The term “artificial intelligence”, was coined in the summer of 1956, on the bucolic grounds of Dartmouth College in Hanover, New Hampshire. There, John McCarthy (who would later go on to teach at Stanford), Marvin Minsky, Claude Shannon, Nathan Rochester and six other conference participants came together to lay out the framework for this exciting new field which would “…find how to make machines use language, form abstractions and concepts, solve kinds of problems now reserved for humans, and improve themselves.” (McCarthy et al., 1955)

Though it was McCarthy who persuaded his nine other colleagues at the conference to adopt the term “artificial intelligence” to describe the nascent field, the seeds of artificial intelligence were planted earlier. Alan Turing, who was instrumental in breaking the German’s Enigma code during WWII, published a paper in 1950 that laid out what came to be known as the “Turing Test:” if a machine could carry out a conversation with a human in such a sophisticated manner as to trick the human into thinking that he or she was conversing with another human, then the machine would have displayed true “intelligence.”

But nearly 60 years later, the world still awaits a machine capable of exhibiting “general A.I.”, instead of the “narrow A.I.” demonstrated by IBM’s chess-playing Deep Blue or Stanford University’s Stanley, an autonomous robotic vehicle, or other impressive albeit limited applications of A.I. For example, Deep Blue may be able to beat Gary Kasparov at chess but can it beat a 10 year-old at a game of checkers? The lack of a general A.I. is made even more stark when juxtaposed with Moore’s Law, a maxim that goes back to 1965 when Intel founder Gordon Moore postulated that the number of transistors on a computer chip would double roughly every 18 months.

There’s even a term - “Singularity” - that is being used to describe the moment when technological progress will leapfrog and herald the creation of computers that not only achieve human-like intelligence, but also give rise to a progeny of computers who will be smarter then their digital forbears. Though he didn’t coin the term (sci-fi writer Vernor Vinge did), the most famous exponent of this belief is inventor Ray Kurzweil. He places the Singularity as occurring sometime before 2050 and believes that with the advent of this unheralded technological progress, mankind may solve some of our society’s most pressing ills, such as global warming, and even conquer death, by uploading one’s consciousness into a virtual medium.

Though this seems a far stretch from engineering a domestic robot like Stanford’s Artificial Intelligence Robot, top A.I. researchers like Stanford’s Andrew Ng and Daphne Koller do believe that computing systems will some day be as smart or smarter than humans. When I spoke with Dharmendra Modha about his work into cognitive computing at IBM, he talked effusively about creating an “i-Brain,” a digital accessory that people could carry around, making decisions and processing information like its human cousin. But if you’re like me, and lament those moments when you’ve misplaced your keys or other instances of poor neural performance, you can’t help but think that such a device can’t arrive soon enough. On second thought, I’ll wait until v2.0 hits the shelves.

Watch the Artificial Intelligence: Thinking Big television story report online.

And don’t miss our Web Extra: A Dose of A.I. In this QUEST web exclusive, Stanford University computer science professor and artificial intelligence (A.I.) researcher Daphne Koller provides an elegant explanation of how A.I. can be employed in the examining room to diagnose a patient’s illness more accurately than a human clinician. Find out more and learn how medical diagnosis is just the tip of the iceberg when it comes to tasks that rely on making sense of a sea of data to arrive at an informed conclusion.

This is the second of two stories born out of an afternoon at UCSF’s Memory and Aging Center, where a team of scientists, led by Dr. Bruce Miller, is trying to tease out the differences between as many as 200 dementias that affect aging brains.

The two stories have a lot in common: Both introduce us to people who have lived with extremely difficult degenerative diseases: ALS in “Decoding the Emotional Brain,” and frontotemporal dementia in this week’s story. Both open up provocative questions about human nature. And neither would have happened without the generosity of a Northern California family – in this case, Cassandra Shafer, who drove down from Forestville with her daughter, Columbia, to tell me about Cassandra’s husband and Columbia’s father, Keith Jordan.

In these video clips, you meet Keith Jordan in the second half of his disease, after doctors at UC Davis and UCSF diagnosed him with frontotemporal dementia. The videos were taken at UCSF over the course of many hours doctors spent studying Keith and his symptoms. In them, we glimpse of two of Keith’s FTD-caused obsessions: joke telling and music. (We also see one of the first symptoms to have emerged: his Jerry Garcia hairdo.)

