New York Times, January 2013
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In November, a team of biologists journeyed to Maria Island, three miles off the Australian island state of Tasmania, taking with them 15 plastic cylinders. They loaded the cylinders into S.U.V.’s, drove them to an abandoned farm and scattered them in the fields.

Before long 15 Tasmanian devils emerged from the containers, becoming the first ever to inhabit the island.

“All indications are that they’re doing very well,” Phil Wise, a government wildlife biologist who leads the project, said of the devils — fierce-looking, doglike marsupials that have become an endangered species on the much larger island for which they are named.

This spring the team plans to take more devils to Maria (pronounced ma-RYE-uh). The goal is to establish a healthy colony that will endure for decades to come. The stakes of the project are high: the survival of the entire species may depend on it.

Many species are threatened with extinction, but the Tasmanian devil faces a singular enemy: an epidemic of cancer. A type of facial tumor has in effect evolved into a parasite, with the ability to spread quickly from one devil to another, killing its victims in a few months.

“We have very little time to save the species,” said Katherine Belov, a biologist at the University of Sydney.

An international network of biologists has spent the past decade figuring out this new kind of disease. “It’s been quite a struggle just to learn some of the basics,” said Elizabeth Murchison, of the University of Cambridge in England.

But recently Dr. Murchison and other experts have gained important insights into how the cancer evolved into a parasite. Some scientists are now trying to translate that knowledge into a treatment, perhaps a cancer vaccine.

There is no guarantee that these projects will save the devils, so Mr. Wise and his colleagues are setting up a drastic Plan B: they are establishing Maria Island as a cancer-free refuge for wild Tasmanian devils.

Then, if the devils die out in Tasmania, Dr. Belov said, “the disease will be gone from the mainland, and then they can be introduced back in the wild.”

Biologists first encountered the cancer in the late 1990s. The tumors grew on the devils’ faces or inside their mouths, and within six months the animals were dead. The first cases appeared in eastern Tasmania, and with each passing year the cancer’s range expanded westward.

When scientists examined the cells in the tumors, they got a baffling surprise. The DNA from each tumor did not match the Tasmanian devil on which it grew. Instead, it matched the tumors on other devils. That meant that the cancer was contagious, spreading from one animal to another.

There are only a few reports of humans developing cancer from other people’s tumors hidden in transplanted skin or other organs. Only one other example of contagious cancer is known from the natural world, a tumor in dogs.

Dr. Murchison led a team of researchers who sequenced the entire genome of two tumor cells. They published the sequences last February, and since then they have launched a project to sequence hundreds more genomes of Tasmanian devil facial tumors.

Their studies and others like them are revealing how the Tasmanian cancer got its start. It probably originated in the 1980s or early 1990s in a single animal, most likely a female. A nerve cell in her face underwent a drastic mutation: its chromosomes shattered and then stitched themselves back together.

“The cell was still able to function, because there wasn’t too much DNA lost,” Dr. Belov said. “It’s a bit of a freak of nature.”

The cancer then spread to other devils by taking advantage of their behavior. The animals frequently fight, biting their opponents’ faces. During these battles, Tasmanian devils sometimes bite off bits of a tumor. The cells slip into the attacker’s own bloodstream and travel to its face. There they grow a new tumor.

Dr. Murchison and her colleagues have identified some 20,000 mutations in the tumors that are not found in normal Tasmanian devil DNA. But they do not know which of those mutations originally gave rise to the cancer.

Recent research is revealing that the cancer has been evolving. “Up until a year ago we thought the tumor was completely stable,” Dr. Belov said. “But now we know that’s not the case.”

She and her colleagues recently examined cancer cells collected from Tasmanian devils in 2007 and 2008, comparing them with cells collected from 2010 to 2012. They surveyed molecular caps that cover some genes, known as methylation marks. These marks can keep genes from producing proteins.

In the Jan. 7 issue of Proceedings of the Royal Society B, Dr. Belov and her colleagues reported that recent cancers have fewer methylation marks than older ones, suggesting that the cancer cells are unmuzzling genes and using their proteins to spread more efficiently. The cancer, she and her colleagues wrote, “should not be treated as a static entity, but rather as an evolving parasite.”

Until recently, most scientists believed Tasmanian devils were uniquely vulnerable to contagious cancers. They have very little genetic diversity, and so they might not be able to recognize a tumor as foreign.

