Posts Tagged brain

[WEB SITE] Research provides insights for why some epilepsy patients continue to experience postoperative seizures

New research from the University of Liverpool, published in the journal Brain, has highlighted the potential reasons why many patients with severe epilepsy still continue to experience seizures even after surgery.

Epilepsy continues to be a serious health problem and is the most common serious neurological disorder. Medically intractable temporal lobe epilepsy (TLE) remains the most frequent neurosurgically treated epilepsy disorder.

Many people with this condition will undergo a temporal lobe resection which is a surgery performed on the brain to control seizures. In this procedure, brain tissue in the temporal lobe is resected, or cut away, to remove the seizure focus.

Unfortunately, approximately one in every two patients with TLE will not be rendered completely seizure free after temporal lobe surgery, and the reasons underlying persistent postoperative seizures have not been resolved.

Reliable biomarkers

Understanding the reasons why so many patients continue to experience postoperative seizures, and identifying reliable biomarkers to predict who will continue to experience seizures, are crucial clinical and scientific research endeavours.

Researchers from the University’s Institute of Translational Medicine, led by Neuroimaging Lead Dr Simon Keller and collaborating with Medical University Bonn (Germany), Medical University of South Carolina (USA) and King’s College London, performed a comprehensive diffusion tensor imaging (DTI) study in patients with TLE who were scanned preoperatively, postoperatively and assessed for postoperative seizure outcome.

Diffusion tensor imaging (DTI) is a MRI-based neuroimaging technique that provides insights into brain network connectivity.

The results of these scans allowed the researchers to examine regional tissue characteristics along the length of temporal lobe white matter tract bundles. White matter is mainly composed of axons of nerve cells, which form connections between various grey matter areas of the brain, and carry nerve impulses between neurons allowing communication between different brain regions.

Through their analysis the researchers could determine how abnormal the white matter tracts were before surgery and how the extent of resection had affected each tract from the postoperative MRI scans.

Surgery outcomes

The researchers identified preoperative abnormalities of two temporal lobe white matter tracts that are not included in standardised temporal lobe surgery in patients who had postoperative seizures but not in patients with no seizures after surgery.

The two tracts were in the ‘fornix’ area on the same side as surgery, and in the white matter of the ‘parahippocampal’ region on the opposite side of the brain.

The tissue characteristics of these white matter tracts enabled researchers to correctly identify those likely to have further seizures in 84% of cases (sensitivity) and those unlikely to have further seizures in 89% of cases (specificity). This is significantly greater than current estimates.

The researchers also found that a particular temporal lobe white matter tract called the ‘uncinate fasciculus’ was abnormal – and potentially involved in the generation of seizures – in patients with excellent and suboptimal postoperative outcomes.

However, it was found that significantly more of this tract was surgically resected/removed in the patients with an excellent outcome.

New insights

Dr Simon Keller, said: “There is scarce information on the prediction of postoperative seizure outcome using preoperative imaging technology, and this study is the first to rigorously investigate the tissue characteristics of temporal lobe white matter tracts with respect to future seizure classifications.

“Although there is some way to go before this kind of data can influence routine clinical practice, these results may have the potential to be developed into imaging prognostic markers of postoperative outcome and provide new insights for why some patients with temporal lobe epilepsy continue to experience postoperative seizures.”

Source: Research provides insights for why some epilepsy patients continue to experience postoperative seizures

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[WEB SITE] Brain surgery helps remove scar tissue causing seizures in epilepsy patients

By the time epilepsy patient Erika Fleck came to Loyola Medicine for a second opinion, she was having three or four seizures a week and hadn’t been able to drive her two young children for five years.

“It was no way to live,” she said.

Loyola epileptologist Jorge Asconapé, MD, recommended surgery to remove scar tissue in her brain that was triggering the seizures. Neurosurgeon Douglas Anderson, MD, performed the surgery, called an amygdalohippocampectomy. Ms. Fleck hasn’t had a single seizure in the more than three years since her surgery.

“I’ve got my life back,” she said. “I left my seizures at Loyola.”

