The journey of a marathon sleeper

A marathon sleeper who got away left some clues for Emory and University of Florida scientists to Read more

A push for reproducibility in biomedical research

At Emory, several scientists are making greater efforts to push forward to improve scientific research and combat what is being called “the reproducibility crisis.” Guest post from Erica Read more

Exosomes as potential biomarkers of radiation exposure

Exosomes = potential biomarkers of radiation in the Read more

Neuro

Brain chemical linked to migraines could be anxiety target

Neuroscientist Michael Davis, PhD, and his colleagues have devoted years to mapping out the parts of the brain responsible for driving fear and anxiety. In a recent review article, they describe the differences between fear and anxiety in this way:

Fear is a generally adaptive state of apprehension that begins rapidly and dissipates quickly once the threat is removed (phasic fear). Anxiety is elicited by less specific and less predictable threats, or by those that are physically or psychologically more distant (sustained fear).

Michael Davis is an investigator at Yerkes National Primate Research Center and Emory School of Medicine

A host of their studies suggest that one part of the brain, the amygdala, is instrumental in producing “phasic fear,” while the bed nucleus of the stria terminalis (BNST) is important for “sustained fear.”

In a new report in the Journal of Neuroscience, Davis’ team describes the effects of a brain communication chemical, which is known primarily for its role in driving migraine headaches, in enhancing anxiety.

“This is the first study to show a role of this peptide, in a brain area we’ve identified as being important for anxiety.  This could lead to new drug targets to selectively reduce anxiety,” Davis says.

His team found that introducing calcitonin gene-related peptide (CGRP) into rats’ BNSTs can increase the anxiety they experience from loud noises or light, in that they startle more and avoid well-lit places. This peptide appears to activate other parts of the brain including the amygdala, hypothalamus and brainstem, producing fear-related symptoms.

Slice of rat brain showing the bed nucleus of the stria terminalis (BNST) and the central amygdala (Ce)

If Davis and his colleagues block CGRP’s function by introducing a short, decoy version of CGRP into the BNST, the reverse does not happen: the rats are not more relaxed. However, the short version does block the startle-enhancing effects of a smelly chemical produced by foxes that scientists use to heighten anxiety-like behavior in rats. This suggests that interfering with CGRP can reduce fear-related symptoms in situations where the rats are already under stress.

“Blockade of CGRP receptors may thus represent a novel therapeutic target for the treatment of stress-induced anxiety and related psychopathologies such as post-traumatic stress disorder,” says the paper’s first author, postdoctoral fellow Kelly Sink.

In fact, experimental drugs that work against CGRP are already in clinical trials to treat migraine headaches. But first, Sink reports that she and her colleagues are examining the relationship between CGRP and the stress hormone CRF (corticotropin-releasing factor) — another target of pharmacological interest — in the parts of the brain important for fear responses.

Posted on by Quinn Eastman in Neuro 1 Comment

National Academy of Sciences recognizes Yerkes Primate Center neuroscientist

Elizabeth A. Buffalo, PhD

The National Academy of Sciences (NAS) has recognized 13 individuals with awards acknowledging extraordinary scientific achievements in the areas of biology, chemistry, physics, economics and psychology.

Elizabeth A. Buffalo, PhD, a researcher at the Yerkes National Primate Research Center, is one of two recipients of the Troland Research Awards. Buffalo is being honored for innovative, multidisciplinary study of the hippocampus and the neural basis of memory. Troland Research Awards of $50,000 are given annually to recognize unusual achievement by young investigators and to further empirical research in experimental psychology.

The recipients will be honored in a ceremony on Sunday, May 1, during the NAS 148th annual meeting.

Posted on by Holly Korschun in Neuro Leave a comment

Shedding light on the vitamin D-Parkinson’s connection

Vitamin D may be called a vitamin, but it’s not. That’s because we can make it by exposing our skin to sunshine. So, technically that makes vitamin D a hormone–a steroid hormone to be exact. In fact, we get most of our exposure to vitamin D directly from sunshine and some from foods such as milk, fortified orange juice and oily fishes like salmon.

But no matter what you call it or where you get it, vitamin D is vital to growth, development and maintenance of our cells. Doctors have known for decades that vitamin D promotes calcium uptake and bone formation, but evidence is accumulating that it regulates the immune system and the development of the nervous system. Growing evidence suggests a link between low vitamin D levels and Parkinson’s disease, but whether this is a cause-and-effect relationship is unknown.

Marian Evatt, MD

That’s why Emory neurologist Marian Evatt, MD, and her colleagues are conducting a clinical trial exploring the effects of vitamin D supplementation on patients with Parkinson’s disease who have low vitamin D levels. The study also includes further epidemiological studies of vitamin D in Parkinson’s disease.