But if that were the case, their immune systems would not reject tissue from other devils. In fact, however, when devils were given skin grafts, “they all rejected really nicely,” said Alexandre Kreiss, a research fellow at the Menzies Research Institute in Tasmania. “So we knew then there was something else to the tumor.”

Instead, it turns out, the cancer cells camouflage themselves. They have stopped making a molecular identity badge that mammal cells normally produce.

All of the scientists studying the tumors know that they cannot afford to dawdle. The cancer has already wiped out 84 percent of the Tasmanian devil population and shows little sign of slowing. “You feel that the clock is always ticking,” Dr. Murchison said.

But she sees some reasons for hope. In the far northwest corner of Tasmania, for example, a population of devils shows signs of resisting the cancer. Some of the animals appear to have destroyed their tumors. As a result, only about 20 percent of the devils there have died.

If the devils do not escape the cancer on their own, scientists may be able to help them. “I think the potential for a vaccine is pretty good if we can understand what is going on there,” Dr. Murchison said.

But Dr. Kreiss warns that with 35,000 devils left in the wild, no vaccine can be a panacea. “Even if we had a perfect vaccine, we’d probably have to vaccinate every animal more than once,” he said. “I don’t see us doing that for the whole population.”

In case no medicine works, the federal and Tasmanian governments are quarantining a so-called “insurance population” of devils. The program now has 500 cancer-free Tasmanian devils in zoos and sanctuaries. It is to ensure they do not become too tame to survive on their own that Mr. Wise and his colleagues are establishing the wild population on Maria Island.

While Tasmanian devils are the first species known to be threatened by a contagious cancer, they may not be the last. “It’s quite likely that there are more out there that haven’t been identified,” Dr. Murchison said. “It might have led to the extinction of other species.”

Copyright 2013 The New York Times Company. Reproduced with permission.

Yale Environment 360, January 2013
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It rises from the chimneys of mansions and from simple hut stoves. It rises from forest fires and the tail pipes of diesel-fueled trucks rolling down the highway, and from brick kilns and ocean liners and gas flares. Every day, from every occupied continent, a curtain of soot rises into the sky.

What soot does once it reaches the atmosphere has long been a hard question to answer. It’s not that scientists don’t know anything about the physics and chemistry of atmospheric soot. Just the opposite: it does so many things that it’s hard to know what they add up to.

To get a clear sense of soot — which is known to scientists as black carbon — an international team of 31 atmospheric scientists has worked for the past four years to analyze all the data they could. This week, they published a 232-page report in the Journal of Geophysical Research. “It’s an important assessment of where we stand now,” says Veerabhadran Ramanathan of the Scripps Institution for Oceanography, an expert on atmospheric chemistry who was not involved in the study.

The big result that jumps off the page is that black carbon plays a much bigger role in global warming than many scientists previously thought. According to the new analysis, it is second only to carbon dioxide in the amount of heat it traps in the atmosphere. The new estimate of black carbon’s heat-trapping power is about twice that made by the Intergovernmental Panel on Climate Change in 2007.

This result suggests that cutting black carbon emissions could go a long way to slowing climate change. But the authors of the new study warn that we’ll need to be careful about the sort of black carbon we choose to cut. “There’s a significant potential, but you have to be very targeted,” said co-author Sarah Doherty of the University of Washington.

Soot is made up of tiny dark particles. When it rises from fires, it mixes with dust, sulphates, and other material rising from the ground. As it ascends through the atmosphere, it can drift into clouds, mixing with the water droplets. Rain and snow then wash out the black carbon particles and bring them back to Earth.

Along the way, black carbon exerts all sorts of influences, some of which help warm the atmosphere and some of which cool it. When sunlight strikes black carbon, its dark hue causes it to heat up, something like the way a black tar roof gets hot on a sunny day. When black carbon falls on ice and snow, it smudges their bright white reflective surfaces. As a result, less sunlight bounces back out to space, leading to more warming.

In clouds, black carbon has a dazzling number of effects. “The more we study it, the more mechanisms people find,” says Doherty.

If black carbon heats up the layer of the atmosphere where clouds are forming, for example, they will evaporate. They can no longer reflect sunlight back into space, and so the soot-laced clouds end up warming the atmosphere. But black carbon that hangs above low-lying stratocumulus clouds has a different effect. It stabilizes the layer of air on top of the clouds, promoting their growth. It just so happens that thick stratocumulus clouds are like shields, blocking incoming sunlight. As a result, black carbon also ends up cooling the planet.