Surgery can be an option for a minority of patients who do not respond to medications or other treatments and have epileptic scar tissue that can be removed safely. In 60 to 70 percent of surgery patients, seizures are completely eliminated, and the success rate likely will improve as imaging and surgical techniques improve, Dr. Anderson said.

Traditionally, patients would have to try several medications with poor results for years or decades before being considered for surgery, according to the Epilepsy Foundation. “More recently, surgery is being considered sooner,” the foundation said. “Studies have shown that the earlier surgery is performed, the better the outcome.” (Ms. Fleck is a service coordinator for the Epilepsy Foundation North/Central Illinois Iowa and Nebraska.)

Dr. Asconapé said Ms. Fleck was a perfect candidate for surgery because the scar tissue causing her seizures was located in an area of the brain that could be removed without damaging critical structures.

Ms. Fleck experienced complex partial seizures, characterized by a deep stare, unresponsiveness and loss of control for a minute or two. An MRI found the cause: A small area of scar tissue in a structure of the brain called the hippocampus. The subtle lesion had been overlooked at another center.

Epilepsy surgery takes about three hours, and patients typically are in the hospital for two or three days. Like all surgery, epilepsy surgery entails risks, including infection, hemorrhage, injury to other parts of the brain and slight personality changes. But such complications are rare, and they pose less risk to patients than the risk of being injured during seizures, Dr. Asconapé said.

Loyola has been designated a Level Four Epilepsy Center by the National Association of Epilepsy Centers. Level Four is the highest level of specialized epilepsy care available. Level Four centers have the professional expertise and facilities to provide the highest level of medical and surgical evaluation and treatment for patients with complex epilepsy.

Loyola’s comprehensive, multidisciplinary Epilepsy Center offers a comprehensive multidisciplinary approach to epilepsy and seizure disorders for adults and children as young as two years old. Pediatric and adult epileptologist consultation and state-of-the-art neuroimaging and electrodiagnostic technology are used to identify and assess complex seizure disorders by short- and long-term monitoring.

Source: Loyola University Health System

Source: Brain surgery helps remove scar tissue causing seizures in epilepsy patients

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[WEB SITE] Study investigates plasticity of motor representations in patients with brain tumors

Winner of the Brainlab Community Neurosurgery Award, Sandro Krieg, MD, presented his research, Plasticity of Motor Representations in Patients with Brain Lesions: a Navigated TMS Study, during the 2017 American Association of Neurological Surgeons (AANS) Annual Scientific Meeting.

This study investigated the spatial distributions of motor representations in terms of tumor-induced brain plasticity by analyzing navigated transcranial magnetic stimulation (nTMS) motor maps derived from 100 patients with motor eloquently located brain tumors in or adjacent to the precentral gyrus (PrG).

The research evoked 8,774 motor potentials (MEPs) that were elicited in six muscles of the upper and lower extremity by stimulating four gyri in patients with five possible tumor locations. Regarding the MEP frequency of each muscle-gyrus subdivision per patient, the expected frequency was 3.53 (8,774 divided by 100 patients, further divided by six muscles and four gyri). Accordingly, the patient ratio for each subdivision was calculated by defining the per-patient minimum data points as three.

The tumor-location specific patient ratios were higher for frontal tumors in both gyri than for other tumor locations. This suggests that the finger representation reorganization in these frontal gyri, which corresponds to location of dorsal premotor areas, might be due to within-premotor reorganization rather than relocation of motor function from PrG into premotor areas one might expect from the Rolandic tumors. The research indicates that reorganization of the finger motor representations might be limited along the middle-to-dorsal dimension of the dorsal premotor areas (posterior MFG and SFG) and might not cross rostrally from the primary motor cortex (PrG) to the dorsal premotor cortex.

Source: Study investigates plasticity of motor representations in patients with brain tumors

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[WEB SITE] Brain Derived Neurotrophic Factor (BDNF) and Exercise

Brain Derived Neurotrophic Factor (BDNF) has been referred to as a fertilizer for your brain. Find out how exercise can help you to get more of it.

