Neuroinflammation as a Target for Blocking Fetal Alcohol Exposure

Research Suggests New Avenue for Exploration in Preventing or Mitigating the Condition

New research using rat models has found that ibuprofen reduced neuroinflammation and behavioral signs of alcohol exposure associated with fetal alcohol spectrum disorders (FASD). As reported by Ohio State University, the study is the first to connect alcohol-induced inflammation in the hippocampus to later cognitive impairment, and the findings could provide new insight into the treatment of FASD in humans. The conclusions also support related prior research demonstrating that anti-inflammatory intervention can prevent cognitive impairment due to neuroinflammation at birth. The CDC has estimated that 2 to 5 out of 100 children in the US exhibit lasting cognitive effects of early alcohol exposure. The findings are published in the journal Behavioral Brain Research.

In the study, rats that were exposed to alcohol at 4 to 9 days after birth, the equivalent of the 3rd trimester of human pregnancy, were administered either ibuprofen or saline solution. The former cohort had lower levels of neuroinflammation and enhanced long-term memory at 25 days, compared to the latter. Lead author Molly Goodfellow, then an Ohio State graduate student commented, “We hope that our work will promote future studies to determine how long neuroinflammation persists after alcohol exposure and if anti-inflammatory therapies might work if administered after birth or later in life to improve cognitive function in people with FASD.” They also noted that, as ibuprofen carries risks of adverse effects for both mother and fetus, alternative anti-inflammatory drugs would be preferable.

Read a news story about the research findings.

The journal abstract may be read here.

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