All these effects depend, ultimately, on how much soot is in the air, which, in turn, depends on the many different kinds of sources of soot all over the world. Estimating that flux is a major challenge, and so it’s not too surprising that different teams of scientists have ended up with markedly different estimates for the net effect of soot on the climate.

In 2009, Doherty and her colleagues set out to make careful estimates of all sources of black carbon, using data from monitoring stations around the world. They then ran computer models of the atmosphere to measure the effects of the black carbon, based on what scientists have learned about chemical reactions in clouds from experiments and observations. Along with the effect that soot had on clouds, the scientists also estimated the total amount of warming that occurred as the soot directly absorbed sunlight, and as it darkened snow and ice.

After the scientists had taken into account all of these effects, they tallied them up to calculate how much extra energy was being stored in the
“It took a while to convince ourselves it was correct,” a co-author of the study says.
atmosphere thanks to black carbon. Climate scientists typically express that energy as watts per square meter of the Earth’s surface. The number they got — 1.1 watts — was enormous. Carbon dioxide, the biggest heat-trapper in the atmosphere, is responsible for an estimated 1.56 watts per square meter. Black carbon takes second place. “It took a while to convince ourselves it was correct,” says Doherty.

If black carbon is responsible for trapping so much heat, then reducing soot may be an effective way to slow down the planet’s warming. It’s even more attractive because black carbon washes quickly out of the atmosphere, and so reducing soot emissions would lead to a fast fall in the concentration of black carbon in the atmosphere. Carbon dioxide, by contrast, lingers for centuries in the atmosphere.

James Hansen of the Goddard Institute for Space Studies has been arguing for such a strategy for over a decade. But the new study reveals a paradox in reducing soot to fight global warming. If tomorrow we could shut down every brick kiln, every burning farm field, and every other source of soot, we would, on balance, have no effect on global warming whatsoever.

How can this be? Because when things burn, black carbon is not the only thing they produce. A forest fire produces black carbon as well as organic carbon molecules. The forest fire black carbon helps to warm the planet, but the organic carbon creates a haze that blocks sunlight, cooling the atmosphere. The two emissions cancel each other out. “In the real world you can’t just get rid of black carbon emissions,” says Doherty. “You get rid of other things as well.”

But Doherty and her colleagues found that some sources of soot — including coal and diesel fuel — produce a lot of warming with very little compensating cooling. They suggest that these sources should be the top priority for efforts to fight global warming.

Diesel fuel looks to be an especially ripe target. “That message is loud and clear,” says Ramanathan. Making diesel an even more attractive candidate for attack is the fact that reducing much of its black carbon emissions might simply be a matter of upgrading old, soot-spewing engines with newer technology. Developing countries, in particular, could put in place regulations about burning diesel to upgrade their rapidly growing auto fleets.

Coal is another potent source of warming from soot, the scientists found, whether burned industrially or at home. So are the small stoves that billions of people use to cook. Fueled by wood or coal, they spew billows of sooty smoke. Engineers in recent years have designed efficient, cheap stoves that release much less black carbon. Getting those stoves into people’s homes would take a lot of warming soot out of the atmosphere.

Doherty does not see her new study as the end of the story. While she and her colleagues conclude that soot most likely produces 1.1 watts per square meter, they still put a margin of error on their results. They calculate that there’s a 90 percent chance the actual figure falls between .17 and 2.1 watts. To tighten that range, they still need to better understand the many ways that soot alters clouds, and also get a better fix on the amount of soot each source produces. “We need to dig deeper on that,” she says.

Nevertheless, Doherty and her colleagues see many good reasons not to wait for a more precise understanding of soot before taking steps to reduce it. Along with its effect on the global climate, a number of studies also indicate it has powerful influences on some regions of the planet. A lot of soot falls onto the glaciers of Himalayas, for example, speeding up their melting. Millions of people depend on that ice for their water supply. Soot also has a particularly large effect on the circulation of the atmosphere around India, which ultimately reduces the amount of rainfall produced by monsoons.

