The authors state the relationship between abnormal behaviours and microRNA changes is not known. The authors state that dysregulation of miR-132 is unlikely to explain sex differences in behaviour or brain morphology.
Declared interests
Funding came from the Japan Society for the Promotion of Science, Dainippon Sumitomo Pharma, the Uehara Memorial Foundation, the Takeda Science Foundation, the Research Foundation for Pharmaceutical Sciences, and the Japan Agency for Medical Research and Development. The supplied text gives no author conflict-of-interest list.
The easy way to misread this
Do not read the increased miR-132 in mouse embryos as evidence that valproic acid causes autism in humans or that therapy should change. The paper tested pregnant mice and embryonic brain RNA, not patients, treatment outcomes, or clinical speech and language function.