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Aging, Genetics, In the News, Mental Health, Neuroscience, Research, Women's Health

Are women at greater risk for Alzheimer’s? Stanford expert to discuss on today’s Science Friday

Are women at greater risk for Alzheimer’s? Stanford expert to discuss on today's Science Friday

2187905205_158290644d_zConfession: I named my parents’ cat (who died recently) Watson after listening to Ira Flatow interview James Watson, PhD, while driving cross country with my dad in 2000. Both before and after the all-critical cat-name-inspiring program, Science Friday has been a part of my Friday as often as I can squeeze it in.

So I was happy to hear that today’s program (which airs locally from 11 a.m. to 1 p.m. on KQED) will feature Stanford’s Michael Greicius, MD, MPH. He’ll be talking about Alzheimer’s disease and why the disease affects men and women differently.

Greicius, medical director of the Stanford Center for Memory Disorders, has worked with the gene variant known as ApoE4 – the largest single genetic risk factor for Alzheimer’s, particularly for women. Last spring, he published a study showing that healthy ApoE4-positive women were twice as likely to contract the disease as their ApoE4-negative counterparts.

Greicius is expected to be on in the second hour, from 12 to 1 p.m. Pacific time.

Previously: Blocking a receptor on brain’s immune cells counters Alzheimer’s in mice, Examining the potential of creating new synapses in old or damaged brains, The state of Alzheimer’s research: A conversation with Stanford neurologist Michael Greicius and Having a copy of ApoE4 gene variant doubles Alzheimer’s risk for women but not for men
Photo by *Ann Gordon

Biomed Bites, Mental Health, Neuroscience, Research, Videos

A visual deluge may provide clues to ADHD treatment

A visual deluge may provide clues to ADHD treatment

It’s time for Biomed Bites, a weekly feature that introduces readers to some of Stanford’s most innovative researchers.

Looking out my window, I see a man dressed in red sweats on a bike. There’s my neighbor’s white truck parked in the street. A tree just starting to bud. A fire hydrant. A woman fertilizing roses. Closer, there’s my grey-and-white cat, Grizzly, bathing in the sun. My glass of ice water. My phone. Scattered papers.

And that’s probably only one-thousandth of the things I see right now. (I didn’t even mention the computer.) How do I make sense of that visual onslaught? How do I navigate, perceive threats, respond to changing conditions?

Well, that’s part of the puzzle Stanford neurobiologist Tirin Moore, PhD, is working to figure out.

“I’m a systems-level neurobiologist, which means I study how networks of neurons combine to either process sensory information or to control complex behaviors,” Moore explains in the video above.

How do we filter out what’s important – seeing the dog darting across the street in front of our car, but not focusing on the bird in the tree?

This process is most obvious when it breaks down, such as in patients with Attention Deficit Hyperactivity Disorder, or other attention disorders that affect from 3 to 8 percent of the population, Moore said:

At present, disorders such as ADHD are treatable, but their underlying neural basis is still very much a mystery… Our hope is that by understanding disorders of attention at the level of the neurocircuitry we will be able to arrive at more effective treatments…

Stay tuned to see what he, and his team, figures out.

Learn more about Stanford Medicine’s Biomedical Innovation Initiative and about other faculty leaders who are driving biomedical innovation here.

Aging, In the News, Neuroscience, Research

The distinctly different brains of “SuperAgers”

The distinctly different brains of “SuperAgers”

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Scientists are gaining insights into the cognitive abilities of “SuperAgers” and why their memories are more resilient against the ravages of time than are other older people’s. ABC News reports today on new research:

The SuperAgers were picked to be studied because all were over age 80 and had the memory capability of a person 20 to 30 years their junior according to the study recently published in the Journal of Neurology.

To understand how SuperAgers managed to keep their mental ability intact, researchers performed a battery of tests on them, including MRI scans on 12 SuperAgers and post-mortem studies on five other SuperAgers to understand the make-up of their brains.

