WASHINGTON — Scientists have new evidence that the brain chemical best known for regulating mood also plays a role in the mystifying killer of seemingly healthy babies — sudden infant death syndrome.

Autopsied brain tissue from SIDS babies first raised suspicion that an imbalance in serotonin might be behind what once was called crib death.

But specialists couldn't figure out how that defect could kill. Now researchers in Italy have engineered mice born with serotonin that goes haywire — and found that the brain abnormality is enough to cause sudden death, in ways that mesh with other clues from human babies.

The work suggests it might one day be possible to test newborns for their risk of SIDS.

For now, even an animal experiment can give devastated families "some sense of comfort that there was nothing they could have done to prevent it," said Dr. Marian Willinger, a SIDS specialist at the National Institute of Child Health and Human Development, who wasn't part of the study. "It is a real disease."

The study is published in today's edition of the journal Science.

AUTOPSY CLUE

More than 2,000 U.S. infants a year die in the sudden and unexplained circumstances called SIDS.

Having babies sleep on their backs appears to reduce the risk of SIDS. And parents are urged not to allow smoking around their babies, or to let their babies get too warm while sleeping.

But beyond those risk factors, doctors have little advice.

In 2006, Dr. Hannah Kinney of Children's Hospital Boston compared brain tissue from 31 SIDS babies and 10 infants who died of other causes. The SIDS babies had abnormalities in their brain stem that led to imbalances in serotonin, a chemical that helps brain cells communicate.

Low serotonin famously plays a role in depression. Less known to laymen is that serotonin also helps regulate some of the body's most basic functions — breathing, heart rate, body temperature, arousal from sleep.

UNEXPECTED RESULTS

Dr. Cornelius Gross and colleagues at the European Molecular Biology Laboratory in Italy were studying how the serotonin system turns itself on and off when they stumbled onto the SIDS connection.

They genetically engineered mice to have an overactive serotonin-regulating receptor, which in turn reduced the amount of serotonin in the brains of otherwise normal baby mice.

More than half of the mice abruptly died before they were 3 months old. More intriguing, they had erratic episodes where their heart rate would drop and, five to 10 minutes later, so would their body temperature, Gross reported. Sometimes they died in the midst of what Gross calls those crises, other times afterward.

The exact cellular defects in the mice and the human babies studied so far aren't identical, researchers caution.

But heart and temperature problems are consistent with what little human data is available, Willinger noted.

Here's another key: Gross could switch on and off the gene defect that controlled serotonin levels in the mice. By doing so, he showed that older baby animals are less likely to die from haywire serotonin than younger ones.

"This is a very exciting part of the research," says Willinger — because doctors have long suspected that if at-risk babies just get through a developmental period, they'll be OK.