Running, Cardio Activities in Young Adulthood May Preserve Thinking Skills in Middle Age

Young adults who run or participate in other cardio fitness activities may preserve their memory and thinking skills in middle age, according to a new study published in the April 2, 2014, online issue of Neurology®, the medical journal of the American Academy of Neurology. Middle age was defined as ages 43 to 55.

“Many studies show the benefits to the brain of good heart health,” said study author David R. Jacobs, Jr, PhD, with the University of Minnesota in Minneapolis. “This is one more important study that should remind young adults of the brain health benefits of cardio fitness activities such as running, swimming, biking or cardio fitness classes.”

Cardiorespiratory fitness is a measure of how well your body transports oxygen to your muscles, and how well your muscles are able to absorb the oxygen during exercise.

For the study, 2,747 healthy people with an average age of 25 underwent treadmill tests the first year of the study and then again 20 years later. Cognitive tests taken 25 years after the start of the study measured verbal memory, psychomotor speed (the relationship between thinking skills and physical movement) and executive function.

For the treadmill test, which was similar to a cardiovascular stress test, participants walked or ran as the speed and incline increased until they could not continue or had symptoms such as shortness of breath. At the first test, participants lasted an average of 10 minutes on the treadmill. Twenty years later, that number decreased by an average of 2.9 minutes. For every additional minute people completed on the treadmill at the first test, they recalled 0.12 more words correctly on the memory test of 15 words and correctly replaced 0.92 more numbers with meaningless symbols in the test of psychomotor speed 25 years later, even after adjusting for other factors such as smoking, diabetes and high cholesterol.

People who had smaller decreases in their time completed on the treadmill test 20 years later were more likely to perform better on the executive function test than those who had bigger decreases. Specifically, they were better able to correctly state ink color (for example, for the word “yellow” written in green ink, the correct answer was “green”).

“These changes were significant, and while they may be modest, they were larger than the effect from one year of aging,” Jacobs said. “Other studies in older individuals have shown that these tests are among the strongest predictors of developing dementia in the future. One study showed that every additional word remembered on the memory test was associated with an 18-percent decrease in the risk of developing dementia after 10 years.”

“These findings are likely to help us earlier identify and consequently prevent or treat those at high risk of developing dementia,” Jacobs said.

Great minds think alike

Study finds pigeons and other animals, like humans, can place everyday things in categories

Pinecone or pine nut? Friend or foe? Distinguishing between the two requires that we pay special attention to the telltale characteristics of each. And as it turns out, us humans aren’t the only ones up to the task.

According to researchers at the University of Iowa, pigeons share our ability to place everyday things in categories. And, like people, they can hone in on visual information that is new or important and dismiss what is not.

“The basic concept at play is selective attention. That is, in a complex world, with its booming, buzzing confusion, we don’t attend to all properties of our environment. We attend to those that are novel or relevant,” says Ed Wasserman, UI psychology professor and secondary author on the paper, published in the Journal of Experimental Psychology: Animal Learning and Cognition.

Selective attention has traditionally been viewed as unique to humans. But as UI research scientist and lead author of the study Leyre Castro explains, scientists now know that discerning one category from another is vital to survival.

“All animals in the wild need to distinguish what might be food from what might be poison, and, of course be able to single out predators from harmless creatures,” she says.

More than that, other creatures seem to follow the same thought process humans do when it comes to making these distinctions. Castro and Wasserman’s study reveals that learning about an object’s relevant characteristics and using those characteristics to categorize it go hand-in-hand.

When observing pigeons, “We thought they would learn what was relevant (step one) and then learn the appropriate response (step two),” Wasserman explains. But instead, the researchers found that learning and categorization seemed to occur simultaneously in the brain.

To test how, and indeed whether, animals like pigeons use selective attention, Wasserman and Castro presented the birds with a touchscreen containing two sets of four computer-generated images—such as stars, spirals, and bubbles.

The pigeons had to determine what distinguished one set from the other. For example, did one set contain a star while the other contained bubbles?

By monitoring what images the pigeons pecked on the touchscreen, Wasserman and Castro were able to determine what the birds were looking at. Were they pecking at the relevant, distinguishing characteristics of each set—in this case the stars and the bubbles?

The answer was yes, suggesting that pigeons—like humans—use selective attention to place objects in appropriate categories. And according to the researchers, the finding can be extended to other animals like lizards and goldfish.