At first glance, Keith’s behavior might strike you as more eccentric than brain-damaged, which is precisely why FTD can take so long to diagnose. If you’re a doctor with a 15-minute appointment slot, frontotemporal dementia might just look like a midlife crisis. What we don’t see in the video clips are the five heartbreaking years that Cassandra spent trying to figure out what was happening to her husband – a search that included marriage and career counseling, the full gamut of conventional western specialists, yoga, meditation, chelation therapy, replacing every household cleaning product, every pot and pan, all the way to shamanic soul retrieval and exorcism – all while his behavior grew more erratic and difficult to be around. It’s impossible to overstate the drain – both emotional and financial — that this search brought on Keith’s family.

Keith died in May and Cassandra is still, she says, “inching her way” out of the “foreign land” that FTD plunged her into. As unlikely as it sounds, I think she takes some comfort in the fact that Keith’s illness also gave doctors a chance to explore profound questions about human nature and the extent to which the structure of our brains determines who we are.

FTD can turn Democrats into Republicans, and vice versa. People with no interest in art begin to paint obsessively. As the neurons in Keith’s right frontotemporal lobe (just behind the right eyebrow) died, his taste in music, his sense of humor, his relationships with his family members and friends changed completely. Our self, in other words, may owe much more to the way our brains are built than we’d care to acknowledge.

And what to make of the fact that this same part of the brain that shapes personality is also responsible for reading other people’s reactions? People with some forms of FTD can’t empathize with others (hear more about this in our slide show about FTD and art) or read the emotion on another person’s face. Not only do they experience radical personality changes, but they lose the ability to sense others’ reactions to them. In other words, how we define ourselves – whether we consider ourselves funny, smart, ambitious — seems to have everything to do with how others define us. We are all, in other words, people people.

Which begs the question: What about people raised in isolation, without the critical feedback loop of social interaction? What does FTD tell us, for example, about children who have been deeply neglected in orphanages? Or – taking another angle entirely — autistic people, who have trouble empathizing with others? What does self-perception look like in those who can’t perceive those around them?

If all this is giving you a headache, you might spend some time exploring the web extras we’ve produced for these two stories. Here, Bruce Miller explains why frontotemporal dementia can bring with it an artistic renaissance. And here, we introduce you to Matt Cheney and find out what his compulsive laughing and crying jags might reveal about emotion and the human brain.

Then use our blog, below, to let us know what you think.

Listen to the Beyond Alzheimer’s radio report online, and watch our Web Extra: Dementia and Artistic Renaissance slideshow.

Scientists have created a mouse that doesn’t get as fat on a high fat diet.

You read that right. In a new study out in Nature Neuroscience, scientists tinkered with a single gene in a mouse and made it less likely to get fat. Finally I can eat as many Double Stufs as I want without worrying about gaining weight. If scientists can turn what they’ve learned into a pill, that is.

How’d the researchers do it? By changing one part of the mouse’s brain, the hypothalamus. One of the hypothalamus’ many jobs is body weight regulation. So it was a logical place to start.

The scientists couldn’t go in with a wrecking ball and tear the hypothalamus apart. It is an important part of the brain with lots of different duties. They needed to something pretty subtle so the mice would survive but be thinner.

What they did was to keep certain cells in the hypothalamus from being able to release a neurotransmitter called GABA. This was enough to make a mouse better able to maintain a lower weight.

This study suggests that GABA’s normal job in the hypothalamus is to keep mice (and probably us) from burning too much energy. Makes sense in the wild. But is quite a pain in my cubicle.

Now, we can’t go changing human genes (at least not yet). But perhaps scientists can come up with a pill that will do the same thing. A pill that keeps AgRP neurons from releasing GABA in the hypothalamus.

This is as hard as it sounds. But now that scientists know what to do, pharmaceutical companies will be able to apply all of their firepower to solving this problem. Given the potential market, if anyone can find a medicine for restricting weight gain using this finding, they will.

Before I get too excited, though, I want to see what happens to these mice as they age. Burning calories makes free radicals which damages DNA which causes aging and can cause cancer. Perhaps burning more calories this way might generate more free radicals.

Of course even if it does, maybe we could just take the pills with cranberries or some other anti-oxidant. Or maybe Nabisco can make an Oreo laced with antioxidants…

Being a neurologist in the era of fMRI scanners must feel like being a kid in a candy shop. What’s going in there while we’re, say, shopping? How about reading? Watching campaign ads? Now that we have a way to take real-time images of the brain at work, the scientific possibilities are endless.