Brain Derived Neurotrophic Factor (BDNF) has been referred to as a fertilizer for your brain. It is a substance that is found in your brain and helps to maintain the life of your brain cells, as well as grow new ones. You’ve probably heard all about ‘neuroplasticity’ and how we used to think our brains, once adult, were like a lump of concrete – unable to change and grow. Scientists now believe our brains are more like plastic – able to adapt, grow and change depending on what we do with them. BDNF is widely accepted as being a key player in this ‘plastic’ ability of the brain – its presence has been shown to make brain cells in petri dishes sprout new branches (necessary activity for a cell to make new connections!).

Low levels of BDNF have been associated with depression, anxiety, poor memory and brain degeneration as seen in conditions such as Alzheimer’s and dementia.

 

Why would you want more BDNF?

  • Improved learning and memory
  • May trigger the production of more serotonin (hello happy feelings!)
  • Helps with new skill acquisition
  • Improved mood (exercise increases BDNF as much or even more than taking antidepressants does)
  • Lower rates of Alzheimer’s disease and dementia in older age may be related to higher levels of BDNF.

Are you getting the picture? Better mood, better mental performance, healthier brain as you age…

How do you get more BDNF?

One word: STIMULATION.  Stimulation of your brain and all its cells can come in many forms. Of course, traditional brain exercise has been thought of as activities such as cross words and Sudoku (which are definitely good!) but here’s another aspect you can add to the list: exercise. As little as 30 minutes of jogging on three days a week has been shown to improve brain functioning, but even better gains have been suggested with more complex activity, which requires you to build or acquire a skill. An example of this is exercise that challenges your balance or thinking, like rock climbing or dancing.

The ultimate brain booster? A bit of aerobic exercise (at least ten minutes) to increase levels of BDNF and other neurotransmitters, as well as all those other wonderful benefits of aerobic exercise, followed by a skill-based exercise to get the new brain cells creating new networks with each other.

TIP: Want to maximize the increased learning capacity of your brain? Don’t try to learn something while exercising (stop taking your study notes to the spin bike!) – blood flow increases to the brain post-exercise, while BDNF levels are still increased, meaning immediately after exercise is the perfect time to take in new information. Put on that French language podcast on the way home from the gym…

 

EXERCISE RIGHT’S FIVE FAVOURITE WAYS TO MOVE FOR MORE BDNF

  • 1. Indoor rock-climbing – especially if you actively commute to the rock wall!
  • 2. Trail running – something with twists, turns and great views is awesome
  • 3. Dancing – where you’re learning new moves and also working your fitness
  • 4. Functional movement – wait until the after school rush has finished then go check out (and play on) your nearest playground – think monkey bars, crawling through tunnels and balancing on beams
  • 5. Team sports – they require you to be getting great aerobic gains by running around, whilst also working your brain in terms of strategy and quick thinking

References:

Aisen, P. S. (2014). Serum brain-derived neurotrophic factor and the risk for dementia. JAMA, 311(16), 1684-1685. doi: 10.1001/jama.2014.3120

Binder, Devin K., & Scharfman, Helen E. (2004). Brain-derived Neurotrophic Factor. Growth factors (Chur, Switzerland), 22(3), 123-131. doi: 10.1080/08977190410001723308

Hagerman, Eric, & Ratey, Dr John J. (2010). Spark! How Exercise Will Improve the Performance of Your Brain (Kindle Edition ed.).

Source: Brain Derived Neurotrophic Factor (BDNF) and Exercise

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[TED Talk] Carl Schoonover: How to look inside the brain.

There have been remarkable advances in understanding the brain, but how do you actually study the neurons inside it? Using gorgeous imagery, neuroscientist and TED Fellow Carl Schoonover shows the tools that let us see inside our brains.

 

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[WEB SITE] Understanding the Human Brain – Neuroscience News

Functional magnetic resonance images reflect input signals of nerve cells.

The development of magnetic resonance imaging (MRI) is a success story for basic research. Today medical diagnostics would be inconceivable without it. But the research took time to reach fruition: it has been nearly half a century since physicists first began their investigations that ultimately led to what became known as nuclear magnetic resonance. In 2001, Nikos K. Logothetis and his colleagues at the Max Planck Institute for Biological Cybernetics in Tübingen devised a new methodological approach that greatly deepened our understanding of the principles of functional MRI.

