While at the World Economic Forum annual meeting in Davos, neuroscientists Tony Wyss-Coray, PhD, and Amit Etkin, MD, PhD, had a webcast conversation with NPR correspondent Joe Palca as part of his series of conversations on brain science. During their conversation, Palca asked about the current state of treatment for mental health and neurodegenerative diseases (bad) and prospects for the future (better).

When asked the single most important thing people could do for their mental health, Etkin answered, “awareness”. He said people need to be aware of their mental health and know that help exists if they seek it out. Current treatments aren’t perfect, but they are better than no treatment at all.

They also discussed molecular tools for diagnosing degenerative diseases, and the goals of the Stanford Neurosciences Institute‘s Big Ideas in Neuroscience teams that the two co-lead to develop new diagnostics and treatments for mental health (Etkin) and neurodegenerative diseases (Wyss-Coray).

At the end, Palca summarized the wide-ranging conversation saying, “I think it’s a time of actually some hope. I feel quite positive that this globby thing that sits inside our skulls is being understood in enough detail to make some precise changes that can be helpful.”

Previously: Neurosciences get the limelight at Davos, Neuroscientists dream big, come up with ideas for prosthetics, mental health, stroke and more

Four faculty from the Stanford Neurosciences Institute have been in Davos for the past few days attending the World Economic Forum along with world leaders and economic illuminati. They were invited to form a panel about the recently announced Big Ideas in Neuroscience, which is a novel way of bringing faculty together around health challenges like stroke, neurodegenerative disease and mental health conditions. If this approach is successful it could help ease the crippling economic and emotional costs of those diseases.

Amit Etkin, MD, PhD, emailed me from the conference that attendees seem to be very excited and focused on the sessions, with lines out the door of people waiting for seating. The entire panel included Etkin, who co-leads a mental health team, Marion Buckwalter, MD, PhD, who leads a stroke collaboration, and Tony Wyss-Coray, PhD, and Anne Brunet, PhD, who are both part of the neurodegenerative disease team.

Tomorrow at 6 a.m. Pacific Time both Etkin and Wyss-Coray will be webcast live in conversation with NPR correspondent Joe Palca. That webcast is available on the World Economic Forum website.

Previously: Neuroscientists dream big, come up with ideas for prosthetics, mental health, stroke and more, Stanford expert responds to questions about brain repair and the future of neuroscience

I had the pleasure of teaching a class this fall to a group of mostly chemistry and chemical engineering graduate students, helping them improve their skills communicating about their science with the public. For her assignment, graduate student Julie Fogarty recorded this Science Friday-style segment on work taking place in the lab of chemical biologist and bioengineer James Swartz, PhD. Swartz and colleagues are trying to develop a universal flu vaccine that would eliminate the need to get a new vaccine each year – something all of us would probably appreciate. (Here I’m thinking about my colleague Michelle Brandt, who recently suffered the woes of not finding time to get her kids vaccinated.)

Julie’s brother Skyped in for his role as Science Friday host extraordinaire Ira Flatow in this segment, while Julie played the enthusiastic and articulate guest. It’s often difficult to explain complex science in audio format, but Julie does a fantastic job explaining the work in way that is very visual. I love her description of the flu virus as a little mushroom.

(A previous blog entry featured another student, Rhiannon Thomas-Tran, who produced a great video about her work.)

Previously: Working to create a universal flu vaccine, Graduate student explains pain research in two-minute video and How one mom learned the importance of the flu shot – the hard way

Earlier this year I wrote about some fascinating research from the lab of chemist Justin Du Bois, PhD, who has been working with naturally occurring toxins with the goal of developing ways of combatting pain. This class of toxins is found in a number of poisonous animals, including the newts scurrying around Stanford campus, puffer fish and mollusks in red tides.

Now, graduate student Rhiannon Thomas-Tran, who has been working with Du Bois, produced a great video describing their approach, complete with some pretty creative drawings.

