Archive for the ‘University of Southern California’ Category


William Gibson’s popular science fiction tale “Johnny Mnemonic” foresaw sensitive information being carried by microchips in the brain by 2021. A team of American neuroscientists could be making this fantasy world a reality. Their motivation is different but the outcome would be somewhat similar. Hailed as one of 2013’s top ten technological breakthroughs by MIT, the work by the University of Southern California, North Carolina’s Wake Forest University and other partners has actually spanned a decade.

But the U.S.-wide team now thinks that it will see a memory device being implanted in a small number of human volunteers within two years and available to patients in five to 10 years. They can’t quite contain their excitement. “I never thought I’d see this in my lifetime,” said Ted Berger, professor of biomedical engineering at the University of Southern California in Los Angeles. “I might not benefit from it myself but my kids will.”

Rob Hampson, associate professor of physiology and pharmacology at Wake Forest University, agrees. “We keep pushing forward, every time I put an estimate on it, it gets shorter and shorter.”

The scientists — who bring varied skills to the table, including mathematical modeling and psychiatry — believe they have cracked how long-term memories are made, stored and retrieved and how to replicate this process in brains that are damaged, particularly by stroke or localized injury.

Berger said they record a memory being made, in an undamaged area of the brain, then use that data to predict what a damaged area “downstream” should be doing. Electrodes are then used to stimulate the damaged area to replicate the action of the undamaged cells.

They concentrate on the hippocampus — part of the cerebral cortex which sits deep in the brain — where short-term memories become long-term ones. Berger has looked at how electrical signals travel through neurons there to form those long-term memories and has used his expertise in mathematical modeling to mimic these movements using electronics.

Hampson, whose university has done much of the animal studies, adds: “We support and reinforce the signal in the hippocampus but we are moving forward with the idea that if you can study enough of the inputs and outputs to replace the function of the hippocampus, you can bypass the hippocampus.”

The team’s experiments on rats and monkeys have shown that certain brain functions can be replaced with signals via electrodes. You would think that the work of then creating an implant for people and getting such a thing approved would be a Herculean task, but think again.

For 15 years, people have been having brain implants to provide deep brain stimulation to treat epilepsy and Parkinson’s disease — a reported 80,000 people have now had such devices placed in their brains. So many of the hurdles have already been overcome — particularly the “yuck factor” and the fear factor.

“It’s now commonly accepted that humans will have electrodes put in them — it’s done for epilepsy, deep brain stimulation, (that has made it) easier for investigative research, it’s much more acceptable now than five to 10 years ago,” Hampson says.

Much of the work that remains now is in shrinking down the electronics.

“Right now it’s not a device, it’s a fair amount of equipment,”Hampson says. “We’re probably looking at devices in the five to 10 year range for human patients.”

The ultimate goal in memory research would be to treat Alzheimer’s Disease but unlike in stroke or localized brain injury, Alzheimer’s tends to affect many parts of the brain, especially in its later stages, making these implants a less likely option any time soon.

Berger foresees a future, however, where drugs and implants could be used together to treat early dementia. Drugs could be used to enhance the action of cells that surround the most damaged areas, and the team’s memory implant could be used to replace a lot of the lost cells in the center of the damaged area. “I think the best strategy is going to involve both drugs and devices,” he says.

Unfortunately, the team found that its method can’t help patients with advanced dementia.

“When looking at a patient with mild memory loss, there’s probably enough residual signal to work with, but not when there’s significant memory loss,” Hampson said.

Constantine Lyketsos, professor of psychiatry and behavioral sciences at John Hopkins Medicine in Baltimore which is trialing a deep brain stimulator implant for Alzheimer’s patients was a little skeptical of the other team’s claims.

“The brain has a lot of redundancy, it can function pretty well if loses one or two parts. But memory involves circuits diffusely dispersed throughout the brain so it’s hard to envision.” However, he added that it was more likely to be successful in helping victims of stroke or localized brain injury as indeed its makers are aiming to do.

The UK’s Alzheimer’s Society is cautiously optimistic.

“Finding ways to combat symptoms caused by changes in the brain is an ongoing battle for researchers. An implant like this one is an interesting avenue to explore,” said Doug Brown, director of research and development.

Hampson says the team’s breakthrough is “like the difference between a cane, to help you walk, and a prosthetic limb — it’s two different approaches.”

It will still take time for many people to accept their findings and their claims, he says, but they don’t expect to have a shortage of volunteers stepping forward to try their implant — the project is partly funded by the U.S. military which is looking for help with battlefield injuries.

There are U.S. soldiers coming back from operations with brain trauma and a neurologist at DARPA (the Defense Advanced Research Projects Agency) is asking “what can you do for my boys?” Hampson says.

“That’s what it’s all about.”



Published: February 3, 2013
New York Times

In the past few years, scientists have learned a lot about fear from a woman who could not experience it. A rare illness had damaged a part of her brain known as the amygdala and left her eerily unafraid.

Both in experiments and in life, the woman, known as SM, showed no fear of scary movies, snakes, spiders or very real domestic assaults, death threats, and robberies at knife- and gunpoint.