The great advantage of functional magnetic resonance imaging (fMRI) is that it requires no major interventions in the body. In fMRI, the human body is exposed to the action of electromagnetic waves. As far as we know today, the process is completely harmless, despite the fact that fMRI equipment generates magnetic fields that are about a million times stronger than the natural magnetic field of the earth.

The physical phenomenon underlying fMRI is known as nuclear magnetic resonance, and the path to its discovery was paved with several Nobel prizes. The story begins in the first half of the 20th century with the description of the properties of atoms. The idea of using nuclear magnetic resonance as a diagnostic tool was mooted as early as the 1950s. But the method had to be refined before finally being realised in the form of magnetic resonance imaging.

Today, MRI not only produces images of the inside of our bodies; it also provides information on the functional state of certain tissues. The breakthrough for fMRI came in the 1980s when researchers discovered that MRI can also be used to detect changes in the oxygen saturation of blood, a principle known as BOLD (blood oxygen level dependent) imaging. There is a 20 percent difference between the magnetic sensitivity of oxygenated arterial blood and that of deoxygenated venous blood. Unlike oxygenated haemoglobin, deoxygenated haemoglobin amplifies the strength of a magnetic field in its vicinity. This difference can be seen on an MRI image.

Resuscitation of the brain after a 15-minute cardiac arrest in fMRI: The pictorial representation provides information about the degree of damage of the brain as well as a detailed analysis of the recovery curve. The top three rows are examples of successful and the bottom row for an unsuccessful resuscitation. The comparison with the concentration images of ATP, glucose and lactate shows that the MR images are in fact closely related to the biochemical changes. Based on such studies, the course of cerebral infarction and the success of various therapeutic measures can be documented. Credit Max Planck Institute.

fMRI has given us new insights into the brain, especially in neurobiology. However, the initial phase of euphoria was followed by a wave of scepticism among scientists, who questioned how informative the “coloured images” really are. Although fMRI can in fact generate huge volumes of data, there is often a lack of background information or basic understanding to permit a meaningful interpretation. As a result, there is a yawning gap between fMRI measurements of brain activity and findings in animals based on electrophysiological recordings.

This is due mainly to technical considerations: interactions between the strong MRI field and currents being measured at the electrodes made it impossible to apply the two methods simultaneously to bridge the gap between animal experiments and findings in humans.

fMRT shows input signals

In 2001, Nikos Logothetis and his colleagues at the Max Planck Institute for Biological Cybernetics in Tübingen were the first to overcome this barrier. With the help of special electrodes and sophisticated data processing, they showed unambiguously that BOLD fMRI actually does measure changes in the activity of nerve cells. They also discovered that BOLD signals correlate to the arrival and local processing of data in an area of the brain rather than to output signals that are transmitted to other areas of the brain. Their paper was a milestone in our understanding of MRI and has been cited over 2500 times worldwide.

Their novel experimental setup enabled the Tübingen scientists to study various aspects of nerve cell activity and to distinguish between action potentials and local field potentials. Action potentials are electrical signals that originate from single nerve cells or a relatively small group of nerve cells. They are all-or-nothing signals that occur only if the triggering stimulus exceeds a certain threshold. Action potentials therefore reflect output signals. These signals are detected by electrodes located in the immediate vicinity of the nerve cells. By contrast, local field potentials generate slowly varying electrical potentials that reflect signals entering and being processed in a larger group of nerve cells.

Applying these three methods simultaneously, the Max Planck researchers examined the responses to a visual stimulus in the visual cortex of anaesthetized monkeys. Comparison of the measurements showed that fMRI data relate more to local field potentials than to single-cell and multi-unit potentials. This means that changes in blood oxygen saturation are not necessarily associated with output signals from nerve cells; instead, they reflect the arrival and processing of signals received from other areas of the brain.

Another important discovery the Tübingen researchers made was that, because of the large variability of vascular reactions, BOLD fMRI data have a much lower signal-to-noise ratio than electrophysiological recordings. Because of this, conventional statistical analyses of human fMRI data underestimate the extent of activity in the brain. In other words, the absence of an fMRI signal in an area of the brain does not necessarily mean that no information is being processed there. Doctors need to take this into account when interpreting fMRI data.

