June 22, 2012

Neuropsychiatric conditions such as autism, schizophrenia and epilepsy involve an imbalance between two types of synapses in the brain: excitatory synapses that release the neurotransmitter glutamate, and inhibitory synapses that release the neurotransmitter GABA. Little is known about the molecular mechanisms underlying development of inhibitory synapses, but a research team from Japan and Canada has reported that a molecular signal between adjacent neurons is required for the development of inhibitory synapses.

Figure 1: Compared with the brains of normal animals (left), mice lacking the Slitrk3 gene (right) have a reduced density of inhibitory synapses in the hippocampus. Reproduced from Ref. 1 © 2012 Jun Aruga, RIKEN Brain Science Institute

In earlier work, the researchers—led by Jun Aruga of the RIKEN Brain Science Institute, Wako, and Ann Marie Craig of the University of British Colombia, Vancouver—showed that a membrane protein called Slitrk2 organizes signaling molecules at synapses. They therefore tested whether five related proteins are involved in inhibitory synapse development. They cultured immature hippocampal neurons with non-neural cells expressing each of the six Slitrk proteins. They found that Slitrk3, but not other Slitrk proteins, induced clustering of VGAT, a GABA transporter protein found only at inhibitory synapses.

The researchers also examined the localization of Slitrk3 by tagging it with yellow fluorescent protein and introducing it into cultured hippocampal cells. This revealed that Slitrk3 co-localizes in the dendrites of neurons with gephyrin, a scaffold protein found only in inhibitory synapses. They then blocked Slitrk3 synthesis, and found that it led to a significant reduction in the number of inhibitory synapses.

To confirm these findings, the researchers generated a strain of genetically engineered mice lacking the Slitrk3 gene. These animals had significantly fewer inhibitory synapses than normal animals (Fig. 1), and therefore impaired neurotransmission of GABA. They were also susceptible to epileptic seizures. From a screen for proteins that bind to Slitrk3, Aruga, Craig and colleagues identified the protein PTPδ as its only binding partner. Introduction of PTPδ fused to yellow fluorescent protein to cultured hippocampal neurons showed that it is expressed in neuronal dendrites and cell bodies, but not in axons. Blocking PTPδ synthesis prevented the induction of inhibitory synapses by the Slitrk3 protein.

These results demonstrated that the interaction between Slitrk3 on dendrites and PTPδ on axons of adjacent cells is required for the proper development of inhibitory synapses and for inhibitory neurotransmission in the brain.

“We are now examining whether the balance of excitatory and inhibitory synapses is affected by other members of the Slitrk protein family,” says Aruga. “It is possible that Slitrk3 and other Slitrk proteins are acting synergistically or antagonistically. We are also clarifying whether Slitrk3 is involved in any neurological disorders.”

Provided by RIKEN

Source: medicalxpress.com

ScienceDaily (June 21, 2012) — Preventing diabetes or delaying its onset has been thought to stave off cognitive decline — a connection strongly supported by the results of a 9-year study led by researchers at the University of California, San Francisco (UCSF) and the San Francisco VA Medical Center.

Earlier studies have looked at cognitive decline in people who already had diabetes. The new study is the first to demonstrate that the greater risk of cognitive decline is also present among people who develop diabetes later in life. It is also the first study to link the risk of cognitive decline to the severity of diabetes.

The result is the latest finding to emerge from the Health, Aging, and Body Composition (Health ABC) Study, which enrolled 3,069 adults over 70 at two community clinics in Memphis, TN and Pittsburgh, PA beginning in 1997. All the patients provided periodic blood samples and took regular cognitive tests over time.

When the study began, hundreds of those patients already had diabetes. A decade later, many more of them had developed diabetes, and many also suffered cognitive decline. As described this week in Archives of Neurology, those two health outcomes were closely linked.

People who had diabetes at the beginning of the study showed a faster cognitive decline than people who developed it during the course of the study — and these people, in turn, tended to be worse off than people who never developed diabetes at all. The study also showed that patients with more severe diabetes who did not control their blood sugar levels as well suffered faster cognitive declines.

"Both the duration and the severity of diabetes are very important factors," said Kristine Yaffe, MD, the lead author of the study. "It’s another piece of the puzzle in terms of linking diabetes to accelerated cognitive aging."