Even before soot gets far into the air, it has a particularly harmful effect: it makes people sick. In recent days, news reports from China have provided startling images of Beijing swaddled in a blanket of sooty smog. That air pollution, from cars and coal-fired plants, takes a terrible toll on the country’s health. Far from the world’s urban centers, poor people suffer from air pollution in their own homes when they cook with smoky stoves and breathe in black carbon and other pollutants.

These benefits of cutting black carbon were already apparent before Doherty and her colleagues published their new study; now it’s clear that cutting soot could help not just personal health, but planetary health as well.

Copyright 2013 Carl Zimmer

The New York Times, December 5, 2012
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In the rain forests of Costa Rica lives Anelosimus octavius, a species of spider that sometimes displays a strange and ghoulish habit.

From time to time these spiders abandon their own webs and build radically different ones, a home not for the spider but for a parasitic wasp that has been living inside it. Then the spider dies — a zombie architect, its brain hijacked by its parasitic invader — and out of its body crawls the wasp’s larva, which has been growing inside it all this time.

The current issue of the prestigious Journal of Experimental Biology is entirely dedicated to such examples of zombies in nature. They are far from rare. Viruses, fungi, protozoans, wasps, tapeworms and a vast number of other parasites can control the brains of their hosts and get them to do their bidding. But only recently have scientists started to work out the sophisticated biochemistry that the parasites use.

“The knowledge that parasites can manipulate their hosts is old. The new part is how they do it,” said Shelley Adamo of Dalhousie University in Nova Scotia, a co-editor of the new issue. “The last 5 to 10 years have really been exciting.”

In the case of the Costa Rican spider, the new web is splendidly suited to its wasp invader. Unlike the spider’s normal web, mostly a tangle of threads, this one has a platform topped by a thick sheet that protects it from the rain. The wasp larva crawls to the edge of the platform and spins a cocoon that hangs down through an opening that the spider has kindly provided for the parasite.

To manipulate the spiders, the wasp must have genes that produce proteins that alter spider behavior, and in some species, scientists are now pinpointing this type of gene. Such is the case with the baculovirus, a virus sprinkled liberally on leaves in forests and gardens. (The cabbage in a serving of coleslaw carries 100 million baculoviruses.)

Human diners need not worry, because the virus is harmful only to caterpillars of insect species, like gypsy moths. When a caterpillar bites a baculovirus-laden leaf, the parasite invades its cells and begins to replicate, sending the command “climb high.” The hosts end up high in trees, which has earned this infection the name treetop disease. The bodies of the caterpillars then dissolve, releasing a rain of viruses on unsuspecting hosts below.

David P. Hughes of Penn State University and his colleagues have found that a single gene, known as egt, is responsible for driving the caterpillars up trees. The gene encodes an enzyme. When the enzyme is released inside the caterpillar, it destroys a hormone that signals a caterpillar to stop feeding and molt.

Dr. Hughes suspects that the virus goads the caterpillar into a feeding frenzy. Normally, gypsy moth caterpillars come out at night to feed and then return to crevices near the bottom of trees to hide from predators. The zombie caterpillars, on the other hand, cannot stop searching for food.

“The infected individuals are out there, just eating and eating,” Dr. Hughes said. “They’re stuck in a loop.”

Other parasites manipulate their hosts by altering the neurotransmitters in their brains. This kind of psychopharmacology is how thorny-headed worms send their hosts to their doom.

Their host is a shrimplike crustacean called a gammarid. Gammarids, which live in ponds, typically respond to disturbances by diving down into the mud. An infected gammarid, by contrast, races up to the surface of the pond. It then scoots across the water until it finds a stem, a rock or some other object it can cling to.

The gammarid’s odd swimming behavior allows the parasite to take the next step in its life cycle. Unlike baculoviruses, which go from caterpillar to caterpillar, thorny-headed worms need to live in two species: a gammarid and then a bird. Hiding in the pond mud keeps a gammarid safe from predators. By forcing it to swim to the surface, the thorny-headed worm makes it an easy target.

Simone Helluy of Wellesley College studies this suicidal reversal. Her research indicates that the parasites manipulate the gammarid’s brain through its immune system.

The invader provokes a strong response from the gammarid’s immune cells, which unleash chemicals to kill the parasite. But the parasite fends off these attacks, and the host’s immune system instead produces an inflammation that infiltrates its own brain. There, it disrupts the brain’s chemistry — in particular, causing it to produce copious amounts of the neurotransmitter serotonin.