“Because a pigeon’s beak is midway between its eyes, we have a pretty good idea that where it is looking is where it is pecking,” Wasserman says. “This could be true of any bird or fish or reptile.

“However, we can’t assume our findings would hold true in an animal with appendages—such as arms—because their eyes can look somewhere other than where their hand or paw is touching,” he explains.

Moonwalker Flies Backing Up

Most land animals walk forward by default, but can switch to backward walking when they sense an obstacle or danger in the path ahead. The impulse to change walking direction is likely to be transmitted by descending neurons of the brain that control local motor circuits within the central nervous system. This neuronal input can change walking direction by adjusting the order or timing of individual leg movements.

Screening for flies with altered walking patterns

In the current study, Dickson and his team aimed to understand the fly’s change in walking direction at the cellular level. Using a novel technology known as thermogenetics, they were able to identify the neurons in the brain that cause a change in locomotion. Their studies involved screening large numbers of flies with it which specific neurons were activated by heat, producing certain behaviors only when warmed to 30°C, but not at 24°C . Analysing several thousand flies, the researchers looked for strains that exhibited altered walking patterns compared to control animals.

Moonwalker-neurons control backward walking

Using the thermogenetic screen, the IMP-researchers isolated four lines of flies that walked backward on heat activation. They were able to track down these changes to specific nerve cells in the fly brain which they dubbed “moonwalker neurons”. They could also show that silencing the activity of these neurons using tetanus toxin rendered the flies unable to walk backward.

Among the moonwalker neurons, the activity of descending MDN-neurons is required for flies to walk backward when they encounter an obstacle. Input from MDN brain cells is sufficient to induce backward walking in flies that would otherwise walk forward. Ascending moonwalker neurons (MAN) promote persistent backward walking, possibly by inhibiting forward walking.

“This is the first identification of specific neurons that carry the command for the switch in walking direction of an insect”, says Salil Bidaye, lead author of the study. “Our findings provide a great entry point into the entire walking circuit of the fly. “
Although there are obvious differences in how insects and humans walk, it is likely that there are functional analogies at a neural circuit level. Insights into the neural basis of insect walking could also generate applications in the field of robotics. To date, none of the engineered robots that are used for rescue or exploration missions can walk as robustly as animals. Understanding how insects change their walking direction at a neuronal level would reveal the mechanistic basis of achieving such robust walking behavior.

(Image credit)

Researchers identify how zinc regulates a key enzyme involved in cell death

Findings may help develop targeted drug interventions and fight cancer and neurodegenerative diseases

The molecular details of how zinc, an essential trace element of human metabolism, interacts with the enzyme caspase-3, which is central to apoptosis or cell death, have been elucidated in a new study led by researchers at Virginia Commonwealth University. The study is featured on the cover of the April issue of the journal Angewandte Chemie’s International Edition.

Dysregulation of apoptosis is implicated in cancer and neurodegenerative disease such as Alzheimer’s disease. Zinc is known to affect the process by inhibiting the activity of caspases, which are important drug targets for the treatment of the above conditions. The findings may help researchers design therapeutic agents that target zinc-caspase interaction to specifically control the activity of caspases, and hence, apoptosis.

“The work is unique in helping to open up a broad new area of research which we call the bioinorganic chemistry of apoptosis – understanding the role of essential metal ions in one of life’s fundamental processes,” said corresponding author Nicholas P. Farrell, Ph.D., member of the Developmental Therapeutics program at VCU Massey Cancer Center and professor of chemistry in the VCU College of Humanities and Sciences.

“Indeed, the zinc inhibition of apoptosis in fact contrasts with the role of its closely related neighbor copper, which is understood to enhance apoptosis,” he said.

In the study, Farrell and his research team, A. Gerard Daniel, Ph.D., and Erica J. Peterson, used conventional enzymology and biophysical techniques combined with state-of-the-art computational methods, to show evidence for a hitherto unrecognized interaction site with caspase-3.

According to Farrell, caspases were discovered in the mid-1990s. There are 11 caspases known humans, and seven of these are involved in cell death. The study suggests a regulatory zinc site that may be common to all caspases. Previous findings have shown other zinc binding sites in caspase-6 and -9. Now, Farrell said, the generality of the team’s observations must be extended and verified in other caspases.