An important question for future studies, she added, would be to ask if interventions that would effectively prevent, delay or better control diabetes would also lower people’s risk of cognitive impairment later in life.

Yaffe is the Roy and Marie Scola Endowed Chair of Psychiatry; professor in the UCSF departments of Psychiatry, Neurology and Epidemiology and Biostatistics; and Chief of Geriatric Psychiatry and Director of the Memory Disorders Clinic at the San Francisco VA Medical Center.

Diabetes and Cognitive Decline

Diabetes is a chronic and complex disease marked by high levels of sugar in the blood that arise due to problems with the hormone insulin, which regulates blood sugar levels. It is caused by an inability to produce insulin (type 1) or an inability to respond correctly to insulin (type 2).

A major health concern in the United States, diabetes of all types affects an estimated 8.3 percent of the U.S. population — some 25.8 million Americans — and costs U.S. taxpayers more than $200 billion annually. In California alone, an estimated 4 million people (one out of every seven adults) has type 2 diabetes and millions more are at risk of developing it. These numbers are poised to explode in the next half century if more is not done to prevent the disease.

Over the last several decades, scientists have come to appreciate that diabetes affects many tissues and organs of the body, including the brain and central nervous system — particularly because diabetes places people at risk of cognitive decline later in life.

In their study the scientists looked at a blood marker known as “glycosylated hemoglobin,” a standard measure of the severity of diabetes and the ability to control it over time. The marker shows evidence of high blood sugar because these sugar molecules become permanently attached to hemoglobin proteins in the blood. Yaffe and her colleagues found that greater levels of this biomarker were associated with more severe cognitive dysfunction.

While the underlying mechanism that accounts for the link between diabetes and risk of cognitive decline is not completely understood, Yaffe said, it may be related to a human protein known as insulin degrading enzyme, which plays an important role in regulating insulin, the key hormone linked to diabetes. This same enzyme also degrades a protein in the brain known as beta-amyloid, a brain protein linked to Alzheimer’s disease.

Source: Science Daily

ScienceDaily (June 21, 2012) — Scientists have developed a small-molecule-inhibiting drug that in early laboratory cell tests stopped breast cancer cells from spreading and also promoted the growth of early nerve cells called neurites.

Researchers from Cincinnati Children’s Hospital Medical Center report their findings online June 21 in Chemistry & Biology. The scientists named their lead drug candidate “Rhosin” and hope future testing shows it to be promising for the treatment of various cancers or nervous system damage.

The inhibitor overcomes a number of previous scientific challenges by precisely targeting a single component of a cell signaling protein complex called Rho GTPases. This complex regulates cell movement and growth throughout the body. Miscues in Rho GTPase processes are also widely implicated in human diseases, including various cancers and neurologic disorders.

"Although still years from clinical development, in principle Rhosin could be useful in therapy for many kinds of cancer or possibly neuron and spinal cord regeneration," said Yi Zheng, PhD, lead investigator and director of Experimental Hematology and Cancer Biology at Cincinnati Children’s. "We’ve performed in silica (computerized) rational drug design, pharmacological characterization and cell tests in the laboratory, and we are now starting to work with mouse models."

Because the role of Rho GTPases in cellular processes and cancer formation is well established, researchers have spent years trying to identify safe and effective therapeutic targets for specific parts of the protein complex. In particular, scientists have focused on the center protein in the complex called RhoA, which is essential for the signaling function of the complex. In breast cancer for example, increased RhoA activity makes the cancer cells more invasive and causes them to spread, while a deficiency of RhoA suppresses cancer growth and progression.

Despite this knowledge, past efforts to develop an effective small-molecule inhibitor for RhoA have failed, explained Zheng, who has studied Rho GTPases for over two decades. Most roadblocks stem from a lack of specificity in how researchers have been able to target RhoA, a resulting lack of efficiency in affecting molecular processes, problems with toxicity, and the inability to find a workable drug design.

For the current study, Zheng and his colleagues started with the extensive body of research from Cincinnati Children’s and other institutions describing the processes and functions of Rho GTPases. They then used high-throughput computerized molecular screening and computerized drug design to reveal a druggable target site. This also provided a preliminary virtual simulation on the potential effectiveness of candidate drugs.