Serotonin influences how neurons transmit signals. Dr. Helluy proposes that the rush of serotonin triggered by the thorny-headed worms corrupts the signals traveling from the eyes to the brain. Normally, an escape reflex causes the gammarid to be attracted to the darkness at the bottom of its pond. Thorny-headed worms may cause their host to perceive sunlight as darkness, and thus swim up instead of down.

Whether humans are susceptible to this sort of zombie invasion is less clear. It is challenging enough to figure out how parasites manipulate invertebrates, which have a few hundred thousand neurons in their nervous systems. Vertebrates, including humans, have millions or billions of neurons, and so scientists have made fewer advances in studying their zombification.

Most of the research on vertebrate zombies has been carried on a single-celled parasite, Toxoplasma gondii. Like thorny-headed worms, it moves between predators and their prey. Toxoplasma reproduces in the guts of cats, which shed it in their feces.

Mammals and birds can pick up the parasite, which invade their brain cells and form cysts. When cats eat these infected animals, Toxoplasma completes its cycle. Scientists have found that Toxoplasma-infected rats lose their fear of cat odor — potentially making them easier prey to catch.

Glenn McConkey of the University of Leeds and his colleagues have found a possible explanation for how Toxoplasma wreaks this change. It produces an enzyme that speeds the production of the neurotransmitter dopamine, which influences mammals’ motivation and how they value rewards. Adding extra dopamine might make Toxoplasma’s hosts more curious and less fearful.

But Ajai Vyas of Nanyang Technological University in Singapore has found evidence that Toxoplasma simultaneously manipulates its hosts in other ways. Infected male rats, he found, make extra testosterone. This change makes the males more attractive to females, and when they mate the males spread the parasite to females.

By causing male rats to make more testosterone, Toxoplasma may do more than spread itself to other rats. Testosterone also tamps down fear. The infected rats may thus become even less concerned when they pick up the scent of a cat.

This research could potentially provide important clues about human behavior. In the case of Toxoplasma, for example, humans can become hosts if they handle contaminated cat litter or eat parasite-laden meat. Some studies have linked Toxoplasma infection with subtle changes in personality, as well as with a higher risk of schizophrenia.

Dr. Adamo, the co-editor of the journal’s new issue, thinks this new science of “neuroparasitology” can offer inspiration to pharmaceutical companies that are struggling to find effective drugs for mental disorders. “A number of the big companies have given up on their neuroscience labs,” she said. “Maybe the parasites can teach us something.”

She points out that the way parasites manipulate brains is profoundly different from drugs like Prozac. “The way that a parasite goes about changing behavior is not the way a neurobiologist would do it,” she said.

A typical drug focuses on just one type of molecule in the brain. Parasites, on the other hand, often launch a much broader attack that still manages to cause a specific change in their host. “Perhaps tweaking several systems simultaneously might give better results than trying to hit one particular system with a sledgehammer,” Dr. Adamo said.

But she added that she and other parasitologists barely understand those zombifying tweaks. “All we know now,” she said, “is they have their own ways.”

Copyright 2012 The New York Times Company. Reproduced with permission.

Discover, December 2012
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I am sitting in a darkened, closet-size lab at Tufts University, my scalp covered by a blue cloth cap studded with electrodes that detect electric signals from my brain. Data flow from the electrodes down rainbow- colored wires to an electroencephalography (eeg) machine, which records the activity so a scientist can study it later on.

Wearing this elaborate setup, I gaze at a television in front of me, focusing on a tiny cross at the center of the screen. The cross disappears, and a still image appears of Snoopy chasing a leaf. Then Charlie Brown takes Snoopy’s place, pitching a baseball. Lucy, Linus, and Woodstock visit as well. For the next half hour I stare at Peanuts comic strips, one frame at a time. The panels are without words, and while sometimes the action makes sense from frame to frame, at other times the Peanuts gang seems to be engaging in a series of unconnected shenanigans.

At the same time, a freshly minted Ph.D. named Neil Cohn is watching the readout from my brain, an exercise he has repeated with some 100 subjects to date. Many people would consider tracking Peanuts or Calvin and Hobbes comic strips unworthy of scientific inquiry, but Cohn begs to differ. His evidence suggests that we use the same cognitive process to make sense of comics as we do to read a sentence. They seem to tap the deepest recesses of our minds, where we bring meaning to the world.