NOTES ABOUT THIS NEUROIMAGING RESEARCH

Contact: Christina Beck – Max Planck Institute
Source: Max Planck Institute press release
Image Source: The image is credited to Max Planck Institute and is adapted from the press release

Source: Understanding the Human Brain – Neuroscience News

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[BLOG POST] Brain Plasticity: How Adult Born Neurons Get Wired – Neuroscience News

FEBRUARY 3, 2017

Summary: Researchers report adult neurogenesis not only helps increase the number of cells in a neural network, it also promotes plasticity in the existing network. Additionally, they have identified the role the Bax gene plays in synaptic pruning.

Source: University of Alabama at Birmingham.

One goal in neurobiology is to understand how the flow of electrical signals through brain circuits gives rise to perception, action, thought, learning and memories.

Linda Overstreet-Wadiche, Ph.D., and Jacques Wadiche, Ph.D., both associate professors in the University of Alabama at Birmingham Department of Neurobiology, have published their latest contribution in this effort, focused on a part of the brain that helps form memories — the dentate gyrus of the hippocampus.

The dentate gyrus is one of just two areas in the brain where new neurons are continuously formed in adults. When a new granule cell neuron is made in the dentate gyrus, it needs to get ‘wired in,’ by forming synapses, or connections, in order to contribute to circuit function. Dentate granule cells are part of a circuit that receive electrical signals from the entorhinal cortex, a cortical brain region that processes sensory and spatial input from other areas of the brain. By combining this sensory and spatial information, the dentate gyrus can generate a unique memory of an experience.

Overstreet-Wadiche and UAB colleagues posed a basic question: Since the number of neurons in the dentate gyrus increases by neurogenesis while the number of neurons in the cortex remains the same, does the brain create additional synapses from the cortical neurons to the new granule cells, or do some cortical neurons transfer their connections from mature granule cells to the new granule cells?

Their answer, garnered through a series of electrophysiology, dendritic spine density and immunohistochemistry experiments with mice that were genetically altered to produce either more new neurons or kill off newborn neurons, supports the second model — some of the cortical neurons transfer their connections from mature granule cells to the new granule cells.

This opens the door to look at how this redistribution of synapses between the old and new neurons helps the dentate gyrus function. And it opens up tantalizing questions. Does this redistribution disrupt existing memories? How does this redistribution relate to the beneficial effects of exercise, which is a natural way to increase neurogenesis?

“Over the last 10 years there has been evidence supporting a redistribution of synapses between old and new neurons, possibly by a competitive process that the new cells tend to ‘win,’” Overstreet-Wadiche said. “Our findings are important because they directly demonstrate that, in order for new cells to win connections, the old cells lose connections. So, the process of adult neurogenesis not only adds new cells to the network, it promotes plasticity of the existing network.”

Image shows a brain.

The study opens the door to look at how this redistribution of synapses between the old and new neurons helps the dentate gyrus function. NeuroscienceNews.com image is for illustrative purposes only.

“It will be interesting to explore how neurogenesis-induced plasticity contributes to the function of this brain region,” she continued. “Neurogenesis is typically associated with improved acquisition of new information, but some studies have also suggested that neurogenesis promotes ‘forgetting’ of existing memories.”

The researchers also unexpectedly found that the Bax gene, known for its role in apoptosis, appears to also play a role in synaptic pruning in the dentate gyrus.

“There is mounting evidence that the cellular machinery that controls cell death also controls the strength and number of synaptic connections,” Overstreet-Wadiche said. “The appropriate balance of synapses strengthening and weakening, collectively termed synaptic plasticity, is critical for appropriate brain function. Hence, understanding how synaptic pruning occurs may shed light on neurodevelopmental disorders and on neurodegenerative diseases in which a synaptic pruning gone awry may contribute to pathological synapse loss.”

ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE

All of the work was performed in the Department of Neurobiology at UAB. In addition to Overstreet-Wadiche and Wadiche, co-authors of the paper, “Adult born neurons modify excitatory synaptic transmission to existing neurons,” published in eLife, are Elena W. Adlaf, Ryan J. Vaden, Anastasia J. Niver, Allison F. Manuel, Vincent C. Onyilo, Matheus T. Araujo, Cristina V. Dieni, Hai T. Vo and Gwendalyn D. King.

