SR-Research Roundup

July 21st-July 28th

Welcome to this week’s Research Roundup. These Friday posts aim to inform our readers about the many stories that relate to animal research each week. Do you have an animal research story we should include in next week’s Research Roundup? You can send it to us via our Facebook page or through the contact form on the website.

  • A protein that may cause Lupus has been identified. Lupus is a chronic inflammatory disease that occurs when your body’s immune system attacks its own tissues and organs. An estimated 1.5 million Americans, and at least 5 million people worldwide, have a form of lupus. Previous research has implicated the gene PRDM1 as a risk factor for lupus. Scientists looking at Blimp-1, a protein that is encoded by the PRDM1 gene, have found in mice thatthat a low level of or no Blimp-1 in a particular cell type led to an increase in the protein cathepsin S (CTSS) which caused the immune system to identify healthy cells as something to attack — particularly in females.” These results are particularly striking as women have an increased risk for lupus compared to men. While this work needs to be replicated and validated, this research provides some valuable insight into the etiology and treatment of lupus. This research was published in the journal Nature Immunology.


  • Vaccine for virus induced Type 1 diabetes successful in mice. Coxsackie B viruses are the most common enteroviruses and are believed to be associated with the development of Type 1 diabetes. Type 1 diabetes is a common human disease defined by a decrease in the production of insulin, which is a hormone that allows blood glucose (sugar) to enter energy producing cells. Thus, without insulin your body cannot effectively produce energy. This week, a team of Finnish researchers published a preclinical evaluation of a Coxsackie B1 vaccine using mice and found that the vaccine successfully protected the mouse after administering the Coxsackie B1 virus. Pre-clinical trials in humans are the next logical step for this vaccine, and the researchers believe that this research will aid in the development of vaccines for other disease caused by enteroviruses such as; hand-foot-and-mouth disease, meningitis, and myocarditis. This research was published in the journal Vaccine.
  • High iron levels in brain linked to progression of Alzheimer’s. Alzheimer’s is a degenerative neurological disease that causes dementia in humans. Previous research has linked Alzheimer’s to the buildup of amyloid protein in the brain, but research on drugs that reduce amyloid levels have not successfully slowed the progression of the disease. New research from the University of Melbourne however, discovered that humans with high levels of iron and amyloid were suffering from rapid dementia, while those with just high levels of amyloid protein were stable. This finding will fuel a five year trial on whether an anti-iron drug can slow the progression of the disease. This research was published the journal Brain.


  • Compound protects macaques from simian HIV. Research being presented this week at the National AIDS Treatment Advocacy Project (NATAP) Conference on HIV Pathogenesis Treatment and Prevention in Paris shows that weekly administration of a compound called MK-8591 repeatedly protected 8 of 8 macaques from simian HIV (SHIV) 6 days after treatment. Researchers from the Aaron Diamond AIDS Research Center in New York, Merck, and the Tulane National Primate Research Center studies 16 male macaques, 8 of which received weekly treatments of MK-8591 for up to 14 weeks, the other 8 of which received a placebo. MK-8591 is a nucleoside reverse transcriptase translocation inhibitor (NRTTI) that thwarts HIV. All 8 monkeys treated with MK-8591 remained SHIV-free even after 12 challenges with SHIV, to the end of the 168-day study. In contrast, the monkeys not treated with the drug all became infected with SHIV. The researchers noted that protective intracellular active MK-8591 concentrations can be attained in humans at low drug doses. These new findings support the potential use of MK-8591 as a prophylactic treatment for high-risk individuals.
  • New drug acting at two opioid receptors shows promise to treat chronic pain without the adverse effects of morphine. An epidemic of opioid abuse is killing people by the hundred of thousands in the United States, becoming the main cause of death for people under 40. The epidemic has been traced to the prescription of new opioid analgesics like Oxycontin over the last years, which has led people to become addicted to it and then to harder drugs like heroin. A group of scientist followed the strategy of creating drugs that bind not only to the receptor for morphine in the brain, the mu-opioid receptor, but also to a new opioid receptor called the nociceptin FQ receptor. The new drug, BU08028, was shown to reduce pain responses in rats as effectively as morphine. Now the drug is being tested in rhesus monkeys, where it also decreased pain. Importantly, the monkeys showed no desire to self-administer BU08028, an indication that the drug is not addictive.
  • Computer-designed opioid drug may decrease pain without producing respiratory arrest. People dying during the current opioid epidemic do so because the drugs inhibit the centers in the brain that drive breathing, leading to suffocation. Scientists proposed that the pain-relieving and breathing-suppressive effects of the opioids depend on different interactions of these drugs with the mu-opioid receptor, and set up to produce a compound that would suppress pain but not breathing. To do that, they modelled the drug binding site at the receptor using computers. After testing millions of compounds in the computer, they found a drug, PZM21, that showed promise. Then they tested PZM21 in mice and found that it suppressed pain but not breathing. They also found that PZM21 did not show the rewarding effect that typically lead to addiction. This demonstrates how even when new drugs are designed using computer models, animal studies are still needed to evaluate their effects.