A key challenge to binding a small-molecule inhibitor to RhoA is the protein’s globular structure and lack of surface pocket areas suitable for easy binding, Zheng said. The unique chemical structure of the lead compound identified by researchers, Rhosin, allows it to effectively bind to two shallow surface grooves on RhoA. This enables the candidate drug to take root and begin affecting cells. The two-legged configuration of Rosin also describes a useful drug design strategy for more effectively targeting difficult molecular sites like RhoA.

The researchers also wanted to make sure Rhosin effectively blocked what are known as guanine nucleotide exchange factors (GEFs). Guanine nucleotide is a critical energy source and signaling component of cells. Activation of GEFs is required to set off the regulatory signaling of GTPases (GTP stands for guanosine triphosphate).

After conducting a series of laboratory cell tests to verify the targeting and binding capabilities of Rhosin to RhoA, the researchers then tested the candidate drug’s impact on cultured breast cancer cells and nerve cells.

In tests on a human breast cancer cells, Rhosin inhibited cell growth and the formation of mammary spheres in a dose dependent manner, acting specifically on RhoA molecular targets without disrupting other critical cellular processes. Rhosin does not affect non-cancerous breast cells. This, along with other tests the scientists performed, indicated Rhosin’s effectiveness in targeting RhoA-mediated breast cancer proliferation, according to the researchers.

Researchers also treated an extensively tested line of neuronal cells with Rhosin, along with nerve growth factor, a protein that is important to the growth and survival of neurons. Rhosin worked with nerve growth factor in a dose-dependent way to promote the proliferation of branching neurites from the neuronal cells. Neurites are young or early stage extensions from neurons required for neuronal communications.

Source: Science Daily

ScienceDaily (June 21, 2012) — Eating disorders are commonly seen as an issue faced by teenagers and young women, but a new study reveals that age is no barrier to disordered eating. In women aged 50 and over, 3.5% report binge eating, nearly 8% report purging, and more than 70% are trying to lose weight. The study published in the International Journal of Eating Disorders revealed that 62% of women claimed that their weight or shape negatively impacted on their life.

The researchers, led by Dr Cynthia Bulik, Director of the University of North Carolina Eating Disorders Program, reached 1,849 women from across the USA participating in the Gender and Body Image Study (GABI) with a survey titled, ‘Body Image in Women 50 and Over — Tell Us What You Think and Feel.’

"We know very little about how women aged 50 and above feel about their bodies," said Bulik. "An unfortunate assumption is that they ‘grow out of’ body dissatisfaction and eating disorders, but no one has really bothered to ask. Since most research focuses on younger women, our goal was to capture the concerns of women in this age range to inform future research and service planning."

The average age of the participants was 59, while 92% were white. More than a quarter, 27%, were obese, 29% were overweight, 42% were normal weight and 2% were underweight.

Results revealed that eating disorder symptoms were common. About 8% of women reported purging in the last five years and 3.5% reported binge eating in the last month. These behaviors were most prevalent in women in their early 50s, but also occurred in women over 75.

When it came to weight issues, 36% of the women reported spending at least half their time in the last five years dieting, 41% checked their body daily and 40% weighed themselves a couple of times a week or more.

62% of women claimed that their weight or shape negatively impacted their life, 79% said that it affected their self-perception and 64% said that they thought about it daily.

The women reported resorting to a variety of unhealthy methods to change their body, including diet pills (7.5%), excessive exercise (7%), diuretics (2.5%), laxatives (2%) and vomiting (1%).

Two-thirds, 66%, were unhappy with their overall appearance and this was highest when it came to their stomach, 84%, and shape, 73%.

"The bottom line is that eating disorders and weight and shape concerns don’t discriminate on the basis of age," concluded Bulik. "Healthcare providers should remain alert for eating disorder symptoms and weight and shape concerns that may adversely influence women’s physical and psychological wellbeing as they mature."

Source: Science Daily

ScienceDaily (June 21, 2012) — A pioneering report of genome-wide gene expression in autism spectrum disorders (ASDs) finds genetic changes that help explain why one person has an ASD and another does not. The study, published by Cell Press on June 21 in The American Journal of Human Genetics, pinpoints ASD risk factors by comparing changes in gene expression with DNA mutation data in the same individuals. This innovative approach is likely to pave the way for future personalized medicine, not just for ASD but also for any disease with a genetic component.

ASDs are a heterogeneous group of developmental conditions characterized by social deficits, difficulty communicating, and repetitive behaviors. ASDs are thought to be highly heritable, meaning that they run in families. However, the genetics of autism are complex.

