Syndicate content

Archive - Mar 12, 2018

Date

Autism's Social Deficits Are Reversed by Epigenetic Anti-Cancer Drug In Animal Models

Of all the challenges that come with a diagnosis of autism spectrum disorder (ASD), the social difficulties are among the most devastating. Currently, there is no treatment for this primary symptom of ASD. New research at the University at Buffalo (UB) in New York reveals the first evidence that it may be possible to use a single compound to alleviate the behavioral symptoms by targeting sets of genes involved in the disease. The research, published online on March 12, 2018 in Nature Neuroscience, demonstrated that brief treatment with a very low dose of romidepsin, an FDA-approved anti-cancer drug, restored social deficits in animal models of autism in a sustained fashion. The three-day treatment reversed social deficits in mice deficient in a gene called Shank 3, an important risk factor for ASD. This effect lasted for three weeks, spanning the juvenile to late adolescent period, a critical developmental stage for social and communication skills. That is equivalent to several years in humans, suggesting the effects of a similar treatment could potentially be long-lasting, the researchers say. The Nature Neuroscience article is titled “Social Deficits in Shank3-Deficient Mouse Models of Autism Are Rescued by Histone Deacetylase (HDAC) Inhibition.” "We have discovered a small molecule compound that shows a profound and prolonged effect on autism-like social deficits without obvious side effects, while many currently used compounds for treating a variety of psychiatric diseases have failed to exhibit the therapeutic efficacy for this core symptom of autism," said Zhen Yan (photo), PhD, Professor in the Department of Physiology and Biophysics in the Jacobs School of Medicine and Biomedical Sciences at UB, and senior author on the paper.

Revolutionary Technique Allows Imaging of All Cells in Entire Regions of Living Brain

Until now, existing microscopy methods to explore living brain tissue have been limited to imaging previously labeled cells only. Yet, owing to technical limitations, not all the cells in a specific region of the brain can be labeled simultaneously, and this has restricted the way we see, and therefore understand, how brain cells, which are highly interconnected, are organized and interact with each other. Dr. Jan Tønnesen, researcher in the Ramón y Cajal Programme at the UPV/EHU-University of the Basque Country’s Department of Neurosciences, and who works at the ACHUCARRO Centre (Achucarro Basque Center for Neuroscience) located in the Basque town of Leioa, is one of the authors of a piece of work published in the February 22, 2018 issue of Cell. The open-access article describes a new microscopy technique known as SUSHI designed to improve the imaging of cells in living brain tissue. The article is titled “Super-Resolution Imaging of the Extracellular Space in Living Brain Tissue.” The new SUSHI (Super-resolution Shadow Imaging) technique allows the tiny space full of liquid surrounding brain cells to be labeled in one sweep, thus obviating the need to individually label all the cells that one is intending to analyze. Given that this "label" also remains outside the cells, a kind of negative image akin to the film used in old cameras is produced. So, the negative image contains the same information about the brain cells as its corresponding positive image, but, thanks to the fact that the labeling procedure is more straightforward, it is much easier to obtain this image and all the information contained in it.

New Treatment for Chronic Neuropathic Pain Targeting FLT3 Molecule Suggested by Mouse Study

Neuropathic pain is a chronic illness affecting 7-10% the population in France and for which there is no effective treatment. Researchers at the Institute for Neurosciences of Montpellier (INSERM/Université de Montpellier) and the Laboratory for Therapeutic Innovation (CNRS/Université de Strasbourg) have uncovered the mechanism behind the appearance and continuation of pain. Based on their discovery, an innovative treatment was developed which produces, in animal subjects, an immediate, robust, and long-lasting therapeutic effect on pain symptoms. This study was published online on March 12, 2018 in Nature Communications. The open-access article is titled “Inhibition of Neuronal FLT3 Receptor Tyrosine Kinase Alleviates Peripheral Neuropathic Pain in Mice.” French researchers have just revealed the unexpected role played by the molecule FLT3 (FMS-like tyrosine kinase 3) in chronic pain, known for its role in different blood functions and produced by the hematopoietic stem cells that generate all blood cells. Neuropathic pain is caused by a lesion in peripheral nerves due to diseases such as diabetes, cancer, or shingles, or to accident- or surgery related trauma. In this study, researchers showed that immune cells in the blood which flood the nerve at the site of the lesion synthesize and release another molecule, FL, which binds with and activates FLT3, triggering a chain reaction in the sensory system, causing pain. It was revealed that FLT3 induces and maintains pain by acting far upstream on other components in the sensory system that are known for making pain chronic (known as "chronicization").