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Archive - Nov 9, 2013

NIH Launches Clinical Trial of Investigational Genital Herpes Vaccine

Researchers have launched an early-stage clinical trial of an investigational vaccine designed to prevent genital herpes disease. The National Institute of Allergy and Infectious Diseases (NIAID), part of the National Institutes of Health, is sponsoring the Phase I trial, which is being conducted at the NIH Clinical Center in Bethesda, Maryland. Genital herpes is one of the most common sexually transmitted infections in the United States. Most genital herpes cases are caused by infection with herpes simplex virus type 2 (HSV-2); however, herpes simplex virus type 1 (HSV-1) can also cause genital herpes. An estimated 776,000 people in the United States are infected with HSV-2 or HSV-1 each year. There is no vaccine to prevent genital herpes. "Although genital herpes is treatable, it is a lifelong infection that can exact a substantial psychological and physical toll on infected individuals and places them at higher risk of acquiring HIV," said NIAID Director Anthony S. Fauci, M.D. "Furthermore, mothers with active genital herpes infection at time of delivery can transmit the virus to their newborns, which can lead to severe illness and death. A protective vaccine would help to reduce significantly the spread of this all-too- common sexually transmitted infection," Dr. Fauci added. Led by principal investigator Lesia K. Dropulic, M.D., of NIAID's Laboratory of Infectious Diseases, the trial will test an investigational HSV-2 vaccine candidate, called HSV529, for safety and the ability to generate an immune system response. The investigational vaccine, manufactured by Sanofi Pasteur, was developed by David Knipe, Ph.D., professor of microbiology and immunobiology at Harvard Medical School, Boston. Preclinical testing of the candidate vaccine involved a 10-year collaborative effort between Dr.

Earliest-Ever Marker for Autism Found in Young Infants

Eye contact during early infancy may be a key to early identification of autism, according to a study funded by the National Institute of Mental Health (NIMH), part of the National Institutes of Health. Published online on November 6, 2013 in Nature, the study reveals the earliest sign of developing autism ever observed—a steady decline in attention to others' eyes within the first two to six months of life. "Autism isn't usually diagnosed until after age 2, when delays in a child's social behavior and language skills become apparent. This study shows that children exhibit clear signs of autism at a much younger age," said Thomas R. Insel, M.D., director of the NIMH. "The sooner we are able to identify early markers for autism, the more effective our treatment interventions can be." Typically developing children begin to focus on human faces within the first few hours of life, and they learn to pick up social cues by paying special attention to other people's eyes. Children with autism, however, do not exhibit this sort of interest in eye-looking. In fact, a lack of eye contact is one of the diagnostic features of the disorder. To find out how this deficit in eye-looking emerges in children with autism, Warren Jones, Ph.D., and Ami Klin, Ph.D., of the Marcus Autism Center, Children's Healthcare of Atlanta, and Emory University School of Medicine, followed infants from birth to age 3. The infants were divided into two groups, based on their risk for developing an autism spectrum disorder. Those in the high-risk group had an older sibling already diagnosed with autism; those in the low-risk group did not. Drs. Jones and Klin used eye-tracking equipment to measure each child's eye movements as they watched video scenes of a caregiver.

RNA Target Identified for ALS and Frontotemporal Degeneration

A team of scientists led by researchers from the University of California, San Diego School of Medicine and Ludwig Institute for Cancer Research have identified a novel therapeutic approach for the most frequent genetic cause of ALS (Lou Gehrig’s disease), a disorder of the regions of the brain and spinal cord that control voluntary muscle movement, and also for frontal temporal degeneration, the second most frequent dementia. Published online on October 29, 2013 in PNAS, the study establishes using segments of genetic material called antisense oligonucleotides – ASOs – to block the buildup and selectively degrade the toxic RNA that contributes to the most common form of ALS, without affecting the normal RNA produced from the same gene. The new approach may also have the potential to treat frontotemporal degeneration or frontotemporal dementia (FTD), a brain disorder characterized by changes in behavior and personality, language, and motor skills that also causes degeneration of regions of the brain. In 2011, scientists found that mutation of a specific gene known as C9orf72 is the most common genetic cause of ALS. It is a very specific type of mutation which, instead of changing the protein, involves a large expansion, or repeated sequence of a set of nucleotides – the basic component of RNA, as well as DNA. A normal C9orf72 gene contains fewer than 30 of the nucleotide repeat unit, GGGGCC. The mutant gene may contain hundreds of repeats of this unit, which generate a repeat containing RNA that the researchers show aggregates into foci.

30,000 Attending Neuroscience Annual Meeting in San Diego

Nearly 30,000 attendees will gather in San Diego for the world’s largest source of emerging news about brain science and health: Neuroscience 2013, November 9–13. With more than 15,000 scientific presentations, 600 exhibitors, and 34 professional development workshops and networking functions, the annual meeting of the Society for Neuroscience (SfN) provides an extraordinary opportunity to share information, learn and discuss the latest brain research findings, and attend public events on the mind, creativity, and art. “Aided by new technology and scientific innovations, neuroscience is on the cusp of revolutionary advances — and nowhere is that better on display than at Neuroscience 2013,” said SfN President Larry Swanson, Ph.D., Professor of Biological Sciences, Neurology, and Psychology at the University of Southern California. “Each year the meeting showcases valuable new research about brain structure, disease, and function in the relentless pursuit of knowledge and understanding and the hope for better medical treatments. The spirit of innovation and creativity is evident in the many lectures and presentations, and in the buzz of scientific discourse on the poster floor,” he added. Recent investment in neuroscience in the U.S., Europe, Canada, China, and elsewhere, has highlighted the importance of scientific discovery in addressing mental and physical health worldwide. More than 1 billion people suffer from 1,000 brain and nervous system diseases and disorders that result in heavy financial burdens to healthcare systems and to families and society each year. Highlights of this year’s diverse program of events include: “Dialogues between Neuroscience and Society” lecture featuring Ed Catmull, Ph.D., president of Pixar and Walt Disney Animation Studios. Dr.

Genetic Variation Increases Risk of Kidney Disease Progression in African-Americans—Link to Sleeping Sickness Resistance

New research provides direct evidence that genetic variations in some African Americans with chronic kidney disease contribute to a more rapid decline in kidney function compared with white Americans. The research, led by investigators from the University of Maryland School of Medicine and Johns Hopkins University, may help explain, in part, why even after accounting for differences in socioeconomic background, end-stage kidney disease is twice as prevalent among blacks as whites. Results were published online on November 9, 2013 in the New England Journal of Medicine. “What we found is pretty remarkable — that variations in a single gene account for a large part of the racial disparity in kidney disease progression and risk for end-stage kidney disease,” says co-lead author and nephrologist Afshin Parsa, M.D., M.P.H., assistant professor of medicine and member of the Program in Personalized and Genomic Medicine at the University of Maryland School of Medicine. “If it were possible to reduce the effect of this gene, there could be a very meaningful decrease in progressive kidney and end-stage kidney disease within blacks.” Previous landmark discoveries had revealed that two common variants within a gene called apolipoprotein L1 (APOL1) were strongly associated with non-diabetic end-stage renal disease in blacks. Having only one copy of the variant APOL1 gene variant is associated with a health benefit – protection against African sleeping sickness, a potentially lethal parasitic infection transmitted by the tsetse fly (image), found only in sub-Saharan Africa. However, people with two copies of the variant are at a higher risk for kidney disease.