Parkinson’s disease affects nerve cells in several parts of the brain, particularly those that use the chemical messenger dopamine to control movement. The most common symptoms of Parkinson’s disease are tremor, stiffness and slowness of movement.

“Vitamin D has become associated with many chronic diseases: diabetes, hypertension, cardiovascular disease, and some of the autoimmune diseases, including multiple sclerosis,” says Evatt. “But we haven’t yet determined the specific effect of vitamin D in specific conditions because it has such broad effects.”

To hear Evatt talk about what vitamin D is, what it does, and why we need it, please go to Emory’s latest Sound Science podcast.

Posted on by Robin Tricoles in Neuro Leave a comment

Smart mice, clever names and some context

This week a variety of media outlets and science-oriented Web sites had fun with research at Emory — published recently in PNAS — investigating a gene that appears to limit some forms of learning and memory.

Mice with a disabled RGS14 gene remembered objects in their cages more easily and learned to navigate water mazes better, pharmacologist John Hepler and his colleagues found. Since the presence of a functional RGS14 gene holds mice back mentally, Hepler and his colleagues have been jokingly calling it “the Homer Simpson gene.”

This description struck a chord; the Atlantic magazine even embellished the story with a video showing the “D’oh”-ey cartoon character evolving from a single cell into a human couch potato.

It’s important to recognize that smart mice are not so surprising to scientists anymore. Back in 1999, scientists at Princeton announced the creation of “Doogie Howser” mice (named after a precocious doctor from another TV series). These critters performed better than normal lab mice in some of the same tests that Hepler’s team used to evaluate the RGS14-deleted mice.

One important difference: the Doogie mice had all their normal genes, and were overproducing a NMDA receptor gene involved in helping neurons communicate. Still, as a helpful 2009 round-up in Nature Reviews Neuroscience explains, scientists have found several single-gene knock-out mice that do better on tests of learning and memory. Many of these genetic alterations affect the process of long term potentiation, a process where neurons that get stimulated at the same time have the connections between them grow stronger.

RGS14 is turned on primarily in the CA2 region of the hippocampus

What makes the RGS14 gene an intriguing case is that it’s primarily turned on in the enigmatic CA2 region of the hippocampus. The CA2 region is normally relatively resistant to long-term potentiation and is also more hardy in situations of stroke or seizure.

Hepler observes that the vasopressin receptor 1b gene is also turned on predominantly in the CA2 region, and seems to be involved in aggression and social memory. He and his colleagues are planning to examine whether the RGS14-disabled mice have altered capabilities in those areas. Conveniently, Larry Young’s laboratory at Yerkes National Primate Research Center has been investigating the functions of vasopressin receptors in voles.

One last note: scientists in Spain have reported in Science that they can generate a variety of smart mice by putting the RGS14 gene on overdrive in a part of the brain where it’s not usually turned on. So whatever precise function RGS14 has, it doesn’t always dumb things down.

Posted on by Quinn Eastman in Neuro 1 Comment

New drug strategy against fragile X

Even as clinical trials examining potential treatments for fragile X syndrome gain momentum, Emory scientists have identified a new strategy for treating the neurodevelopmental disorder.

In a paper recently published in Journal of Neuroscience, a team led by cell biologist Gary Bassell shows that PI3 kinase inhibitors could restore normal appearance and levels of protein production at the synapses of hippocampal neurons from fragile X model mice. The next steps, studies in animals, are underway.

“This is an important first step toward having a new therapeutic strategy for fragile X syndrome that treats the underlying molecular defect, and it may be more broadly applicable to other forms of autism,” he says.

A recent Nature Biotechnology article describes pharmaceutical approaches to autism and fragile X.

Posted on by Quinn Eastman in Neuro 1 Comment

Alzheimer’s expert weighs in on proposed guidelines

Scans can show beta amyloid, a protein associated with Alzheimer’s disease (right)

For the first time in 25 years, medical experts are proposing new diagnostic criteria aimed at better and earlier detection of Alzheimer’s disease (AD).

The guidelines, proposed by the National Institute on Aging (NIA) and the Alzheimer’s Association, update and revise the current Alzheimer’s criteria with modern technologies and the latest research advances.

According to the Alzheimer’s Association, an estimated 5.3 million Americans have AD, most of them 65 and older. The disease is thought to begin years, possibly even decades, before symptoms are noticeable. But there is no single, generally accepted way to identify the disease in its earliest stages before symptoms are evident.

The new diagnostic guidelines focus on advances in detecting biomarkers for the disease, such as substances found in spinal fluid or appearing on cutting-edge brain imaging scans conducted with PET or MRI.

Emphasis will be on diagnosing early stages of the disease as soon as possible so that patients can take measures to slow the progression or prevent further damage.