Previously: Toxins in newts lead to new way of locating pain

It wasn’t long ago that my kids could barely identify all the letters in the alphabet and now I have to yell at them to put down books and eat dinner. That transition, from identifying symbols to learning how to interpret them in math and reading, is something that involves creating new pathways in the brain.

Neuroscientists have long known that those changes must be taking place in the brain, but only recently has brain imaging been good enough to reveal where and how those changes are taking place. With that advance, neuroscientists and faculty in the School of Education are now starting to work together to better understand the changes and also come up with ways of using what’s learned in neuroscience to develop ways of helping kids who fall behind.

I recently wrote about a new education professor, Bruce McCandliss, PhD, who is pulling together the interdisciplinary team of faculty from across Stanford to build the educational neuroscience program here. From my story:

In one set of experiments, McCandliss used a type of brain imaging that reveals connections or tracts of neurons to look at the brains of kids who were good readers and others who showed signs of dyslexia. He found that the kids who were better readers had stronger brain connections in that region.

“There is a profound relationship between the way a person’s brain is organized and how well that person masters abstract intellectual skills, such as reading or mathematics,” he said.

In a follow-up study, he and a team that included Allan Reiss, the Howard C. Robbins Professor of Psychiatry and Behavioral Sciences and professor of radiology, found that kids with dyslexia who activate a particular brain region when trying to read went on to make much greater improvements in their reading ability. Kids who did not activate that region made very little reading gain after the age of 14.

“The hope is that by understanding the nature of these differences we might be able to tailor interventions for those individuals,” McCandliss said.

The people I talked with for my story all said that we have many years to go before discoveries made in the lab start showing up as personalized learning in the classroom. Still, it’s nice to think that some of the kids who are struggling with reading or math might one day be able to get help that’s based on what’s actually known about learning in the brain.

Previously: Learning how we learn to read, Study shows brain scans could help identify dyslexia in children before they start to read and Stanford study furthers understanding of reading disorders
Photo by John Morgan

These days, a person can get through graduate school in the sciences practically without touching a physical publication. Most journals are available online going back decades. So it was a bit unusual when graduate student Jason Yeatman and postdoctoral scholar Kevin Weiner found themselves in the basement of Lane Medical Library trying to get to the bottom of a medical mystery.

It all started when Yeatman found a nerve pathway in brain images he’d taken as part of his work studying brain changes as kids learn to read.  This pathway didn’t appear anywhere in the available literature. He and Weiner became curious how this pathway – which clearly showed up in their work – could have escaped the notice of previous neuroscientists.

Their curiosity eventually led them back to an 1881 publication, still available in the basement of Lane Medical Library, where Carl Wernicke, MD, described identifying this brain pathway. Weier said, “That was a really cool experience that most people don’t have anymore, when you have to check your belongings at the door because the book you are about to look at is worth thousands of dollars per page. You are literally smelling 100 year-old ink as you find the images you have been searching for.”

Wernicke’s discovery contradicted theories by the eminent neuroanatomist at the time, Theodor Meynert, MD. I describe the controversy that led to this pathway expulsion from the literature in this Stanford News story:

Meynert strongly believed that all of the brain’s association pathways run from front to back – horizontal. This pathway, which Wernicke had called the vertical occipital fasciculus, or VOF, ran vertically. Although Yeatman and Weiner found references to the VOF under a variety of different names in texts published for about 30 years after Wernicke’s original discovery, Meynert never accepted the VOF and references to it became contentious before eventually disappearing entirely from the literature.

The group, whose work was published this week in the Proceedings of the National Academy of Sciences, says this was all more than just an exercise in curiosity. Psychologist Brian Wandell, PhD, in whose lab Yeatman was working, says it also shows the value of modern publishing methods, where making data available means scientists worldwide can try to reproduce results. He says it’s now less likely that a dispute could lead to a discovery being lost to history.

