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Archive - Mar 18, 2019

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Scientists Characterize, Target, & Manipulate Critical Subset of Neurons Responsible for Excessive Drinking; Major Breakthrough in Identifying Key Brain Cells May Open Door to Developing Drug Therapies or Even Gene Therapies for Alcohol Addiction

Scientists at Scripps Research Institute (La Jolla, California) have found that they can reverse the desire to drink in alcohol-dependent rats--with the flip of a switch. The researchers were able to use lasers to temporarily inactivate a specific neuronal population, reversing alcohol-seeking behavior and even reducing the physical symptoms of withdrawal. "This discovery is exciting--it means we have another piece of the puzzle to explain the neural mechanism driving alcohol consumption," says Olivier George, PhD, an Associate Professor at Scripps Research and senior author of the new study, published on March 18, 2019 in Nature Communications. The open-access article is titled “Inactivation of a CRF-Dependent Amygdalofugal Pathway Reverses Addiction-Like Behaviors in Alcohol-Dependent Rats.” Although the laser treatment is far from ready for human use, Dr. George believes identifying these neurons opens the door to developing drug therapies or even gene therapies for alcohol addiction. "We need compounds that are specific to this neuronal circuitry," Dr. George says. According to the National Institute on Alcohol Abuse and Alcoholism, more than 15.1 million adults in the United States suffer from alcohol use disorder. Previous work at Scripps Research has shown that transitioning from casual drinking to dependent drinking occurs alongside fundamental changes in how the brain sends signals. These signals drive the intense cravings that make it so difficult for many people to scale back their alcohol consumption. Dr. George and his colleagues have been hunting for the brain cells that driving drinking in an alcohol-addicted rat model. In 2016, they reported that they had found a possible source: a neuronal "ensemble," or group of connected cells in a brain region called the central nucleus of the amygdala (CeA).

Inflammation Links Heart Disease & Depression, New Study Finds

People with heart disease are more likely to suffer from depression, and the opposite is also true. Now, scientists at the University of Cambridge (UK) believe they have identified a link between these two conditions: inflammation - the body's response to negative environmental factors, such as stress. While inflammation is a natural response necessary to fight off infection, chronic inflammation (which may result from psychological stress as well as lifestyle factors such as smoking, excessive alcohol intake, physical inactivity, and obesity) is harmful. The link between heart disease and depression is well documented. People who have a heart attack are at a significantly higher risk of experiencing depression. Yet, scientists have been unable to determine whether this is due to the two conditions sharing common genetic factors or whether shared environmental factors provide the link. "It is possible that heart disease and depression share common underlying biological mechanisms, which manifest as two different conditions in two different organs--the cardiovascular system and the brain," says Dr Golam Khandaker (https://www.neuroscience.cam.ac.uk/directory/profile.php?Golam), PhD, a Wellcome Trust Intermediate Clinical Fellow at the University of Cambridge in the UK. "Our work suggests that inflammation could be a shared mechanism for these conditions." In a study published on March 19, 2019 in Molecular Psychiatry, Dr. Khandaker and colleague Dr Stephen Burgess led a team of researchers from Cambridge who examined this link by studying data relating to almost 370,000 middle-aged participants of UK Biobank.

New Evidence Supports Suggestion That Narcolepsy Is Autoimmune Disease; Cytotoxic Autoreactive CD8 T Cells Found in Patients with Narcolepsy

Researchers from the University of Copenhagen have discovered autoreactive cells in persons suffering from narcolepsy. This is a new, important proof that the sleep disorder is an autoimmune disease. This knowledge may lead to better treatment of the chronic condition, the researchers behind the new discovery believe. For many years, scientists have suspected that the sleep disorder narcolepsy is an autoimmune disease, though without being able to prove it conclusively. Now, researchers from the Faculty of Health and Medical Sciences at the University of Copenhagen, together with the Technical University of Denmark and Rigshospitalet, have found a new, important proof that their presumptions were correct. The new research results were on February 19, 2019 in Nature Communications. The open-access article is titled “CD8+ T Cells from Patients with Narcolepsy and Healthy Controls Recognize Hypocretin Neuron-Specific Antigens.” “We have found autoreactive cytotoxic CD8 T cells in the blood of narcolepsy patients. That is, the cells recognize the neurons that produce hypocretin, which regulates a person's waking state. It does not prove that they are the CD8 T cells are the ones that killed the neurons, but it is an important step forward. Now we know what the cells are after,” says the article’s senior author, Associate Professor Birgitte Rahbek Kornum (photo), PhD, from the Department of Neuroscience at the University of Copenhagen. The immune system is designed to recognize viruses and bacteria. When its cells are autoreactive - which is the case in autoimmune diseases - the immune system recognizes the body's own cells as foreign and attacks them. That the immunr cells are cytotoxic means that they are capable of killing other cells.

Blood Test Using Vibrational Spectroscopy Accurately Spots Molecular Signature of Fibromyalgia; “Could Lead to Better, More Directed Treatment for Patients," Lead Researcher Says; Unusual Collaboration with Food Science Group Key to Advance

For the first time, researchers have evidence that fibromyalgia can be reliably detected in blood samples -- work they hope will pave the way for a simple, fast diagnosis. In a study published in the February 15, 2019 issue of the Journal of Biological Chemistry, researchers from The Ohio State University report success in identifying biomarkers of fibromyalgia and differentiating it from a handful of other related diseases. Their article is titled “Metabolic Fingerprinting for Diagnosis of Fibromyalgia and Other Rheumatologic Disorders.” The discovery could be an important turning point in care of patients with a disease that is frequently misdiagnosed or undiagnosed, leaving them without proper care and advice on managing their chronic pain and fatigue, said lead researcher Kevin Hackshaw (photo), MD, an Associate Professor in Ohio State's College of Medicine and a rheumatologist at the University's Wexner Medical Center. Identification of biomarkers of the disease - a "metabolic fingerprint" like that discovered in the new study - could also open up the possibility of targeted treatments, he said. To diagnose fibromyalgia, doctors now rely on patient-reported information about a multitude of symptoms and a physical evaluation of a patient's pain, focusing on specific tender points, he said. But there's no blood test - no clear-cut, easy-to-use tool to provide a quick answer. "We found clear, reproducible metabolic patterns in the blood of dozens of patients with fibromyalgia. This brings us much closer to a blood test than we have ever been," Dr. Hackshaw said.