Researchers have found rare changes in the number of copies of defined genetic regions that associate with ASD. Although there are some hot-spot regions containing these alterations, very few genetic changes are exactly alike. Similarly, no two autistic people share the exact same symptoms. To discover how these genetic changes might affect gene transcription and, thus, the presentation of the disorder, Rui Luo, a graduate student in the Geschwind lab at UCLA, studied 244 families in which one child (the proband) was affected with an ASD and one was not.

In addition to identifying several potential new regions where copy-number variants (CNVs) are associated with ASDs, Geschwind’s team found genes within these regions to be significantly misregulated in ASD children compared with their unaffected siblings. “Strikingly, we observed a higher incidence of haploinsufficient genes in the rare CNVs in probands than in those of siblings, strongly indicating a functional impact of these CNVs on expression,” says Geschwind. Haploinsuffiency occurs when only one copy of a gene is functional; the result is that the body cannot produce a normal amount of protein. The researchers also found a significant enrichment of misexpressed genes in neural-related pathways in ASD children. Previous research has found that these pathways include other genetic variants associated with autism, which Geschwind explains further legitimizes the present findings.

Source: Science Daily

June 21, 2012 By Janice Wood

Thanks to science, we know that love lives in the brain, not the heart.

Now a new international study has mapped out where love and sexual desire are in the brain.

“No one has ever put these two together to see the patterns of activation,” says Dr. Jim Pfaus, professor of psychology at Concordia University.

“We didn’t know what to expect –the two could have ended up being completely separate. It turns out that love and desire activate specific but related areas in the brain.”

Working with colleagues in the United States and Switzerland, Pfaus analyzed the results of 20 separate studies that examined brain activity while subjects engaged in tasks such as viewing erotic pictures or looking at photographs of their significant others. Pooling this data enabled the scientists to form a map of love and desire in the brain.

They found that two brain structures, the insula and the striatum, are responsible for tracking the progression from sexual desire to love.

The insula is a portion of the cerebral cortex folded deep within an area between the temporal lobe and the frontal lobe, while the striatum is located nearby, inside the forebrain.

According to the researchers, love and sexual desire activate different areas of the striatum. The area activated by sexual desire is usually turned on by things that are inherently pleasurable, such as sex or food.

The area activated by love is involved in the process of conditioning in which things paired with reward or pleasure are given inherent value. That is, as feelings of sexual desire develop into love, they are processed in a different place in the striatum, the researchers explain.

This area of the striatum is also the part of the brain associated with drug addiction. Pfaus says there is good reason for this.

“Love is actually a habit that is formed from sexual desire as desire is rewarded,” he explains. “It works the same way in the brain as when people become addicted to drugs.”

However, the habit is not a bad one, he said, noting that love activates different pathways in the brain that are involved in monogamy and pair bonding. Some areas in the brain are actually less active when a person feels love than when they feel desire, he added.

“While sexual desire has a very specific goal, love is more abstract and complex, so it’s less dependent on the physical presence someone else,” says Pfaus.

Source: PsychCentral

June 20, 2012 By Robin Erb

Go ahead - do it: Grab a pencil. Right now. Write your name backward. And upside down. Awkward, right?

But if researchers and neurologists are correct, doing exercises like these just might buy you a bit more time with a healthy brain.

Some research suggests that certain types of mental exercises - whether they are memory games on your mobile device or jotting down letters backward - might help our gray matter maintain concentration, memory and visual and spatial skills over the years.

"There is some evidence of a use-it-or-lose-it phenomenon," says Dr. Michael Maddens, chief of medicine at Beaumont Hospital, Royal Oak, Mich.

Makers of computer brain games, in fact, are tapping into a market of consumers who have turned to home treadmills and gym memberships to maintain their bodies, and now worry that aging might take its toll on their mental muscle as well.

But tweaking every day routines can help.

Like brushing your teeth with your non-dominant hand. Or crossing your arms the opposite way you’re used to, says Cheryl Deep, who leads “Brain Neurobics” sessions on behalf of the Wayne State Institute of Gerontology.

At a recent session in Novi, Mich., Deep encouraged several dozen senior citizens to flip the pictures in their homes upside-down. It might baffle houseguests, but the exercise crowbars the brain out of familiar grooves cut deep by years of mindless habit.