Although she lived in an area “replete with crime, drugs and danger,” according to an earlier study, because she lacked a functioning amygdala, an evolutionarily ancient part of the brain long known to process fear, nothing scared her.

But recently SM had a panic attack. And the simple fact that she was able to feel afraid without a working amygdala, experts say, illuminates some of the brain’s most fundamental processes and may have practical value in the study of panic attacks.

SM’s moments of fear occurred during an experiment that involved inhaling carbon dioxide through a mask in amounts that are not harmful but create a momentary feeling of suffocation. Not only SM, but two other women, identified as AM and BG, identical twins with amygdala damage similar to SM’s, showed all the physical symptoms of panic, and reported that, to their surprise, they felt intense fear.

The researchers, who report on the experiment in the current issue of Nature Neuroscience, had hypothesized that SM would not panic. John A. Wemmie, a neuroscientist at the University of Iowa and the senior author of the paper, said, “We saw the exact opposite.”

Antonio Damasio, of the University of Southern California, who had worked with SM and some of the researchers involved in this study on previous papers but did not participate in this research, said he was delighted with the results. It confirmed his own thinking, he said, that while the amygdala was central to fear generated by external threats, there was a different brain path that produced the feeling of fear generated by internal bodily experiences like a heart attack. This idea was put forth in a 2011 paper about SM on which he was a co-author.

“I think it’s a very interesting and important result,” he said.

Dr. Joseph E. LeDoux, of New York University, who has extensively studied the amygdala but was not involved in the research, said in an e-mail, “This is a novel and important paper” in an area where there is much left to learn. He said scientists still did not understand “how the brain creates a conscious experience of fear,” whether the amygdala or other systems are involved.

SM scores in the normal range on I.Q. and other tests, and she voluntarily participated in this and earlier studies, all of which showed her lacking in any sort of fear response until now. In one, for example, she walked through a Halloween haunted house and never gasped, recoiled or screamed, as others did, when a person in a costume leapt out of the dark. She also did not seem to learn fear from life experiences.

So what was so unusual about carbon dioxide?

The answer seems to lie in the way the brain monitors disturbances in the world outside the body — snakes and robbers — compared with the way it monitors trouble inside the body — hunger, heart attacks, the feeling of not being able to breathe. External threats clearly are processed by the amygdala. But she had never been tested for internal signals of trouble.

In the experiment that SM and others participated in, they took one deep breath with plenty of oxygen but much more carbon dioxide than air usually contains. Humans are actually not sensitive to how much oxygen they are breathing, but they are sensitive to how much carbon dioxide is accumulating in the body, since it builds up quickly when a person cannot breathe. The sensation is familiar to people who have tried to hold their breath.

The researchers suggest that excess carbon dioxide produces signals that may be picked up in the brainstem and elsewhere, activating a fear-generating system in the brain that a venomous snake or a mugger with a gun would not set off.

One puzzling aspect of the results is that SM and the two other women all reacted so strongly. Among people with normal brains, only those with panic disorder are reliably terrified in carbon dioxide experiments. Most people are not so susceptible, said Colin Buzza, a co-author of the study and a medical student at the University of Iowa Carver College of Medicine, suggesting that perhaps the amygdala is not functioning properly in people with panic disorder.

Since the Viking Mars probes traveled to the red planet back in 1976, NASA has sent several more probes, landers, and rovers to the Martian surface to study the planet’s geology and search for signs of microbial life. But the evidence for life may have been hidden in Viking’s data all along. A new analysis of the data collected by probes Viking 1 and Viking 2 suggest the missions found evidence of microbial life more than three decades ago.

The new analysis centres on one of the three experiments carried by the probe: the Labeled Release (LR) experiment. This instrument searched for signs of life by mixing samples of Martian soil with droplets of water containing nutrients and radioactive carbon. If the soil contained microbes, the reasoning went, they would metabolise these carbon atoms and nutrients and release either methane gas or radioactive carbon dioxide, either of which would tip off the probes that life existed in the soil.

That’s exactly what happened. But other experiments aboard Viking didn’t back up the LR, and NASA scientists had to dismiss the LR’s findings as anomalous.

But now an analysis by a University of Southern California neurobiologist (and former NASA space shuttle project director) and a mathematician from Italy’s University of Siena could reverse that thinking. They used a technique called cluster analysis, which clusters together similar-looking data sets, to see what would happen. They found the analysis created two clusters: one for the two active experiments on Viking and the other for five control experiments.

Further, when they compared Viking’s data to confirmed biological sources on Earth, like temperature readings from a lab rat, the analysis correctly clustered the biological readings with the active Viking experiment data, separate from the non-biological data in the control experiments. All that essentially means that the cluster analysis, when fed a good deal of data from both biological and non-biological sources, correctly separates the two types of data. And when it does so, it lumps the Viking data into the “biological” category.

That’s not concrete evidence for microbial life on Mars. It’s merely concrete evidence that there is a stark difference between Viking’s LR experiment data and the control experiment data. And it’s evidence that the Viking data tracks with biological rather than non-biological data. More study is necessary (isn’t it always?), but if the cluster analysis is to be believed then our first shot at detecting microbial life in the soils of Mars may have hit pay dirt – and we didn’t even realise it.