Comics have been part of Cohn’s life as long as he can remember. He was drawing them by age 8. As a teenager he began to sell his own comics–a graphic novel about two people falling in love in one case, a dreamy series of meditations about philosophy in another. By the time he entered the University of California, Berkeley, as an undergraduate, he was a regular at Comic-Con, the gigantic annual comic book and fantasy convention in San Diego. “If you had asked my friends if I would end up as a scientist,” he says, “they would have all said, ‘No way.’ ”

That changed at Berkeley, where Cohn discovered linguistics. He was fascinated by how our brains find meaning in strings of words. Individual languages differ in terms of particular words and grammar, but all are just systems for building sentences. You could split any sentence into smaller units–the subject and the predicate, for example–and these could be broken down into smaller units still.


This hierarchy of big units and small ones helps make language both versatile and easy. Even though each of us has only a finite number of words in our brain (100,000 or so), we can use the rules of language to combine them into a practically endless number of sentences, conveying an infinite set of meanings.

“I started making connections between what was going on in language and what was going on in comics,” Cohn says. A comic strip is a string of panels, just as a sentence is a string of words. From Cohn’s own experience designing comic strips, he was convinced that both followed a similar set of rules. “Sequential images have a grammar like sequential words do,” he says.

It further seemed to Cohn that comic strips are made up of smaller units, just as sentences are. The narrative arc of a comic strip is made up of an initial group of panels that set up the story, followed by those that convey a narrative peak. These units, in turn, are made up of smaller units that accomplish other tasks, like establishing new characters and resolving conflicts.

Cohn suspected this was no coincidence: Comic strip artists were unwittingly exploiting the brain’s grammar- generating function. “The brain is processing these different kinds of grammars in a common way,” Cohn says.

After this epiphany, Cohn decided to go to graduate school and become a cognitive scientist who studied comics. And he knew whom he wanted to study with: Ray Jackendoff, a linguist then at Brandeis University who had done some of the most important research into language’s hierarchy.

Cohn wrote to Jackendoff, asking if he would take on a student who wanted to study how people’s brains make sense of comics. But Jackendoff couldn’t do it at the time. Crestfallen, Cohn applied to other graduate schools instead, supporting himself in the meantime by drawing comics.

As the years passed, his pile of grad school rejection letters grew. In a typical one, Cohn was informed that he was a great candidate, but there was no way a comic book artist could fit in to the school’s graduate program. Cohn’s ideas were just too far off the map.

After four years of such replies, Cohn was close to giving up. But then he heard that Jackendoff had just moved from Brandeis to Tufts to direct its Center for Cognitive Studies. Cohn worked up the courage to send a second letter. To his surprise, Jackendoff invited him to earn a Ph.D. with him.

In 2006 Cohn came to Tufts and began his experiments. To test his hypothesis that the brain uses a visual grammar to make sense of comics, he designed a series of experiments that updated some classic language studies. In one set of experiments, subjects read sentences in different forms while wearing an EEG cap. Some of the sentences were grammatically correct, while others were scrambled.

When subjects encountered a sentence with an unexpected grammatical error, EEG readings picked up a distinctive signal: The voltage in an area of the left brain briefly dropped. Scientists call this drop, which takes place directly over the left temple, 
the “left anterior negativity” and see it as a sign the brain is struggling to make sense of a sentence with a scrambled structure.


The Peanuts strips that Cohn showed me also came in different forms. Some combined Charles Schulz’s original panels to make strips that made sense. (Cohn selected comics with little language in them and stripped out any speech bubbles, so that his subjects wouldn’t be processing language as well as the images.) In other cases, Cohn jumbled panels from different strips so that they had none of the ordinary structure found in comics–the visual equivalent of stringing together a randomly chosen set of words. Cohn found that subjects experienced the left anterior negativity effect when they were shown the random panels, just as if they were reading sentences with grammatical errors.

The most tantalizing result of Cohn’s study (recently published in Cognitive Psychology) emerged when he showed subjects panels arranged so that they had a narrative arc but didn’t add up to a meaningful story. They were the equivalent of grammatically correct but meaningless sentences. The linguist Noam Chomsky, who published pioneering ideas about language in the 1950s, offered a famous example of such a sentence: “Colorless green ideas sleep furiously.”