“The [journal] cover epitomizes the contrasting but interdependent roles of the metal ions copper/zinc in the regulation of apoptosis and perfectly captures the duality of this most fundamental of biological processes,” Farrell said.

Muscle paralysis eased by light-sensitive stem cells

A genetic tweak can make light work of some nervous disorders. Using flashes of light to stimulate modified neurons can restore movement to paralysed muscles. A study demonstrating this, carried out in mice, lays the path for using such “optogenetic” approaches to treat nerve disorders ranging from spinal cord injury to epilepsy and motor neuron disease.

Optogenetics has been hailed as one of the most significant recent developments in neuroscience. It involves genetically modifying neurons so they produce a light-sensitive protein, which makes them “fire”, sending an electrical signal, when exposed to light.

So far optogenetics has mainly been used to explore how the brain works, but some groups are exploring using it as therapy. One stumbling block has been fears about irreversibly genetically manipulating the brain.

In the latest study, a team led by Linda Greensmith of University College London altered mouse stem cells in the lab before transplanting them into nerves in the leg – this means they would be easier to remove if something went wrong.

"It’s a very exciting approach that has a lot of potential," says Ziv Williams of Harvard Medical School in Boston.

Muscles in action

Greensmith’s team inserted an algal gene that codes for a light-responsive protein into mouse embryonic stem cells. They then added signalling molecules to make the stem cells develop into motor neurons, the cells that carry signals to and from the spinal cord to the rest of the body. They implanted these into the sciatic nerve – which runs from the spinal cord to the lower limbs – of mice whose original nerves had been cut.

After waiting five weeks for the implanted neurons to integrate with the muscle, Greensmith’s team anaesthetised the mice, cut open their skin and shone pulses of blue light on the nerve. The leg muscles contracted in response. “We were surprised at how well this worked,” says Greensmith.

Most current approaches being investigated to help people who are paralysed involve electrically stimulating their nerves or muscles. But this can be painful because they may still have working pain neurons. Plus, the electricity makes the muscles contract too forcefully, making them tire quickly.

Using the optogenetic approach, however, allows the muscle fibres to be stimulated more gently, because the light level can be increased with each pulse. “It gives a very smooth contraction,” says Greensmith.

Breathing restoration

To make the technique practical for use in people, the researchers are developing a light-emitting diode in the form of a cuff that would go around the nerve, which could be connected to a miniature battery pack under the skin.

They are also trying to develop an alternative to using embryonic stem cells, as these would require the recipient to take drugs to stop their immune system attacking the transplanted neurons. Instead the team is working with induced pluripotent stem cells, cells that have been reprogrammed to behave like embryonic stem cells, but can be made from a small sample of the intended recipient’s own skin.

The team’s first goal is to help people with motor neuron disease who lose the ability to control their breathing muscles. “Walking involves contracting about 40 different muscles in complex sequences,” says Greensmith. “Breathing is very simple – one muscle contracts and relaxes.”

They plan to test the restoration of breathing ability in pigs, and are developing a pacemaker that could repeatedly illuminate the phrenic nerve in the chest, which controls the diaphragm.

Other groups are exploring different therapeutic applications of optogenetics, including treatments for epilepsy and Parkinson’s disease

Bioengineer Studying How the Brain Controls Movement

A University of California, San Diego research team led by bioengineer Gert Cauwenberghs is working to understand how the brain circuitry controls how we move. The goal is to develop new technologies to help patients with Parkinson’s disease and other debilitating medical conditions navigate the world on their own. Their research is funded by the National Science Foundation’s Emerging Frontiers of Research and Innovation program.

"Parkinson’s disease is not just about one location in the brain that’s impaired. It’s the whole body. We look at the problems in a very holistic way, combine science and clinical aspects with engineering approaches for technology," explains Cauwenberghs, a professor at the Jacobs School of Engineering and co-director of the Institute for Neural Computation at UC San Diego. "We’re using advanced technology, but in a means that is more proactive in helping the brain to get around some of its problems—in this case, Parkinson’s disease—by working with the brain’s natural plasticity, in wiring connections between neurons in different ways."

Outcomes of this research are contributing to the system-level understanding of human-machine interactions, and motor learning and control in real world environments for humans, and are leading to the development of a new generation of wireless brain and body activity sensors and adaptive prosthetics devices. Besides advancing our knowledge of human-machine interactions and stimulating the engineering of new brain/body sensors and actuators, the work is directly influencing diverse areas in which humans are coupled with machines. These include brain-machine interfaces and telemanipulation.