Image courtesy of PNAS

The ever-funny Andy Borowitz has written in The New Yorker about a previously unreported challenge in the fight against Ebola: It might make Americans believe in science. He writes:

In interviews conducted across the nation, leading anti-science activists expressed their concern that the American people, wracked with anxiety over the possible spread of the virus, might desperately look to science to save the day.

“It’s a very human reaction,” said Harland Dorrinson, a prominent anti-science activist from Springfield, Missouri. “If you put them under enough stress, perfectly rational people will panic and start believing in science.”

For someone who left science to become a writer specifically to help explain science to the public, this piece is both funny and also so very not funny at the same time. Almost 20 years after I put down my pipette, Americans are, if anything, less willing to let science guide their health, energy, or environmental decisions than they were back when I started – thus the humor in Borowitz’ piece.

All of this makes me wonder if I could have spared myself several decades of worrying about clever analogies, agonizing about transitions, and racing the clock to make deadlines and done something less stressful with my life. Something fulfilling. Something where at the end of the day, my work would help people live happier, healthier lives rather than producing something people will ignore if it doesn’t fit their ideology.

Matthew Nisbet and Dietram Scheufele have written a number of articles about science communication and its effects on public perception of science. In the American Journal of Botony they write, “Often when the relationship between science and society breaks down, science illiteracy is typically blamed, the absence of quality science coverage is bemoaned, and there is a call put out for ‘more Carl Sagans.’”

In a nutshell, that sums up my career switch. I bemoaned the absence of quality science coverage and fully intended to fill that gap.

Then, they go on to shatter my reasons for writing by pointing out that at a period of time when the public’s regard for science was at it’s highest – soon after the Sputnik launch – science literacy was abysmal. In one survey at the time, just 12 percent of people understood the scientific method, yet 90 percent of people believed that science was making their lives better.

What that survey suggests is that even a scientific challenge like Ebola is unlikely to push Americans to be better educated about science. But perhaps with the perfect transition, or really outstanding analogy, those same scientifically illiterate Americans can be convinced that science is making life better and – I’m really dreaming here -should be funded?

If yes, maybe Borowitz’ fictional anti-science advocate will be proved right, and we will head down that slippery slope “in which a belief in science leads to a belief in math, which in turn fosters a dangerous dependence on facts.” One can hope!

Previously: Scientist: Just because someone’s on TV doesn’t mean they’re an expert

One cool thing about being at Stanford is access to really, really smart people. Case in point, I get to work with William Newsome, PhD, who, in addition to doing really interesting neuroscience research, co-leads the group that made recommendations to the national BRAIN Initiative, and also directs the new Stanford Neurosciences Institute. He has a lot of insight into the state of neuroscience, where the field is headed, and what challenges scientists face in trying to better understand the brain and develop new therapies.

Newsome recently participated in an Open Office Hours, in which Stanford faculty take questions through Facebook, essentially opening their office doors to anyone with questions. He later recorded answers to those questions in the video above.

In addition to the full- length video, we’ve been posting short excerpts on Facebook. In this clip, Newsome discusses the dynamic nature of our brain’s connections. As he explains, the brain can switch connectivity to let us have one set of behaviors with our boss and another with our spouse.

In today’s installment, Newsome discusses efforts to repair nerves that are damaged in stroke, spinal cord injuries, traumatic brain injuries or other conditions. Stroke is of particular interest right now – the Neurosciences Institute that Newsome leads recently announced the creation of an interdisciplinary consortium at Stanford focused on stroke as one of their Big Ideas in Neuroscience.

In that segment, Newsome points out that nerves of our arms or legs, the so-called peripheral nervous system, can regrow if they get damaged. If you cut your finger, the nerves regrow. If you have a stroke or damage your spinal cord, the nerves don’t regrow. Newsome said:

What’s the difference between the central nervous system and the peripheral nervous system such that the central nervous system does not regrow most of the time yet the peripheral nervous system does? … When we get that knowledge the hope is that we’ll be able to set the conditions right for regrowth when there’s an injury and we’ll actually be able to help people recover function.