Cohn found that when he showed subjects such “colorless green” panels, they experienced a weaker left anterior negativity response than when they read garbled panels. The result suggests that although participants struggled to understand the panels, they still recognized an underlying logic to them, supporting the idea that we depend on a visual grammar in comics in order to make sense of them.

Cohn has gotten similar results from other experiments in which people had to press a button every time they saw one particular panel in a strip. It took them longer to hit the button if the strip was a random jumble than if it was in its original order. If the strip was “colorless green,” on the other hand, people could press the button at an intermediate speed.

“People are able to predict what’s coming next,” Cohn says, “even if there’s no meaning to it.”

Cohn hopes his research will bring a deeper appreciation of comics as more than entertainment. He sees them as windows to the evolution of fundamental structures in the human mind, which is wired to use strings of signals to communicate. Sometime more than 50,000 years ago, our ancestors evolved the ability to string spoken words together. Much later, they used that ability to create written language. But Cohn has shown that the same cognitive processes also gave rise to a visual language–one that can be found on the comics pages in American newspapers, in Japanese manga, and in many other forms.

English and Japanese are not identical, of course; despite being based on the same underlying rules of grammar, they have developed into different languages. Cohn sees the same cultural changes driving different styles of graphic storytelling. When he is not recording brains, Cohn is comparing comics from different cultures to learn 
how this diversity springs from a universal biology.

“My goal is to create a field of study for this stuff,” he says.

Copyright 2012 Carl Zimmer

Discover, November 2012
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Ian Reid, a psychiatrist at the Royal Cornhill Hospital in the Scottish city of Aberdeen, has treated people with severe depression for 25 years. “It’s a very nasty illness, depression,” he says. “I have worked with people who have cancer and depression, and more than one of them has said, ‘If I had to choose one of those two diseases, I’d go for the cancer.’ ”

When patients come to Royal Cornhill with major depression, they’re first treated with psychotherapy and antidepressants. Only about 40 percent respond to their first medication. Sometimes a different one will do the trick, but in Reid’s experience, about 10 to 20 percent of depressed people respond to no drug at all. In those cases, Reid regularly shifts to a third option. It’s officially called electroconvulsive therapy, or ECT– better known by its unofficial name, shock therapy.

Reid is an expert on ECT, and over the years he has received plenty of grief for it. “There are people on the Internet who describe me as a Nazi, as a barbarian,” he says. “And there’s one person who suggested I should get ECT so I know what I’m doing.”

Reid is not surprised by the reactions. For many people, the sum of their knowledge about ECT comes from the 1975 movie One Flew Over the Cuckoo’s Nest. Jack Nicholson plays Randle McMurphy, a criminal hoping to escape hard labor by spending his term in a mental institution. But McMurphy gets more than he bargained for, including a harrowing session of ECT. The hospital staff straps him down, puts a piece of rubber in his mouth so he won’t bite off his own tongue, and delivers a blast of electricity to his temples. He writhes in agony and then slumps back, his body limp.

That scene bears no resemblance to what Reid does for his patients. For one thing, he gives them anesthesia and muscle relaxants so they don’t experience any flailing. But most crucially, ECT works. “You can watch someone going from being unresponsive and soiling themselves to being completely transformed,” Reid says.

In Scotland, a country of 5 million, 400 people receive the treatment each year. And for about 75 percent of them, it brings relief. “ECT outperforms psychotherapeutic treatments and antidepressant drugs,” Reid notes. Yet its effectiveness is a mystery. “It doesn’t sound intuitive at all,” he admits. “Making someone have a seizure, giving them an electric shock, and making something as complex as depression better just seems crazy.”

Fortunately, we don’t have to understand why a treatment works before using it. “Captain Cook was handing out limes to his crew for scurvy before anyone knew what vitamin C is,” Reid says. But since ECT is so invasive, and since its effects can fade, he has long wanted to figure out how shock therapy works, in the hopes of tapping the same mechanism to find a longer-lasting, less arduous means of beating back depression. “Always in the back of my mind has been the thought that it would be awfully nice to know what was going on here,” he says.