Much of the data came from the doctoral thesis research of Adlaf, a former UAB Neuroscience graduate student who is now a postdoctoral fellow at Duke University.

Funding: Funding for this research came from Civitan International Emerging Scholars awards, and National Institutes of Health awards or grants NS098553, NS064025, NS065920 and NS047466.

Source: Jeff Hansen – University of Alabama at Birmingham
Image Source: NeuroscienceNews.com image is in the public domain.
Original Research: Full open access research for “Adult-born neurons modify excitatory synaptic transmission to existing neurons” by Elena W Adlaf, Ryan J Vaden, Anastasia J Niver, Allison F Manuel, Vincent C Onyilo, Matheus T Araujo, Cristina V Dieni, Hai T Vo, Gwendalyn D King, Jacques I Wadiche, and Linda Overstreet-Wadiche in eLife. Published online January 30 2017 doi:10.7554/eLife.19886

Birmingham “Brain Plasticity: How Adult Born Neurons Get Wired.” NeuroscienceNews. NeuroscienceNews, 3 February 2017.
<http://neurosciencenews.com/neuroplasticity-neuroscience-6053/&gt;.

Abstract

Did You Know How Loud Balloons Can Be?

Adult-born neurons are continually produced in the dentate gyrus but it is unclear whether synaptic integration of new neurons affects the pre-existing circuit. Here we investigated how manipulating neurogenesis in adult mice alters excitatory synaptic transmission to mature dentate neurons. Enhancing neurogenesis by conditional deletion of the pro-apoptotic gene Bax in stem cells reduced excitatory postsynaptic currents (EPSCs) and spine density in mature neurons, whereas genetic ablation of neurogenesis increased EPSCs in mature neurons. Unexpectedly, we found that Bax deletion in developing and mature dentate neurons increased EPSCs and prevented neurogenesis-induced synaptic suppression. Together these results show that neurogenesis modifies synaptic transmission to mature neurons in a manner consistent with a redistribution of pre-existing synapses to newly integrating neurons and that a non-apoptotic function of the Bax signaling pathway contributes to ongoing synaptic refinement within the dentate circuit.

“Adult-born neurons modify excitatory synaptic transmission to existing neurons” by Elena W Adlaf, Ryan J Vaden, Anastasia J Niver, Allison F Manuel, Vincent C Onyilo, Matheus T Araujo, Cristina V Dieni, Hai T Vo, Gwendalyn D King, Jacques I Wadiche, and Linda Overstreet-Wadiche in eLife. Published online January 30 2017 doi:10.7554/eLife.19886

Source: Brain Plasticity: How Adult Born Neurons Get Wired – Neuroscience News

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[TED Talk] Carl Schoonover: How to look inside the brain

There have been remarkable advances in understanding the brain, but how do you actually study the neurons inside it? Using gorgeous imagery, neuroscientist and TED Fellow Carl Schoonover shows the tools that let us see inside our brains.

 

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[TEDx Talk] After watching this, your brain will not be the same | Lara Boyd | TEDxVancouver

 

In a classic research-based TEDx Talk, Dr. Lara Boyd describes how neuroplasticity gives you the power to shape the brain you want. Recorded at TEDxVancouver at Rogers Arena on November 14, 2015.

YouTube Tags: brain science, brain, stroke, neuroplasticity, science, motor learning, identity, TED, TEDxVancouver, TEDxVancouver 2015, Vancouver, TEDx, Rogers Arena, Vancouver speakers, Vancouver conference, ideas worth spreading, great idea,

Our knowledge of the brain is evolving at a breathtaking pace, and Dr. Lara Boyd is positioned at the cutting edge of these discoveries. In 2006, she was recruited by the University of British Columbia to become the Canada Research Chair in Neurobiology and Motor Learning. Since that time she has established the Brain Behaviour Lab, recruited and trained over 40 graduate students, published more than 80 papers and been awarded over $5 million in funding.