Uncovering the underlying causes of Parkinson’s disease

A breakthrough investigation by UTS researchers into the underlying causes of Parkinson’s disease has brought us a step closer to understanding how to manage the condition.

The team, led by UTS postdoctoral fellow Dr Dominic Hare and Professor Philip Doble, has produced the first empirical evidence that an imbalance of iron and dopamine in the substantia nigra pars compacta (SNc) region of the brain is the root cause of the neurodegenerative condition.

Caused by the slow loss of neurons in the SNc that control autonomous movement, Parkinson’s disease causes persistent shaking, gastrointestinal problems and a variety of other ailments.

More than 80,000 Australians suffer from the illness, most over the age of 60.

Hare’s findings, before only assumptions in the scientific community, finally validate the theory that iron and dopamine react to create free radicals in the brain that slowly destroy neuron pathways and bring about the onset of Parkinson’s.

"When these two chemicals react, it forms a toxic species of dopamine that essentially reacts like bleach in the brain," said Hare.

To conduct their research Hare and his team used a unique tagging technique using antibodies labelled with gold nanoparticles that acted as proxies for dopamine molecules. This enabled the team to monitor and “co-localise” metals with other molecules and proteins in the brain.

And the findings of this work, said Hare, were revelatory.

"What we found is those particular cells (in the SNc) have what you could call an ‘anti-Goldilocks effect’ – they have just the right amount of iron and just the right amount of dopamine to cause damage," said Dr Hare.

"When we give mice a toxin that mimics the effects of Parkinson’s disease, these cells degenerate."

Hare theorises that this effect is likely a natural result of aging, when the brain’s ability to securely store iron diminishes and allows iron molecules to “leak” into critical areas such as the SNc.

Finding ways to design drugs that can get into the brain and eliminate surplus iron – an initiative that is already well underway in the process of treating other illnesses like cancer and Alzheimer’s disease – is now the next step forward in research.

Preventative measures to halt the build-up of iron in the brain as humans undergo the aging process are also touted by Hare as an important next step, and is something he is now working on.

"I think the real hope is, while we might not necessarily find a cure, prevention is actually not that far away," said Hare.

"So it’s a case where you can wake up and say, ‘my Parkinson’s is flaring up again’, take a tablet and go about your business."

(Image caption: In this microscope photo of motor neurons created in the laboratory of Su-Chun Zhang, green marks the nucleus and red marks the nerve fibers. Zhang and co-workers at the Waisman Center have identified a misregulation of protein in the nucleus as the likely first step in the pathology of ALS. Credit: Hong Chen, Su-Chun Zhang/Waisman Center)

Study helps unravel the tangled origin of ALS

By studying nerve cells that originated in patients with a severe neurological disease, a University of Wisconsin-Madison researcher has pinpointed an error in protein formation that could be the root of amyotrophic lateral sclerosis.

Also called Lou Gehrig’s disease, ALS causes paralysis and death. According to the ALS Association, as many as 30,000 Americans are living with ALS.

After a genetic mutation was discovered in a small group of ALS patients, scientists transferred that gene to animals and began to search for drugs that might treat those animals. But that approach has yet to work, says Su-Chun Zhang, a neuroscientist at the Waisman Center at UW-Madison, who is senior author of the new report, published April 3 in the journal Cell Stem Cell.

Zhang has been using a different approach — studying diseased human cells in lab dishes. Those cells, called motor neurons, direct muscles to contract and are the site of failure in ALS.

About 10 years ago, Zhang was the first in the world to grow motor neurons from human embryonic stem cells. More recently, he updated that approach by transforming skin cells into iPS (induced pluripotent stem) cells that were transformed, in turn, into motor neurons.

IPS cells can be used as “disease models,” as they carry many of the same traits as their donor. Zhang says the iPS approach offers a key advantage over the genetic approach, which “can only study the results of a known disease-causing gene. With iPS, you can take a cell from any patient, and grow up motor neurons that have ALS. That offers a new way to look at the basic disease pathology.”

In the new report, Zhang, Waisman scientist Hong Chen, and colleagues have pointed a finger at proteins that build a transport structure inside the motor neurons. Called neurofilament, this structure moves chemicals and cellular subunits to the far reaches of the nerve cell. The cargo needing movement includes neurotransmitters, which signal the muscles, and mitochondria, which process energy.

