Scorpion venom to the rescue
Compound found to reverse negative effects of fetal alcohol disorder in mice
Don’t drink when pregnant. It’s a well known adage for any expectant mother, as exposure to alcohol can cause fetal alcohol spectrum disorder — a condition marked by physical and learning disabilities for the baby. Now, a new study has found that a compound derived from scorpion venom can reverse some of the negative effects of the disorder in mice, and researchers hope this could one day lead to a treatment.
“I thought this was an important public health issue,” said Kazue Hashimoto-torii, the lead researcher from the Children’s National Hospital in Washington, D.C. Hashimoto-torii became interested in studying fetal alcohol spectrum disorder after having her own child in 2005. Although she never drank during her pregnancy, she was curious about how alcohol could affect development and was concerned about the 119,000 children born globally with the disorder.
“We need some kind of treatment and that’s what drives me to do this research,” she said.
How alcohol causes the disorder is complicated, but broadly speaking, alcohol activates something called the “heat shock pathway,” a flurry of cellular activity that can have a strong effect on fetal development. For the new study, published in the journal Nature Neuroscience, the research team discovered that the heat shock pathway changes a specific part on the surface of brain cells that are important for motor control. These brain cells then act abnormally and affect the baby’s co-ordination. A compound derived from scorpion venom, called tamapin, was then applied to reverse the abnormal brain cells.
To tease apart how this mechanism works, researchers gave pregnant mice alcohol and tracked the effects on the developing brain. Thirty days after birth — roughly translating to the teenage years on a human time-scale — the research team then gave the mice tamapin for a few days. They followed their brain activity and found that about 70 per cent of the damage had been reversed.
Hashimoto-torii reasoned that tamapin might be effective in treating other neurological problems as well. Other diseases that involve a loss of motor control such as Alzheimer’s or dementia are thought to damage brain cells in a similar way, so it’s possible that tamapin can be applied to those, too.
“I can’t say enough positive things — its really a cool paper,” said Rajesh Miranda, a fetal alcohol spectrum disorder neuroscientist who was not involved with the research.
Miranda said that to him, the most interesting and innovative thing is that the study was able to follow very specifically how alcohol affected the developing brain and how the impaired brain cells were rectified with tamapin.
But Miranda warned that although the research was fascinating as a scientist, possible treatments are a long way off. “It’s one thing to be excited about a paper that identifies the mechanism. It’s a very different thing to say that the mechanism can be targeted by therapies anytime soon,” he said.
The mice didn’t develop any side-effects, but Hashimoto-torii would have to determine the compound is entirely safe before human test trials. Her research would have to determine how tamapin can be taken. The study used a very controlled scenario with mice, but figuring out a treatment regimen for patients would be complicated. Miranda also warned that tamapin could be a tricky drug to deal with — too much or too little could both have terrible side-effects.
Still, the paper takes an important stride in figuring out the complex puzzle of how fetal alcohol spectrum disorder is caused and how it might be treated. “Usually investigators looking for the molecular mechanisms behind disease stop there, but we want to move forward to have a real impact on public health,” said Hashimoto-torii. “We really want to give patients the hope of having a better life through treating the neurodevelopmental problems caused by fetal alcohol spectrum disorder.”