“The brains of the SuperAgers are either wired differently or have structural differences when compared to normal individuals of the same age,” Changiz Geula, a study senior author and a research professor at the Cognitive Neurology and Alzheimer’s Disease Center, said in a prepared statement. “It may be one factor, such as expression of a specific gene, or a combination of factors that offers protection.”

The article goes on to explain that participants’ unusual brain signature had three common components in comparison to normal people of similar ages: notably fewer tangles (a primary marker of Alzheimer’s disease), a thicker region of the cortex and a significant supply of a neuron called von Economo, which is linked to higher social intelligence.

Previously: What brain scans reveal about “super agers”, The secret to living longer? It’s all in the ‘tude and Healthy aging the focus of Stanford study
Photo by Fiona Shields

Imaging, Mental Health, Neuroscience, NIH, Research, Stanford News

Study: Major psychiatric disorders share common deficits in brain’s executive-function network

Study: Major psychiatric disorders share common deficits in brain's executive-function network

marble brainPsychiatric disorders, traditionally distinguished from one another based on symptoms, may in reality not be as discrete as we think.

In a huge meta-analysis just published in JAMA Psychiatry, Stanford neuroscientist and psychiatrist Amit Etkin, MD, PhD, and his colleagues pooled the results from 193 different studies. This allowed them to compare brain images from 7,381 patients diagnosed with any of six conditions – schizophrenia, bipolar disorder, major depression, addiction, obsessive-compulsive disorder, and a cluster of anxiety syndromes – to one another, as well as to brain images from 8,511 healthy patients.

Compared with healthy brains, patients in all six psychiatric categories showed a loss of gray matter in each of three separate brain structures. These three areas, along with others, tend to fire in synchrony and are known to participate in the brain’s so-called “executive-function network,” which is associated with high-level functions including planning, decision-making, task-switching, concentrating in the face of distractions, and damping counterproductive impulses.

The findings call into question a longstanding tendency to distinguish psychiatric disorders chiefly by their symptoms

(“Gray matter” refers to information-processing nerve-cell concentrations in the brain, as opposed to the “white matter” tracts that, like connecting cables, shuttle information from one part of the brain to another.)

As Etkin told me when I interviewed him for the news release we issued on this study, “these three structures can be viewed as the alarm system for the brain.” More from our release:

“They work together, signaling to other brain regions when reality deviates from expectations – that something important and unpredicted has happened, or something important has failed to happen.” That signaling guides future behavior in directions more likely to obtain desired results.

The studies of psychiatric patients that Etkin’s team employed all used a technique that yields high-resolution images of the brain’s component structures but can say nothing about how or when these structures work or interact with one another. However, that kind of imaging data was available for the healthy subjects. And, on analysis, those healthy peoples’ performance on classic tests of executive-function (such as  asking the test-taker to note the color of the word “blue,” displayed in a color other than blue, after seeing it briefly flashed on a screen) correlated strongly with the volume of gray matter in the three suspect brain areas, supporting the idea that the anatomical loss in psychiatric patients was physiologically meaningful.

The findings call into question a longstanding tendency to distinguish psychiatric disorders chiefly by their symptoms rather than their underlying brain pathology – and, by implication, suggest that disparate conditions may be amenable to some common remedy.

As National Institute of Mental Health Director Thomas Insel, MD, told me in an interview about the study, the Stanford investigators “have stepped back from the trees to look at the forest and see a pattern in that forest that wasn’t apparent when you just look at the trees.”

Previously: Hope for the globby thing inside our skulls, Brain study offers intriguing clues toward new therapies for psychiatric disorders and Study shows abnormalities in brains of anxiety-disorder patients
Photo by Philippe Put

Aging, Immunology, Neuroscience, Research, Stanford News, Stroke

Can immune cells’ anomalous presence in brain explain delayed post-stroke dementia?

Can immune cells' anomalous presence in brain explain delayed post-stroke dementia?

bees in the bonnetAbout every 40 seconds, someone in the United States has a stroke. About one in three of those people will eventually suffer from dementia if they live long enough, even if there’s been no initial damage to brain structures involved in memory and cognition. That’s a mystery.

