Experiments that elude the senses

Mind / Body
Researchers in Sweden have found a way to trick sensory perceptions so that test subjects experience the body of a mannequin - or even the body of another person - as their own.

The experiment, conducted by cognitive neuroscientists at the Karolinska Institute in Sweden, sounds like a strange party prank. A mannequin was outfitted with small television cameras for "eyes" and a volunteer wore a head-mounted display over his eyes to allow him to see, through closed circuit television, what the mannequin was "seeing." When both mannequin and man tilted their heads downward, the human saw the mannequin's abdomen rather than his own.

Using a short rod in each hand, a researcher standing between the volunteer and the mannequin stroked the abdomens of both at the same time. Volunteers reported that the stroking sensation combined with the visual image created a powerful illusion of having swapped bodies.

To test the illusion, researchers "threatened" the mannequin's abdomen with a knife and measured the volunteer's skin conductance response, a measure of anxiety used in polygraph testing. The anxiety response was significantly higher than when researchers substituted a non-threatening object - a spoon - of similar size.

In another experiment, the mannequin was replaced by a researcher wearing the TV "eyes." When the researcher and volunteer shook hands, the volunteer experienced a vivid illusion that the experimenter's arm was the volunteer's own arm.

"This shows how easy it is to change the brain's perception of the physical self," says Henrik Ehrsson, who led the project. "By manipulating sensory impressions, it's possible to fool the self not only out of its body but into other bodies too."

BOTTOM LINE: Human sense of self can be shifted from one body to another.

CAUTIONS: It was not possible to fool the self into identifying with a nonhuman-like object.

WHAT'S NEXT: Using the techniques to advance virtual reality and robot technology.

WHERE TO FIND IT: The online, open-access journal Public Library of Science, or PLoS ONE

LEIGH HOPPER

OBERHOLZER

Sickle cell anemia, the most common inherited blood disorder, affects 70,000 people in the United States and millions worldwide. Patients with the disease have a mutation in hemoglobin, the protein normally responsible for supplying the body with oxygen. Failure in oxygen transport causes repeated attacks of severe pain, and increased risk of stroke and organ failure. Current therapies do not work consistently for everyone and can have serious side effects. Now, according to a new study led by Dr. Stuart Orkin from the Children's Hospital Boston, Vijay Sankaran, an MD-PhD student in Orkin's lab, as well as collaborators at the Broad Institute of Harvard and MIT, a gene called BCL11A has entered the spotlight as a potential drug target for treating sickle cell patients.

Researchers found when they switched off the gene, blood cells reverted to making a form of hemoglobin seen in babies, called hemoglobin F. Cranking up hemoglobin F production could make up for the faulty hemoglobin, ultimately allowing for better oxygen transport to tissues.

"Ideally, we could take cells that predominantly make hemoglobin F, and transplant them into the patient's bone marrow," says Orkin, who went on to suggest that a useful therapeutic strategy stemming from this discovery may not be far away.
BOTTOM LINE: Shutting down the gene BCL11A causes increased production of hemoglobin F - a form of hemoglobin that compensates for the defective hemoglobin present in patients with sickle cell anemia.
CAUTIONS: These studies were done on cells, rather than in patients with sickle cell disease.
WHAT'S NEXT: Translating these findings into a useful treatment strategy.
WHERE TO FIND IT: Science, Dec. 4, 2008. SUSHRUT JANGI