Motor neurons that control foot muscles are about three feet long, so neurotransmitters must be moved a yard from their origin in the cell body to the location where they can signal the muscles, Zhang says. A patient lacking this connection becomes paralyzed; tellingly, the first sign of ALS is often paralysis in the feet and legs.

Scientists have known for some time that in ALS, “tangles” along the nerve’s projections, formed of misshapen protein, block the passage along the nerve fibers, eventually causing the nerve fiber to malfunction and die. The core of the new discovery is the source of these tangles: a shortage of one of the three proteins in the neurofilament.

The neurofilament combines structural and functional roles, Zhang says. “Like the studs, joists and rafters of a house, the neurofilament is the backbone of the cell, but it’s constantly changing. These proteins need to be shipped from the cell body, where they are produced, to the most distant part, and then be shipped back for recycling. If the proteins cannot form correctly and be transported easily, they form tangles that cause a cascade of problems.”

Finding neurofilament tangles in an autopsy of an ALS patient “will not tell you how they happen, when or why they happen,” Zhang says. But with millions of cells — all carrying the human disease — to work with, Zhang’s research group discovered the source of the tangles in the protein subunits that compose the neurofilaments. “Our discovery here is that the disease ALS is caused by misregulation of one step in the production of the neurofilament,” he says.

Beyond ALS, Zhang says “very similar tangles” appear in Alzheimer’s and Parkinson’s diseases. “We got really excited at the idea that when you study ALS, you may be looking at the root of many neurodegenerative disorders.”

While working with motor neurons sourced in stem cells from patients, Zhang says he and his colleagues saw “quite an amazing thing. The motor neurons we reprogrammed from patient skin cells were relatively young, and we found that the misregulation happens very early, which means it is the most likely cause of this disease. Nobody knew this before, but we think if you can target this early step in pathology, you can potentially rescue the nerve cell.”

In the experiment just reported, Zhang found a way to rescue the neural cells living in his lab dishes. When his group “edited” the gene that directs formation of the deficient protein, “suddenly the cells looked normal,” Zhang says.

Already, he reports, scientists at the Small Molecule Screening and Synthesis Facility at UW-Madison are looking for a way to rescue diseased motor neurons. These neurons are made by the millions from stem cells using techniques that Zhang has perfected over the years.

Zhang says “libraries” of candidate drugs, each containing a thousand or more compounds, are being tested. “This is exciting. We can put this into action right away. The basic research is now starting to pay off. With a disease like this, there is no time to waste.”

New hope for treating ALS

Patient stem cells help identify common problem, leading to clinical trials

Harvard stem cell scientists have discovered that a recently approved medication for epilepsy might be a meaningful treatment for amyotrophic lateral sclerosis (ALS), also known as Lou Gehrig’s disease, a uniformly fatal neurodegenerative disorder. The researchers are now collaborating with Massachusetts General Hospital (MGH) to design an initial clinical trial testing the safety of the treatment in ALS patients.

The investigators all caution that a great deal of work needs to be done to assure the safety and efficacy of the treatment in ALS patients before physicians should start offering it.

The work, laid out in two related advance online publications in April by Cell Stem Cell and Cell Reports, is the long-term fruit of studies by Harvard Stem Cell Institute (HSCI) principal faculty member Kevin Eggan, who in a 2008 Science paper first raised the possibility of using ALS patient-derived stem cells to better understand the disease and identify therapeutic targets for new drugs.

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Meditation as object of medical research

Mindfulness meditation produces personal experiences that are not readily interpretable by scientists who want to study its psychiatric benefits in the brain. At a conference near Boston April 5, 2014, Brown University researchers will describe how they’ve been able to integrate mindfulness experience with hard neuroscience data to advance more rigorous study.

Mindfulness is always personal and often spiritual, but the meditation experience does not have to be subjective. Advances in methodology are allowing researchers to integrate mindfulness experiences with brain imaging and neural signal data to form testable hypotheses about the science — and the reported mental health benefits — of the practice.

A team of Brown University researchers, led by junior Juan Santoyo, will present their research approach at 2:45 p.m on Saturday, April 5, 2014, at the 12th Annual International Scientific Conference of the Center for Mindfulness at the University of Massachusetts Medical School. Their methodology employs a structured coding of the reports meditators provide about their mental experiences. That can be rigorously correlated with quantitative neurophysiological measurements.