In a recent study in The Journal of Neuroscience, Stanford neurologist and stroke expert Marion Buckwalter, MD, PhD, points a bony scientific finger at a major likely reason why having a stroke doubles a person’s risk of incurring dementia within the next decade.

The culprit, surprisingly, seems to be a type of normally very beneficial immune cells that under ordinary circumstances have no business being in the brain. These trespassers, called B cells, are best known for generating antibodies that fight off invading pathogens. As I wrote in my release on the new study:

The antibodies that B cells produce are normally of great value to us. They circulate throughout blood and lymph, and bind to microbial invaders, gumming up the pathogens’ nefarious schemes and marking them for destruction by other immune cells. Occasionally, B cells wrongly begin generating antibodies that bind to the body’s own healthy tissues, causing certain forms of autoimmune disease, such as rheumatoid arthritis. Rituxan, a drug approved by the Food and Drug Administration for this condition, is actually an antibody itself: Its target is a protein found on the surface of every B cell. Use of this drug depletes B cells in the body, relieving the symptoms of rheumatoid arthritis and other B-cell-mediated disorders.

The blood-brain barrier, which tightly controls what enters and what leaves the brain, can be disrupted by a stroke, permitting the anomalous appearance of B cells there. Buckwalter and her colleagues showed that in mice experiencing strokes, the affected brain region – immune-cell-free at least one week later – started filling up with B cells until, at seven and twelve weeks post-stroke, there were “tons” of them, she told me. Around the same time, these mice started showing signs of dementia that hadn’t been at all evident a mere week after the stroke.

But in mice of a strain that is genetically incapable of producing B cells, no such cognitive loss occurred. Not only that, but giving plain old ordinary mice Rituxan five days after a stroke prevented this post-stroke dementia.

Then Buckwalter and her team looked at preserved, autopsied brain-tissue samples from people who had had stroke and dementia. Once again, they observed inordinate numbers of B cells in the majority of these brains, suggesting that humans, too, can experience late but lasting infiltration of rampaging B cells into our brains after a stroke.

So maybe giving a Rituxan-like B-cell-depleting compound to these people within that first week after their stroke could stave off dementia.

This wouldn’t by advisable for all stroke patients. You don’t want to wipe out somebody’s B cells (usually, they’re good guys) unless they are causing trouble. And, as seen in the autopsied tissue samples, not all stroke sufferers’ brains fall into that category.

But, Buckingham noted, Rituxan or something like it could work a double shift as both a therapeutic and a diagnostic. Rituxan pretty much binds only to B cells (a prelude to killing them), so tagging the drug with an imaging agent that could be picked up by, say, an MRI scan might tell clinicians which stroke patients have, or don’t have, B’s in their bonnets.

Previously: Targeted stimulation of specific brains cells boosts stroke recovery in mice, Calling all pharmacologists: Stroke-recovery mechanism found, small molecule needed and Brain sponge: Stroke treatment may extend time to prevent brain damage
Photo by _annamo

Aging, Neuroscience, Stanford News, Stroke, Videos

Bio-X undergraduate student finds direction through research

Bio-X undergraduate student finds direction through research

Richie Sapp arrived to Stanford as an undergraduate already interested in studying neuroscience. After talking with several faculty members, he ended up working in the lab of Carla Shatz, PhD, director of Stanford Bio-X.

I interviewed Sapp recently for a series of stories I was working on about undergraduate research opportunities at Stanford. He had participated in a terrific summer program run by Bio-X. I was struck by a few things when we talked, one of which was Sapp’s sincere interest in helping people. He had grown up with a twin brother who had been born with hydrocephaly and as a result had learning delays and is on the autism spectrum. That experience shaped his interest in helping people with similar challenges.

Sapp said that through his experience in the lab he got more out of his undergraduate classes and learned a lot about where he wants to go with his life. He loves the research and discovery, but also wants to go the medical school before pursuing research. Without the experience provided by the Bio-X summer program he might not have known which direction to go.