"Every time you walk past and look, your brain has to rotate that image," Deep says. "Brain neurobics is about getting us out of those ruts, those pathways, and shaking things up."

Participants were asked to call out the color of ink that flashed on a screen in front them. The challenge: The colors spelled out names of other colors. Blue ink spelled o-r-a-n-g-e, for example.

Several in the crowd at Waltonwood Senior Living hesitated - a few scrunching up faces in concentration. The first instinct is to say “orange.”

In another exercise, participants had to try to name as many red foods as possible. Apple? Sure that’s an easy one. It took a while, but the crowd eventually made its way to pomegranate and pimento.

Elissa and Hal Leider chuckled with friends as they tested their recall.

Hal Leider, 82, a retired carpenter, was diagnosed with early-stage Alzheimer’s, and he tries to challenge himself mentally and physically - bowling and shooting pool and playing poker: “I think anything we can do might be helpful,” says Elissa Leider, 74.

The idea of mental workouts marks a dramatic shift in how we understand the brain these days.

"We want to stretch and flex and push" the brain, says Moriah Thomason, assistant professor in Wayne State University School of Medicine’s pediatrics department and in the Merrill Palmer Skillman Institute for Child and Family Development

Thomason also is a scientific adviser to http://www.Lumosity.com, one of the fastest-growing brain game websites.

"We used to think that what you’re born with is what you have through life. But now we understand that the brain is a lot more plastic and flexible than we ever appreciated," she says.

Still, like the rest of your body, aging takes its toll, she says.

The protective covering of the neural cells - white matter - begins to shrink first. Neural and glial cells, often called the gray matter, begin to shrink as well, but more slowly. Neurotransmitters, or chemical messengers, decrease.

But challenging the brain stimulates neural pathways - those tentacles that look like tree branches in a cluster of brain cells. It boosts the brain’s chemistry and connectivity, refueling the entire engine.

"Certain activities will lay more neural pathways that can be more readily re-engaged," Thomason says. "The hope is that there are ways to train and strengthen these pathways."

Maddens explains it this way: Consider the neurons of your brain like electrical wires and the white matter like the insulation. When the insulation breaks down over time, things can misfire.

In labs, those who engaged in mentally challenging games do, in fact, show improvement in cognitive functioning. They get faster at speed games and stronger in memory games, for example.

What’s less clear is whether this improvement transfers to everyday tasks, like remembering where you parked the car or the name of your child’s teacher, both Thomason and Maddens say.

But when it comes to the link between physical exercise and the brain, researchers and clinicians agree: physical exercise is good for the brain; it has also been linked to lower rates of chronic disease. Good nutrition is essential too.

Oxygen, itself, is essential, Deep said: “Your brain is an oxygen hog.”

Diet, exercise and mental maneuvers all may boost brain health in ways science still doesn’t understand. In the best cases, the right mix might stave off the effects of Alzheimer’s and other age-related disease too, Maddens says.

All this is good news for an aging, stressed out, and too-busy society, he says.

Reading a book, engaging with friends or going out for a walk and paying attention to what’s around you - that’s not really about goofing off. Rather, it’s critical time that stimulates neural pathways and boosts the odds of long-time brain health.

"It’s talking to friends. It’s getting out socially. It’s engaging in life. The question is ‘How do I force myself to learn?’" Thomason says.

The same might be true when it comes to mentally changing computer games.

Says Maddens: “Would I have patients playing computer games eight hours a day in hopes that they can delay Alzheimer’s by two months? No. But you can enjoy (playing such games) and possibly get a benefit from it, too.”

Read more …

ScienceDaily (June 20, 2012) — Most of us assume that confidence and certainty are preferred over uncertainty and bewilderment when it comes to learning complex information. But a new study led by Sidney D’Mello of the University of Notre Dame shows that confusion when learning can be beneficial if it is properly induced, effectively regulated and ultimately resolved.

Most of us assume that confidence and certainty are preferred over uncertainty and bewilderment when it comes to learning complex information. But a new study shows that confusion when learning can be beneficial if it is properly induced, effectively regulated and ultimately resolved. (Credit: © Ana Blazic Pavlovic / Fotolia)

The study will be published in a forthcoming issue of the journal Learning and Instruction.