Doctors in Italy first used electroconvulsive therapy in 1938 to treat schizophrenia; in the decades that followed, the treatment spread to other countries and other disorders, especially depression. Although ECT was clearly effective, it could be a frightening experience. Patients remained conscious until their seizures made them black out. Sometimes they broke bones during the process. In the 1960s, psychiatrists added anesthesia and muscle relaxants to ECT to eliminate some of this trauma, but memory loss was still a common complaint. Amnesia became less of a problem in the 1980s, when pulses were reduced to brief, sharp stimulations.

By the 21st century, the negatives surrounding ECT had been mitigated to a large degree. In a 2010 study, Maria Semkovska and Declan M. McLoughlin of Trinity College in Dublin reviewed 84 studies of 2,981 patients who received ECT. The only significant memory troubles they found occurred within three days after treatment; by 15 days, the patients’ memories actually improved.
With safety questions put to rest, Reid and his colleagues have been trying to find out how ECT works. Beginning in 2009, they used functional magnetic resonance imaging (fMRI) to scan the brains of patients prior to treatment for depression; they then followed the patients through the course of therapy, generally for four weeks. Successfully treated patients, nine in all, returned for follow-up scans. Reid knew from previous studies that depression reduces the size of certain brain regions, including the hippocampus and gray matter, both generally implicated in emotion. After ECT, Reid’s team measured the volume of each subject’s brain. The researchers found an increase in hippocampus size but not in gray matter.

They also investigated a second, potentially more significant change: how ECT altered the brain’s ability to talk to itself. Each region of the brain specializes in certain mental tasks. The hippocampus, for example, helps us encode and retrieve memories. If we try to recall a memory while lying in an fMRI scanner, the machine can detect extra activity occurring in the hippocampus.

If brain regions are like self-contained computers, then the brain as a whole is a computer network. The activity in one region is influenced by neurons sending signals from other regions. This communication can lead two regions to work together closely. When one region is active, so is the other; when one is quiet, the other tends to be as well.

An effort to establish the relationship between this interconnectivity and neuropsychiatric disease was already under way. Researchers found that some disorders, including schizophrenia and Alzheimer’s disease, appear to alter the connectivity of certain networks. In 2010 University of Aberdeen neuroscientist Christian Schwarzbauer measured brain connectivity in people who have lost consciousness. He found that the connectivity of people in permanently vegetative states turns out to be different from that of people who eventually regain awareness.

In 2011 Schwarzbauer teamed up with Reid on a new ECT study. His job was to analyze the brain scans for changes in connectivity. It would be the first time anyone looked for such a link and also the first time Schwarzbauer used a new method he had devised for measuring connectivity. Typically neuroscientists select a few large regions of the brain to study before they start their experiment. They then compare the activity in these regions by measuring the flow of blood into them. Schwarzbauer came up with a way to conduct a much more fine-grained survey. Instead of picking out regions in advance, he divided the entire brain into 25,000 chunks. He then measured the links among all of them, looking for significant changes before and after ECT.

This approach revealed much more than Reid’s study of brain size. “The communication structure of the brain dramatically changed after treatment,” Schwarzbauer says. ECT weakened the same connective network in all nine patients–a network that surrounds a single hub located above the left eye, in a brain region called the left dorsolateral prefrontal cortex.

Reid and his colleagues didn’t know it at the time, but in St. Louis another team was also studying the connectivity of depression. Yvette Sheline and her colleagues at Washington University scanned the brains of 18 people with major depression and compared them with the brains of 17 healthy individuals. They found evidence that in depressed people, the network centered on the left dorsolateral prefrontal cortex was “hyperconnected.”

When Reid and Schwarzbauer found out about Sheline’s research, it got them thinking about how ECT rewires the brain. When people are depressed, they speculated, these hyperconnected regions might bounce thoughts back and forth around the brain. “This could cause an internal information overflow,” Schwarzbauer says, making it hard to process external information. By getting rid of those hyperconnections, ECT might let depressed people get out of their own head.

Reid is testing this hypothesis by following his patients and waiting to see if they relapse. If he and Schwarzbauer are right, a relapse ought to include the detectable return of hyperconnectivity in the depression network.

Reid’s study leaves unanswered the question of how a jolt of electricity gets rid of hyperconnections. But he hopes that brain scans and other sophisticated methods will eventually reveal how ECT works. From there, it might be possible to come up with a less invasive way to get the same effect.
“If you could put it in a bottle,” Reid says, “that would be great.”

Copyright 2012 Carl Zimmer