“The experience of designing experiments and seeing a project through to the end is going to be important for me in whatever I do next,” he said.

Here is the full profile about Sapp, with more about his research experiences.

Previously: Drug helps old brains learn new tricks, and heal

Neuroscience, Parenting, Research, Stanford News

Math and the brain: Memorization is overrated, says education expert

Math and the brain: Memorization is overrated, says education expert

4008476814_a7d70651f7_zRemember being drilled multiplication tables? Or taking a timed math exam? These have been common activities in school, but Stanford experts say they’re not really helpful to kids learning math facts. In fact, they deter students who might otherwise be excellent mathematicians.

Jo Boaler, PhD, is a professor of mathematics education and lead author on a new working paper, “Fluency without Fear.” As part of the research, educators looked at MRI scans of students who are better and worse at math memorization. The only difference in the brain shows up in the hippocampus, the working memory center, leading researchers to believe that there are no differences in math ability, analytical thought, or IQ between the groups. Moreover, the working memory shuts down when under stress. This makes it harder to recall facts when under time pressure, and seems to particularly affect high-achieving and female students.

Boaler’s research shows that students are better at math when they’ve developed “number sense,” or the ability to use numbers flexibly and understand their logic, which comes from relaxed, enjoyable, and exploratory work. Investigators found that high-achievers actually use number sense, and not rote memorization; likewise, it’s not that low-achieving students know less, but that they don’t use numbers flexibly.

Boaler told Stanford News, “They have been set on the wrong path, often from an early age, of trying to memorize methods instead of interacting with numbers flexibly… Number sense is the foundation for all higher-level mathematics.”

So, good math students are not necessarily fast math students, which is a common misconception. In fact, many mathematicians are slow with numbers, because they think carefully about them. The danger is that kids who aren’t fast with math sometimes become convinced they’re not good at it, and they turn away.

Compare times-tables drilling with how English is commonly taught. Students learn words by using them in many different settings: reading novels or poetry, writing thoughtful pieces, speaking about their thoughts or observations. “No English student would say or think that learning about English is about the fast memorization and fast recall of words,” says Boaler.

Boaler teaches a class for educators, “How to learn math,” in which she encourages a variety of math activities, including those that focus on the visual representation of number facts. Visual and symbolic number associations use different pathways in the brain, and connecting them deepens learning, as shown by recent brain research.

Photo by Jimmie

Neuroscience, Research, Stanford News

Face blindness stems from differences in neurocircuitry

Face blindness stems from differences in neurocircuitry

14769-faces_newsA recent Stanford News article stopped me in the first paragraph with its line, “One in 50 people can’t recognize faces.” That’s a huge number of people, including, somewhat disappointingly, Brad Pitt, whose face I would certainly recognize anywhere… These folks see eyes, a nose and a mouth — but they don’t put it together into a coherent whole.

Now, Stanford researchers have discovered that’s because their neurocircuitry is a bit different.

From the article:

The brain’s regions for face recognition and space recognition each perform similar functions, and they are located near each other.

For people with normal face and space recognition, the brain’s wiring for each region appears the same.

But in adults with face blindness, the wiring of the face-recognition region is different from the wiring of space-recognition center. Using that difference alone, researchers successfully predicted the presence of face blindness in adults who had previously been tested for the condition using only behavioral measures.

Stanford neuroscience graduate student Jesse Gomez helped solve the mystery by mastering a software model that shows how naturally occurring water in the brain moves through white matter. Axons, or the networking extensions of neurons, are sheathed in a substance called myelin, which is white. He found that a specific pattern of water movement predicts face blindness.

Next, he hopes to examine 5- to 11-year-old children to see how white matter changes during development, to figure out if a certain white-matter network will predict future face recognition ability.