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Posted on by Jennifer Johnson in Neuro Leave a comment

Untangling the mysteries of Alzheimer’s disease

Lary Walker, PhD

Consider this: Alzheimer’s is a uniquely human disorder. But why? Why don’t nonhuman primates, such as monkeys, get Alzheimer’s disease. Monkeys form the senile plaques that are identical to the plaques found in humans. So do other animals.

“Yet, despite the fact that nonhuman primates make this protein that we know is very important in the pathogenesis of Alzheimer’s disease, they don’t develop the full disease,” says Lary Walker, PhD. Walker is an associate professor at Yerkes National Primate Research Center.

“They don’t develop the tangles we associate with Alzheimer’s disease, the neuronal loss, the shrinkage of the brain, and they don’t get demented in the sense that humans do,” says Walker.

When our bodies make a protein, the protein tends to fold into a functional form. But when it comes to Alzheimer’s disease, some proteins misfold, becoming sticky and then combining with one another. In their collective form, the proteins can then form plaques or tangles, the two types of lesions associated with Alzheimer’s disease.

And for some unknown reason, people who have plaques usually go on to form tangles. But people who have tangles don’t always go on to form plaques. No one is sure why. But that’s what researcher Walker wants to find out.

To listen to Walker’s own words about Alzheimer’s disease, access Emory’s new Sound Science podcast.

Posted on by Robin Tricoles in Neuro Leave a comment

Study: ADHD linked to pesticide exposure

A study published in the May 17, 2010, issue of the journal Pediatrics found that one type of pesticide commonly used on fruits and vegetables may be contributing to attention deficit hyperactivity disorder, or ADHD, in children.

The study measured the levels of pesticide byproducts in the urine of 1,139 children from across the United States. Children with the highest concentration of pesticides in their urine were more likely to have symptoms of ADHD.

Dana Boyd Barr, PhD, a research professor in the Rollins School of Public Health at Emory, spent more than 20 years studying pesticide exposure at the Centers for Disease Control and Prevention (CDC). Barr was not a member of the research team that published these findings on pesticides and ADHD, but data generated in her former CDC lab was analyzed for this particular study.

Barr says while the study doesn’t prove causality between pesticide exposures and ADHD, it does shed light on how even low level daily exposures to pesticides could potentially impact cognitive health.

“It seems very plausible that low-level daily exposures to pesticides can produce some subtle effects like ADHD or other neurological delays,” she says.

Barr notes that additional research is needed to confirm a connection to pesticides and ADHD, but says there are tips for limiting your exposure to commonly used pesticides.

“We’ve done studies here at Emory and also at CDC that have indicated that if you use organic food or if you wash your food properly prior to preparation, you can reduce the levels of these metabolites in your urine.  Eat as much organic produce as possible, or wash your fruits and vegetables very well and that likely could decrease the chances of your children developing ADHD,” says Barr.

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Quirky little prairie voles hold answers

Larry Young, PhD

So says Larry Young, PhD, chief of the Division of Behavioral Neuroscience and Psychiatric Disorders at the Yerkes National Primate Research Center, Emory University.

Young, who is world-renowned for his work on the role of neuropeptides in regulating social behavior, uses voles to investigate the neurobiological and genetic mechanisms underlying social behavior. Using the monogamous prairie vole (vs. the promiscuous meadow vole) as a model organism, Young and his research team identified the oxytocin and vasopressin receptors as key mediators of social bonding and attachment. In addition, they are examining the consequences of social bond disruption as a model of social loss-induced depression.

This work has important implications for developing novel treatment strategies for psychiatric disorders associated with social cognitive deficits, including autism spectrum disorders and schizophrenia.

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Posted on by Holly Korschun in Neuro Leave a comment

Combined MR/PET imaging

On Thursday, April 8, Emory’s Center for Systems Imaging, directed by Department of Radiology Chair Carolyn Meltzer, MD, and the Atlanta Clinical & Translational Science Institute celebrated the launch of the CSI’s prototype MR/PET imaging scanner.

View of MR/PET

View of MR/PET scanner from front, with Ciprian Catana of MGH and Larry Byars of Siemens

The scanner is one of four world-wide and one of two in the United States, and permits simultaneous MR (magnetic resonance) and PET (positron emission tomography) imaging in human subjects. This provides the advantage of being able to combine the anatomical information from MR with the biochemical/metabolic information from PET. Potential applications include functional brain mapping and the study of neurodegenerative diseases, drug addiction and brain cancer.

Thursday’s event brought together leaders of the three other MR/PET programs in Boston, Jülich and Tübingen, the Siemens engineers who designed the device, and the Atlanta research community to explore the possibilities of the technology.

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Posted on by Quinn Eastman in Neuro Leave a comment