Exercise during pregnancy may benefit baby's brain

DEVELOPMENT

Can a pregnant woman make her baby's brain grow bigger just by exercising? That is the intriguing question raised by German researchers who compared brain development in mice born to mothers that ran on an exercise wheel with mice born to sedentary mothers. The offspring of the running mothers showed slower brain development prior to birth, but by the time the pups were seven weeks old, they had 40 percent more of a common brain cell than the pups of inactive mothers. The researchers did not measure whether the extra cells in the hippocampus area -- a brain region vital for learning and memory -- made the mice any smarter, but they said the findings should prompt research into how a pregnant woman's exercise affects her offspring. Until now, most research into exercise by pregnant women has focused on the health of the woman, not her fetus.

BOTTOM LINE: One study of mice is not enough to give pregnant women advice, but the results underscore a biological principle: A pregnant woman's lifestyle can affect her offspring's brain development even after the child is born. For instance, rats whose mothers were deliberately put under stress during pregnancy show signs of anxiety months after birth. The exercise study ''opens up the opportunity for a fresh look on the factors that positively influence brain development," lead researcher Gerd Kempermann of the Max Delbruck Center for Molecular Medicine in Berlin said in an e-mail.

CAUTIONS: This study is closer to basic science than practical advice. The researchers don't even know whether it applies to people.

WHAT'S NEXT: The researchers want to do a larger study that would allow them to calculate how much maternal exercise causes the most brain development and to determine whether more brain cells translates into more intelligent mice.

WHERE TO FIND IT: Proceedings of the National Academy of Sciences, March 7, 2006

SCOTT ALLEN

ALZHEIMER'S

Pill boosts memory and fights disease hallmarks

Scientists experimenting with mice have found a pill that improves memory as well as eliminates two hallmarks of Alzheimer's disease -- amyloid plaques and tau tangles in the brain. It's the first medication that appears to affect all three. The pill, called AF267B, appears to work by improving the brain's use of acetylcholine, a natural chemical that helps transmit messages. In the experiment, mice genetically altered to have symptoms similar to Alzheimer's were fed the pill daily for eight weeks. They performed better than similar mice who did not get the pill in remembering the location of a submerged platform in a tank of murky water, although they did not improve on a second memory task. In addition, autopsies of the brains of ''sick" mice who took the pill showed fewer plaques and tangles.

BOTTOM LINE: ''AF267B could be a tremendous step forward in the treatment of Alzheimer's disease," according to Frank LaFerla, a professor of neurobiology and behavior at the University of California at Irvine, who led the study.

CAUTIONS: ''It does a lot of good things, but this is just mice," Dr. Sam Gandy, chairman of the medical and scientific advisory council of the Alzheimer's Association, said in an interview. Earlier tests of similar substances in mice have failed. In addition, some proposed treatments that were shown to work well in mice failed -- or caused damage -- to people.

WHAT'S NEXT: A California biotechnology company is testing the safety of the drug in healthy young people. If the drug is safe in healthy people, it would next be tested in people with Alzheimer's.

WHERE TO FIND IT: Neuron, March 2, 2006

ALICE DEMBNER

MACULAR DEGENERATION

Two key genes may help identify those at risk

More than 10 million Americans suffer from macular degeneration, which causes blindness in older people and has been on the rise recently as the population ages. Although the disease is poorly understood, recent studies have suggested that macular degeneration may be related to abnormal inflammation. The researchers studied 900 patients with macular degeneration and 400 patients without the disease and identified several genetic variations that seem to affect the risk for macular degeneration, including some variations that appear to protect against the disease as well as others that appear to increase the risk. The researchers also created a computer model to predict whether a person will develop macular degeneration based on which genes they have. The model's predictions are accurate 50 to 75 percent of the time, the study showed.

BOTTOM LINE: Two genes important to the immune system appear to be involved in macular degeneration. It may be possible to determine an individual's risk for this disease based on their genes.

CAUTIONS: This study suggests that certain genes are associated with macular degeneration, but it does not prove that these genes cause the disease. Other factors -- such as smoking history -- may be what is responsible for the development of macular degeneration rather than specific genes.

WHAT'S NEXT: More work is needed to determine the physiologic mechanisms, if any, by which these genes lead to macular degeneration.

WHERE TO FIND IT: Nature Genetics, March 5, 2006

MICHAEL E. HOCHMAN