“In the neuroscience of mindfulness and meditation, one of the problems that we’ve had is not understanding the practices from the inside out,” said co-presenter Catherine Kerr, assistant professor (research) of family medicine and director of translational neuroscience in Brown’s Contemplative Studies Initiative. “What we’ve really needed are better mechanisms for generating testable hypotheses – clinically relevant and experience-relevant hypotheses.”

Now researchers are gaining the tools to trace experiences described by meditators to specific activity in the brain.

“We’re going to [discuss] how this is applicable as a general tool for the development of targeted mental health treatments,” Santoyo said. “We can explore how certain experiences line up with certain patterns of brain activity. We know certain patterns of brain activity are associated with certain psychiatric disorders.”

Structuring the spiritual

At the conference, the team will frame these broad implications with what might seem like a small distinction: whether meditators focus on their sensations of breathing in their nose or in their belly. The two meditation techniques hail from different East Asian traditions. Carefully coded experience data gathered by Santoyo, Kerr, and Harold Roth, professor of religious studies at Brown, show that the two techniques produced significantly different mental states in student meditators.

“We found that when students focused on the breath in the belly their descriptions of experience focused on attention to specific somatic areas and body sensations,” the researchers wrote in their conference abstract. “When students described practice experiences related to a focus on the nose during meditation, they tended to describe a quality of mind, specifically how their attention ‘felt’ when they sensed it.”

The ability to distill a rigorous distinction between the experiences came not only from randomly assigning meditating students to two groups – one focused on the nose and one focused on the belly – but also by employing two independent coders to perform standardized analyses of the journal entries the students made immediately after meditating.

This kind of structured coding of self-reported personal experience is called “grounded theory methodology.” Santoyo’s application of it to meditation allows for the formation of hypotheses.

For example, Kerr said, “Based on the predominantly somatic descriptions of mindfulness experience offered by the belly-focused group, we would expect there to be more ongoing, resting-state functional connectivity in this group across different parts of a large brain region called the insula that encodes visceral, somatic sensations and also provides a readout of the emotional aspects of so-called ‘gut feelings’.”

Unifying experience and the brain

The next step is to correlate the coded experiences data with data from the brain itself. A team of researchers led by Kathleen Garrison at Yale University, including Santoyo and Kerr, did just that in a paper in Frontiers in Human Neuroscience in August 2013. The team worked with deeply experienced meditators to correlate the mental states they described during mindfulness with simultaneous activity in the posterior cingulate cortex (PCC). They measured that with real-time functional magnetic resonance imaging.

They found that when meditators of several different traditions reported feelings of “effortless doing” and “undistracted awareness” during their meditation, their PCC showed little activity, but when they reported that they felt distracted and had to work at mindfulness, their PCC was significantly more active. Given the chance to observe real-time feedback on their PCC activity, some meditators were even able to control the levels of activity there.

“You can observe both of these phenomena together and discover how they are co-determining one another,” Santoyo said. “Within 10 one-minute sessions they were able to develop certain strategies to evoke a certain experience and use it to drive the signal.”

Toward therapies

A theme of the conference, and a key motivator in Santoyo and Kerr’s research, is connecting such research to tangible medical benefits. Meditators have long espoused such benefits, but support from neuroscience and psychiatry has been considerably more recent.

In a February 2013 paper in Frontiers in Human Neuroscience, Kerr and colleagues proposed that much like the meditators could control activity in the PCC, mindfulness practitioners may gain enhanced control over sensory cortical alpha rhythms. Those brain waves help regulate how the brain processes and filters sensations, including pain, and memories such as depressive cognitions.

Santoyo, whose family emigrated from Colombia when he was a child, became inspired to investigate the potential of mindfulness to aid mental health beginning in high school. Growing up in Cambridge and Somerville, Mass., he observed the psychiatric difficulties of the area’s homeless population. He also encountered them while working in food service at Cambridge hospital.

“In low-income communities you always see a lot of untreated mental health disorders,” said Santoyo, who meditates regularly and helps to lead a mindfulness group at Brown. He is pursuing a degree in neuroscience and contemplative science. “The perspective of contemplative theory is that we learn about the mind by observing experience, not just to tickle our fancy but to learn how to heal the mind.”

It’s a long path, perhaps, but Santoyo and his collaborators are walking it with progress.