On the surface, the experiment at the heart of this story might seem pretty narrow. It focuses on a rare disorder called pseudobulbar affect, which afflicts only people with ALS, or Lou Gehrig’s disease — a far cry from the universal rites of shopping or reading. But what’s fascinating about pseudobulbar is the light it might shed on all of us, and one of the most primal and mysterious human experiences of all: emotion.

People with pseudobulbar get happy and sad, just like the rest of us. They laugh and cry like the rest of us too. But then sometimes, something else happens: They keep going. And going. In this video, you can see how what looks like a laughing fit morphs into something else entirely. It’s as if the laughing and crying mechanisms have become detached from whatever part of the brain triggered the emotion in the first place. Maybe – and this is the hope of scientists Howard Rosen and Robert Levenson – by seeing that disconnect take place in real time through the fMRI, we’ll understand, for the first time, how emotion plays out in people without pseudobulbar affect.

(And it doesn’t stop there. Listen to the radio piece to hear Rosen’s theory about what PBA might mean for depression, obsessive compulsive disorder, and, particularly, PTSD.)

Finally, a note about Matt Chaney. As Rosen and Levenson remarked many times, science can’t happen without people like Chaney. While the rest of us sat comfortably in front of the fMRI monitors, Chaney spent an hour and a half lying in the cramped quarters of an MRI tube, watching highly emotional videos designed to make him sad. Moving his head by a millimeter would blur the image, so not only is Chaney being taken on an emotional roller coaster, he’s doing it without moving a muscle – a lot to ask from anyone, let alone someone with a degenerative muscular disease like ALS.

Journalism is a little less demanding (at least I hope so) but Chaney added to an already long day by spending time in an interview with me. He and his wife, Liz, were also extremely generous in allowing us to share videos of them, which illustrate pseudobulbar far more movingly and effectively than anything I could have written.

Listen to the Decoding the Emotional Brain radio report online, and watch our Web Extra: Emotions from the Inside and Out video.

A look into the science of skin.

In an article this week in the New York Times, brainpower was correlated with the complexity of nerve synapses. Leading researcher Dr. Grant, who has studied the interconnectedness of neurons, likened this connection to technology; “From the evolutionary perspective, the big brains of vertebrates not only have more synapses and neurons, but each of these synapses is more powerful - vertebrates have big Internets with big computers and invertebrates have small Internets with small computers.” The brain has been made analogous to a computer before in order to study evolutionary adaptation. However, the brain was not the organ being studied, rather it was human skin.

Have you ever wondered why we have hair only on the tops of our heads and the rest of our skin is relatively bare? Why does our skin come in so many pigmentations? And why does our skin sweat? Dr. Nina Jablonski kept asking why and attributes these adaptations to the need to keep our brain cool. I first heard Dr. Nina Jablonski speak about her most recent book, Skin: A Natural History, in early 2007. I was absolutely enthralled and two hours raced by as she articulated her fascination with skin. Dr. Jablonski divulged into why our skin appears and acts the way it does from an evolutionary standpoint. Her findings showed that about two million years ago our ancestors were running long distances in Africa under the heat of the equatorial sun. To keep their brains cool, sweat glands became more prominent. This in turn let brain size expand and evolve. In the fossil record, it shows after this increase in brain size, Homo sapiens left Africa to migrate into Mainland China.

Skin:A Natural History

So skin was an evolutionary adaptation to keep our large brains cool and working effectively. Skin color, Dr. Jablonski surmised, was what regulated our body’s reaction to the sun and its rays. Dark skin evolved to protect the body of those of our ancestors close to the equator. Those ancestors further away evolved light skin in order to take in Vitamin D in less sunny climates. After her talk about Rosacea, which is a condition of constant blushing found in Eastern European nationalities, I asked Dr. Jablonski why. She told me this might have been attributed to ancestors of light skin being overly bundled and getting over-heated. It might have been an adaptation to release heat and cool the brain from the only exposed skin.

In her lecture, Dr. Jablonski did not stop with touching upon evolutionary adaptations, she also delved into how we associate and identify through our skin. We decorate our skin, clothe it, paint it, tattoo it, scar and pierce it. She elucidated skin as an intimate connection with the world as well as our presentation of individuality. Skin: A Natural History and Dr. Nina Jablonski have gained national recognition. She was even invited as a guest on the Colbert Report to talk about her findings. It is rumored that she is following up Skin with more in-depth research. Until then, this is an outstanding look at a very under-appreciated organ, one that might have made the complex nuances of our brain and its synapses possible.

Watch Dr. Nina Jablonski on The Colbert Report: