New device visualizes DBS for Parkinson's treatment . . . Great Lakes NeuroTechnologies (Valley View, Ohio) reported the product launch of Kinesia ProView to visualize motor symptom severity response during programming of deep brain stimulation (DBS) for Parkinson's disease. Kinesia ProView provides a standardized platform to quantitatively assess how symptoms such as tremor, bradykinesia, and dyskinesias change in response to specific DBS settings during outpatient programming procedures. Developed in collaboration with clinical studies at the Cleveland Clinic and University of Minnesota, the system is FDA cleared to market in the U.S., is CE marked, and has Health Canada and Australian TGA approval for distribution in international markets. The system integrates a secure, HIPAA compliant web application and a broadband enabled tablet interface with wireless patient sensors. “Parkinson's disease is an incredibly complex and challenging disease for both patients and physicians,“ said Joseph Giuffrida, PhD, president and principal investigator at Great Lakes NeuroTechnologies. “Patients may encounter a wide variety of constantly changing symptoms while clinicians have the challenge of matching patient characteristics to an increasingly complex array of treatment options and settings. The Kinesia product suite was developed to improve disease management of Parkinson's through quantitative assessment and telemedicine with targeted clinical applications. Kinesia ProView builds on that momentum for the application of DBS programming.“ Kinesia ProView quantitatively assesses motor symptoms in response to stimulation settings and provides tools to quickly visualize the programming space. During a programming assessment, the patient wears a wireless sensor to assess motor symptoms such as tremor, bradykinesia, and dyskinesia at each DBS setting. A tablet PC application creates color-coded tuning maps as the programming session progresses, which display specific symptom severities as a function of stimulation settings. These tuning maps allow physicians to visually assess the programming parameter space and optimize the final settings for specific symptoms and battery consumption. Once the programming session is complete, patient data and tuning maps are transmitted via broadband connectivity to a cloud-based server for storage, reporting, and trending using the Kinesia web application.

Cocaine vaccine close to human trials . . . A novel anti-cocaine vaccine has been successfully tested in primates, suggesting that human clinical trials are not far off, according to new research by Weill Cornell Medical College (New York). The finding, published in the journal Neuropsychopharmacology, used a radiological method to show that the anti-cocaine vaccine stopped the drug from reaching the brain as well as from causing a dopamine-induced high. The study's lead researcher, Ronald Crystal, PhD, chairman of the Department of Genetic Medicine at Weill Cornell Medical College, said: “The vaccine eats up the cocaine in the blood like a little Pac-man before it can reach the brain. We believe this strategy is a win-win for those individuals, among the estimated 1.4 million cocaine users in the U.S., who are committed to breaking their addiction to the drug,“ he says. “Even if a person who receives the anti-cocaine vaccine falls off the wagon, cocaine will have no effect.“ Cocaine is a tiny molecule drug which functions by causing feelings of pleasure. It blocks the recycling of dopamine – the “pleasure“ neurotransmitter – in two regions of the brain, the putamen in the forebrain and the caudate nucleus in the center of the brain. After dopamine builds up at the nerve endings, it results in a large flooding of dopamine and that is the “feel good“ part of the cocaine high. Crystal and his colleagues developed a novel vaccine that is a combination of the common cold virus with a particle that acts like the structure of cocaine. After the vaccine is given to an animal, its body “sees“ the cold virus and produces an immune response to fight it off, as well as the cocaine impersonator that it is attached to. This way, the immune system learns to see cocaine as a trespasser. As soon as the immune system cells learn that cocaine is an enemy, from that point on they make antibodies that fight against cocaine as soon as it enters the body. In the current study, investigators set out to define how successful the anti-cocaine vaccine is in non-human primates – which are biologically closer to humans than mice. Researchers configured a tool to examine how much cocaine attaches to the dopamine transporter – which collects dopamine in the synapse between neurons and takes it out to be recycled. If cocaine is in the brain, it binds on to the transporter, successfully blocking the transporter from transporting dopamine out of the synapse – allowing the neurotransmitter to be active, resulting in a drug high. Investigators attached a short-lived isotope tracer to the dopamine transporter. The activity of the tracer could be measured using positron emission tomography (PET). The tool calculated how much of the tracer attached to the dopamine receptor in the presence or absence of cocaine. The PET studies revealed no difference in the binding of the tracer to the dopamine transporter in vaccinated animals when compared with unvaccinated animals when cocaine was not present. When cocaine was administered to the primates, there was a prominent decrease in activity of the tracer in the non-vaccinated animals. This finding suggests that without the vaccine, cocaine stopped the tracer from binding to the dopamine receptor. “This is a direct demonstration in a large animal, using nuclear medicine technology, that we can reduce the amount of cocaine that reaches the brain sufficiently so that it is below the threshold by which you get the high,“ said Crystal.

Gender differences in brain anatomy of dyslexia . . . Using MRI, neuroscientists at Georgetown University Medical Center (Washington) found significant differences in brain anatomy when comparing men and women with dyslexia to their non-dyslexic control groups, suggesting that the disorder may have a different brain-based manifestation based on sex. Their study, investigating dyslexia in both males and females, is the first to directly compare brain anatomy of females with and without dyslexia (in children and adults). Their findings were published online in the journal Brain Structure and Function. Because dyslexia is two to three times more prevalent in males compared with females, “females have been overlooked,“ said senior author Guinevere Eden, PhD, director for the Center for the Study of Learning and past-president of the International Dyslexia Association. “It has been assumed that results of studies conducted in men are generalizable to both sexes. But our research suggests that researchers need to tackle dyslexia in each sex separately to address questions about its origin and potentially, treatment,“ Eden said. Previous work outside of dyslexia demonstrates that male and female brains are different in general, said the study's lead author, Tanya Evans, PhD. “There is sex-specific variance in brain anatomy and females tend to use both hemispheres for language tasks, while males just the left,“ Evans said. “It is also known that sex hormones are related to brain anatomy and that female sex hormones such as estrogen can be protective after brain injury, suggesting another avenue that might lead to the sex-specific findings reported in this study.“ The study of 118 participants compared the brain structure of people with dyslexia to those without and was conducted separately in men, women, boys and girls. In the males, less gray matter volume is found in dyslexics in areas of the brain used to process language, consistent with previous work. In the females, less gray matter volume is found in dyslexics in areas involved in sensory and motor processing. The results have important implications for understanding the origin of dyslexia and the relationship between language and sensory processing, said Evans.

Cells aid in scar formation after CNS injury . . . By monitoring the behavior of a class of cells in the brains of living mice, neuroscientists at Johns Hopkins (Baltimore) discovered that these cells remain highly dynamic in the adult brain, where they transform into cells that insulate nerve fibers and help form scars that aid in tissue repair. Published online recently in the journal Nature Neuroscience, their work sheds light on how these multipurpose cells communicate with each other to maintain a highly regular, grid-like distribution throughout the brain and spinal cord. The disappearance of one of these so-called progenitor cells causes a neighbor to quickly divide to form a replacement, ensuring that cell loss and cell addition are kept in balance. “There is a widely held misconception that the adult nervous system is static or fixed, and has a limited capacity for repair and regeneration,“ said Dwight Bergles, PhD, professor of neuroscience and otolaryngology at the Johns Hopkins University School of Medicine. “But we found that these progenitor cells, called oligodendrocyte precursor cells (OPCs), are remarkably dynamic. Unlike most other adult brain cells, they are able to respond to the repair needs around them while maintaining their numbers.“ OPCs can mature to become oligodendrocytes – support cells in the brain and spinal cord responsible for wrapping nerve fibers to create insulation known as myelin. Without myelin, the electrical signals sent by neurons travel poorly and some cells die due to the lack of metabolic support from oligodendrocytes. It is the death of oligodendrocytes and the subsequent loss of myelin that leads to neurological disability in diseases such as multiple sclerosis. Using special microscopes that allow imaging deep inside the brain, the team watched the activity of individual cells in living mice for over a month. The researchers discovered that, far from being static, the OPCs were continuously moving through the brain tissue, extending their “tentacles“ and repositioning themselves. Even though these progenitors are dynamic, each cell maintains its own area by repelling other OPCs when they come in contact. “The cells seem to sense each other's presence and know how to control the number of cells in their population,“ says Bergles. “It looks like this process goes wrong in multiple sclerosis lesions, where there are reduced numbers of OPCs, a loss that may impair the cells' ability to sense whether demyelination has occurred. We don't yet know what molecules are involved in this process, but it's something we're actively working on.“

— Compiled by Robert Kimball, MDD

robert.kimball@ahcmedia.com