Dr. Boyd’s efforts are leading to the development of novel, and more effective, therapeutics for individuals with brain damage, but they are also shedding light on broader applications. By learning new concepts, taking advantage of opportunities, and participating in new activities, you are physically changing who you are, and opening up a world of endless possibility.

This talk was given at a TEDx event using the TED conference format but independently organized by a local community. Learn more at http://ted.com/tedx

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[WEB SITE] ADD Program receives $19.5 million NIH contract to test drugs for treating epilepsy

The University of Utah College of Pharmacy’s Anticonvulsant Drug Development (ADD) Program has been awarded a five-year $19.5 million contract renewal with the National Institutes of Health (NIH) to test drugs to treat epilepsy, and the major focus of the project is to address needs that affect millions of people worldwide -identify novel investigational compounds to prevent the development of epilepsy or to treat refractory, or drug-resistant, epilepsy.

The ADD program began in 1975 and since then has tested the vast majority of drugs used to control seizures in patients with epilepsy, helping millions of people worldwide. Unfortunately, almost one-third of the estimated 50 million people with the disorder has refractory, or unresponsive, epilepsy that isn’t adequately controlled by medications currently available. The contract renewal, awarded through the National Institute of Neurological Disorders and Stroke (NINDS) to the U Department of Pharmacology and Toxicology, represents a shift in the mission to identify new therapies, according to ADD Director Karen S. Wilcox, Ph.D., professor and chair of pharmacology and toxicology and principal investigator of the contract.

“We’re proud that over the past 41 years, the ADD program has played a key role in identifying and characterizing many of the drugs now available to treat patients with epilepsy and to control their seizures,” Wilcox says. “Now, we’re looking for drugs that can modify or prevent the disease, particularly in those patients either with refractory epilepsy or at risk for developing epilepsy following a brain injury.”

Epilepsy is a group of neurological disorders characterized by a tendency for repeated seizures over time. It occurs when permanent changes in the brain result in abnormal or excessive neuronal activity in the brain. An estimated 2.9 million people in the United States and 50 million people worldwide have active epilepsy, according the Centers for Disease Control and World Health Organization. There is no cure for epilepsy and the mainstay of treatment is anti-seizure medications.

ADD is a long-standing program dedicated to testing drugs to treat epilepsy. It has received continuous funding from NINDS’ Epilepsy Therapy Screening Program (ETSP) (formerly known as the Anticonvulsant Screening Program) since its founding in 1974. In collaboration, the ETSP and the ADD Program have evaluated more than 32,000 compounds. ADD received the contract in a competitive bidding process. The renewal of the contractual relationship between the NINDS and the University of Utah reflects the ongoing commitment of the NIH and the ETSP to finding and developing novel therapies for epilepsy and represents a unique partnership between government, industry, and academia.

“The NIH-NINDS ETSP is pleased to continue the productive relationship with the University of Utah,” says Dr. John Kehne, a Program Director at NINDS and head of the ETSP. “These and other efforts supported by the NINDS will help to discover new pharmacotherapies to address the unmet medical needs of people living with epilepsy.”

In addition to its focus on evaluating potential candidate drugs for the treatment of therapy-resistant epilepsy, the mission of the ADD Program includes efforts to identify novel therapies for different types of epilepsy. The program also serves as a base for innovative basic research that sheds new light on the pathophysiology of epilepsy and provides a unique training environment for students, research fellows, and visiting scientists. Currently, the ADD program employ18 researchers, technicians, and staff. Cameron S. Metcalf, Ph.D is associate director and a co-Investigator of the contract and Peter J. West, Ph.D., and Misty D. Smith, Ph.D, research assistant professors of pharmacology and toxicology, are also co-investigators on the contract renewal.

Although there currently is no cure for epilepsy, Wilcox, who previously served as a co-Investigator of ADD before taking over as PI in 2016, believes that can be changed.

“The brain has remarkable plasticity throughout a person’s life,” she says. “If we learn enough about neuroscience and the details of how the brain works, it’s very possible to find a cure.”

Source: University of Utah Health Sciences

Source: ADD Program receives $19.5 million NIH contract to test drugs for treating epilepsy

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