Notre Dame psychologist and computer scientist D’Mello, whose research areas include artificial intelligence, human-computer interaction and the learning sciences, together with Art Graesser of the University of Memphis, collaborated on the study, which was funded by the National Science Foundation.

They found that by strategically inducing confusion in a learning session on difficult conceptual topics, people actually learned more effectively and were able to apply their knowledge to new problems.

In a series of experiments, subjects learned scientific reasoning concepts through interactions with computer-animated agents playing the roles of a tutor and a peer learner. The animated agents and the subject engaged in interactive conversations where they collaboratively discussed the merits of sample research studies that were flawed in one critical aspect. For example, one hypothetical case study touted the merits of a diet pill, but was flawed because it did not include an appropriate control group. Confusion was induced by manipulating the information the subjects received so that the animated agents sometimes disagreed with each other and expressed contradictory or incorrect information. The agents then asked subjects to decide which opinion had more scientific merit, thereby putting the subject in the hot spot of having to make a decision with incomplete and sometimes contradictory information.

In addition to the confusion and uncertainty triggered by the contradictions, subjects who were confused scored higher on a difficult post-test and could more successfully identify flaws in new case studies.

"We have been investigating links between emotions and learning for almost a decade, and find that confusion can be beneficial to learning if appropriately regulated because it can cause learners to process the material more deeply in order to resolve their confusion," D’Mello says.

According to D’Mello, it is not advisable to intentionally confuse students who are struggling or induce confusion during high-stakes learning activities. Confusion interventions are best for higher-level learners who want to be challenged with difficult tasks, are willing to risk failure, and who manage negative emotions when they occur.

"It is also important that the students are productively instead of hopelessly confused. By productive confusion, we mean that the source of the confusion is closely linked to the content of the learning session, the student attempts to resolve their confusion, and the learning environment provides help when the student struggles. Furthermore, any misleading information in the form of confusion-induction techniques should be corrected over the course of the learning session, as was done in the present experiments."

According to D’Mello, the next step in this body of research is to apply these methods to some of the more traditional domains such as physics, where misconceptions are common.

Source: Science Daily

ScienceDaily (June 20, 2012) — Cedars-Sinai’s Regenerative Medicine Institute has pioneered research on how motor-neuron cell-death occurs in patients with spinal muscular atrophy, offering an important clue in identifying potential medicines to treat this leading genetic cause of death in infants and toddlers.

The study, published in the June 19 online issue of PLoS ONE, extends the institute’s work to employ pluripotent stem cells to find a pharmaceutical treatment for spinal muscular atrophy or SMA, a genetic neuromuscular disease characterized by muscle atrophy and weakness.

"With this new understanding of how motor neurons die in spinal muscular atrophy patients, we are an important step closer to identifying drugs that may reverse or prevent that process," said Clive Svendsen, PhD, director of the Cedars-Sinai Regenerative Medicine Institute.

Svendsen and his team have investigated this disease for some time now. In 2009, Nature published a study by Svendsen and his colleagues detailing how skin cells taken from a patient with the disorder were used to generate neurons of the same genetic makeup and characteristics of those affected in the disorder; this created a “disease-in-a-dish” that could serve as a model for discovering new drugs.

As the disease is unique to humans, previous methods to employ this approach had been unreliable in predicting how it occurs in humans. In the research published in PLoS ONE, the team reproduced this model with skin cells from multiple patients, taking them back in time to a pluripotent stem cell state (iPS cells), and then driving them forward to study the diseased patient-specific motor neurons.

Children born with this disorder have a genetic mutation that doesn’t allow their motor neurons to manufacture a critical protein necessary for them to survive. The study found these cells die through apoptosis — the same form of cell death that occurs when the body eliminates old, unnecessary as well as unhealthy cells. As motor neuron cell death progresses, children with the disease experience increasing paralysis and eventually death. There is no effective treatment now for this disease. An estimated one in 35 to one in 60 people are carriers and about in 100,000 newborns have the condition.

"Now we are taking these motor neurons (from multiple children with the disease and in their pluripotent state) and screening compounds that can rescue these cells and create the protein necessary for them to survive," said Dhruv Sareen, director of Cedars-Sinai’s Induced Pluripotent Stem Cell Core Facility and a primary author on the study. "This study is an important stepping stone to guide us toward the right kinds of compounds that we hope will be effective in the model — and then be reproduced in clinical trials."

Source: Science Daily