Previously: Deciphering “three pounds of goo” with Stanford neurobiologist Bill Newsome, Open Office Hours: Stanford neurobiologist taking your questions on brain research, Neuroscientists dream big, come up with ideas for prosthetics, mental health, stroke and more, Co-leader of Obama’s BRAIN Initiative to direct Stanford’s interdisciplinary neuroscience institute and Brain’s gain: Stanford neuroscientist discusses two major new initiatives

Our brains go through remarkably flexible periods in childhood when they can form new connections in a flash and retain information at a rate that leaves adults (or at least me) both impressed and also deeply jealous.

Now neurobiologist Carla Shatz, PhD, has developed a drug that at least in mice can briefly open that window for making new connections in the adult brain. It works as a sort of decoy, tricking other molecules in the cell into binding to it rather than to the “real” protein on the neuron’s surface. Without the bound molecules, the protein on the neuron’s surface releases its brake on synapse formation.

There are still a number of hurdles to overcome before the drug could work in people. The human version of the protein she studied is slightly different than the mouse version, and she had to inject the drug directly into the mouse brain. She would need to find a way of delivering the drug as a pill before it could be useful in people.

Despite those hurdles, the possibilities are exciting. From a story I wrote on the possible uses for such a drug, which she had tested in a form of blindness in mice:

This model that the team studied in mice directly applies to forms of blindness in people. Children who are born with cataracts need to have the problem repaired while the vision processing region of the brain is still able to form new connections with the eyes. “If the damage isn’t repaired early enough then it’s extremely difficult if not impossible to recover vision,” Shatz said.

If a version of the decoy protein could work in people, then kids born with cataracts in countries with limited access to surgery could potentially have their cataracts removed later, receive a drug, and be able to see. Similarly, the window could be briefly opened to help people recover from stroke or other conditions.

Previously: How villainous substance starts wrecking synapses long before clumping into Alzheimer’s plaques, “Pruning synapses” and other strides in Alzheimer’s research
Image, which shows neurons of the visual system in mice that have formed new connections, courtesy of the Shatz lab

Here’s one thing I didn’t know: For every person who goes to the doctor to be treated for chronic pain, less than a half get their pain reduced even by half. I learned that from anesthesiologist David Clark, MD, who recently received a grant from Stanford Bio-X, which supports interdisciplinary teams working on biomedical problems, to improve those odds.

One of Clark’s collaborators is Scott Delp, PhD, who last spring developed a way of using light to activate and deactivate pain neurons in mice. To be clear, the nerves had to be genetically engineered to allow the light to work – not something that can currently be done in humans.

That work pointed to new ways of studying pain, but had a glitch. The light was delivered through fiber optic cables and the mice couldn’t behave normally in their cages. That’s where engineer Ada Poon, PhD, enters the picture. She’s been developing a variety of devices that work wirelessly in the body, and she’s now working on a wireless device to deliver the light to nerves in mice. Here’s what I wrote in an online story yesterday:

Coupling a wireless technology to optogenetics eliminates the wire and allows a mouse to move freely, use an exercise wheel and socialize. Clark said this combination will allow researchers to design experiments that more closely mirror a patient’s experience.

For example, Clark said that when he sees patients they don’t necessarily complain only about the pain. They complain about not wanting to see friends, not being able to go to work, or not being able to do activities they enjoy.

“What we will be able to look at is a more natural measure of pain relief,” Poon said. They could assess whether a treatment allows mice to return to normal activities by tallying time spent on an exercise wheel or socializing.

Clark went on to tell me the value of working in this team: “When you combine people with different skills you will come up with something with truly high impact.”

Previously: Using light to get muscles moving and Stanford researchers demonstrate feasibility of ultra-small, wirelessly powered cardiac device
Image courtesy of Ada Poon