Previously: In a human brain, knowing a face and naming it are separate worries, Metamorphosis: At the push of a button, a familiar face becomes a strange one and Image of the week: Oligodendrocyte
Photo by L.A. Cicero

Genetics, Neuroscience, Stanford News

“The uncertainty was killing me”: A student’s tale of genetic testing for Huntington’s disease

"The uncertainty was killing me": A student's tale of genetic testing for Huntington’s disease

happyImagine you had a 50 percent chance of being diagnosed with a disease that progressively breaks down the nerve cells of your brain, and that as early as your 30s or 40s you could begin exhibiting a range of symptoms of including involuntary movements, emotional problems and cognitive impairment. Such was the fate of Stanford student Kristen Powers.

Powers was three years old when her mother began experiencing symptoms of an incurable neurodegenerative disorder called Huntington’s disease, which claimed her mother’s life in 2011 at the age of 45. By the time she was 11, Powers became fully aware that she and her brother, Nate, had a 50/50 chance of someday developing the disease. Not long after, she learned that a genetic test could tell her if she carried the gene mutation that causes Huntington’s. The only problem was, she had to be 18 in order to take the test.

“The uncertainty was killing me,” said Powers, who was recently named one of the “15 incredibly impressive students at Stanford” by Business Insider. “I was constantly thinking about this ‘What if?’ scenario and it was very consuming in terms of my thoughts and conversations with my best friend. It was getting very tiresome.”

But rather than letting frustration and anxiety dominate her life, Powers channeled her energy into producing a documentary film, titled Twitch, about her experience growing up with her mother’s illness and the potential of carrying the Huntington’s gene.

“My film helped prepare me a lot because it gave me a sense of control in a process that was, very much, out of my control,” she said. “I could distract myself constructively and positively. My film was also a very important process for preparing for the results.”

Distraction came in the form of learning the documentary film business before she was barely old enough to drive a car. Powers had to pitch the idea of potential investors, raise money, hire a film crew, learn about film rights and copyright laws, work with attorneys to draft contracts, and make sure the production didn’t go broke.

To fund the film, she launched a crowdfunding campaign on Indiegogo. “I had decided that if the fundraising campaign was a failure I would take it as sign that I shouldn’t make the film,” she said.

But in the end she raised $18,025, 80 percent more than the goal amount. “I was so surprised. I had never raised more than $300. Within the first night we hit $1,000 and we hit our goal amount on the one-year anniversary of my mom’s passing,” said Powers.

On May 18, 2012, the long-awaited day finally arrived. Accompanied by her family and best friend, Powers took the test that, in her mind, would dictate major life decisions such as if she would have children. When the test results came back two weeks later, she learned the good news: She tested negative.

Continue Reading »

Behavioral Science, Complementary Medicine, Neuroscience, Videos

This is your brain on meditation

This is your brain on meditation

For years, friends have been telling me I should try meditation. I’m embarrassed to admit it’s mostly because of (how can I put this delicately?) a temper that flares when I’m anxious or stressed out. But, as it is for many people, it’s one of those things I haven’t gotten around to. This video by AsapSCIENCE, though, describing the things scientists have discovered about meditators has me thinking about it again.

Meditation is linked to a decreased anxiety and depression, and increased pain tolerance. Your brain tunes out the outer world during meditation, and on brain scans of meditators, scientists can see increased activity in default mode network – which is associated with better memory, goal setting, and self-awareness. The part of the brain that controls empathy has also been shown to be more pronounced in monks who are long-time meditators. From the video:

“[Meditation] also literally changes your brain waves, and we can measure these frequencies. Medidators have higher levels of alpha waves, which have been shown to reduce feelings of negative mood, tension, sadness and anger.”

Much like hitting the gym can grow your muscles and increase your overall health, it seems that meditation may be a way of working out your brain—with extra health benefits.”

Other demonstrated benefits include better heart rate variability and immune system function. I’m glossing over a lot of the information that’s packed into this entertaining little video, but if you’re curious, check out this less-than-three-minute video yourself.

Previously: Study shows benefits of breathing meditation among veterans with PTSDResearch brings meditation’s health benefits into focusUsing meditation to train the brainCan exercise and meditation prevent cold and flu? and How meditation can influence gene activity
Video by AsapSCIENCE

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