A sense-mixing condition in which people taste colors or see smells tends to run in families, and recent studies have homed in on a selection of genes that may contribute to the phenomenon, called synesthesia. Understanding the condition’s genetic basis might reveal why it has perpetuated in humans and help scientists develop cures for degenerative neurological diseases.
Only about 3 percent of the population claim to experience some form of synesthesia, but nearly half of those report having a close family member whose senses become similarly entangled. “We know that synesthesia tends to travel in families,” says experimental psychologist David Brang of the University of California, San Diego who, along with V.S. Ramachandran, discusses synesthesia genetics in an article published online November 22 in PLoS Biology.
But children often exhibit different forms of synesthesia than do their parents. This “complicates the picture and hints at the idea that more than one gene is involved,” says Brang.
A recent study led by neuroscientist David Eagleman from the Baylor College of Medicine in Houston zeroed in on a region on chromosome 16, which he and his colleagues believe holds the gene responsible for the most common form of the condition, colored sequence synesthesia (where letters and numbers are associated with a specific color). “We don’t know which gene it is yet, but we’re getting closer every day,” says Eagleman, who published his findings September 30 in Behavioural Brain Research.
It’s possible that the gene Eagleman’s group and others are searching for helps “prune” connections in the brain, Brang suggests. Synesthesia may result from a defect in such a gene, leading to insufficient regulation or removal of the brain’s many neural bridges. “It could be that everyone is born with global connectivity in the brain, and over time most undergo a refining process,” says Brang. Synesthetes may retain pathways linking different parts of the brain that most people shut down as they get older.
Another theory suggests synesthesia is caused not by excess wiring, but by a shift in the brain’s balance of chemicals. “Synesthesia waxes and wanes depending on if a person is extremely tired or if they’re on drugs,” Eagleman says. Furthermore, people can have synesthetic experiences if they take hallucinogens or if they suffer severe damage to one sense. To him this suggests that everyone has the neural circuitry connecting the senses, and that people with synesthesia just happen to have innately stronger linkages in the brain.
Brang believes that a combination of both a faulty pruning gene and a unique chemical mixture — usually treated as dueling hypotheses — could cause senses to collide more frequently and dramatically in synesthetes.
Continued study of synesthesia could also provide a more complete picture of how a genetic change spins its way up to a change in brain function, and potentially help solve some major medical issues. “Synesthesia provides a very powerful inroad into learning how different brain areas interact with each other,” says Eagleman. “And a lot of interesting diseases have to do with networking problems in the brain.”