A microbiome-sparing antibiotic, tau’s role in AD, the latest and strongest data on the Zika-microcephaly connection, and a look at gene therapy in diabetes. This week in Abstract Science.
(The Scientist, 5/9/2016, Amanda Keener)
One of the problems with antibiotics is that they can also harm helpful bacteria that live in the gut. A drug developed by St. Jude’s Children’s Research Hospital in Memphis to treat Staphylococcus aureus could change that. The researchers found that when the drug, which is designed to inhibit an enzyme called Fabi, is administered orally in high doses it has little impact on intestinal communities in mice. The reason may be due to the fact that the drug, Debio1452, targets a site unique to the staphylococcal version of he enzyme. The findings appear this week in the journal Antimicrobial Agents and Chemotherapy.
(Science, 5/11/2016, Emily Underwood)
Sticky plaques of ß-amyloid protein have long been considered the key culprit in Alzheimer’s disease. But a new imaging study published this week in Science Translational Medicine suggests that the protein tau might be the bigger driver of the neurodegenerative condition that affects tens of millions worldwide. The small study of 10 individuals with mild AD used a PET tracer that binds to tau in the brain in tandem with a separate amyloid-binding tracer to analyze protein deposits in the brain. The more tau protein found in the temporal lobe, a brain region associated with memory, the more likely a person was to show deficits on a battery of memory and attention tests, the team led by scientists from Washington University in St. Louis found. The same results did not apply to ß-amyloid, suggesting that tau might be a better predictor of when people transition from asymptomatic to symptomatic stages of the disease. A larger, longer study is now underway that is tracking these two proteins in the brain.
(Science, 5/11/2016, Jon Cohen)
Since Zika became associated with an alarming surge in microcephaly cases, scientists have been trying to determine if the mosquito-borne virus was the reason for an increase in the birth defect. Recent studies in mice suggest yes. Mouse studies published this week in Cell, its sister journal Cell Stem Cell and in Nature show precisely how the virus slows fetal growth, damages the brain, and leads to miscarriage. Two of them also prove for the first time in an animal model that Zika virus can cause microcephaly in fetuses. Together, the findings indicate that the virus by itself can wreak havoc, says Michael Diamond, a viral immunologist at Washington University in St. Louis, Missouri, who led the Cell study.
(DNA Science Blog, 5/12/2016, Ricki Lewis)
Does gene therapy hold the answer to Type 1 Diabetes? T1D is usually autoimmune, with inherited risk factors such as certain HLA haplotypes contributing to, but not directly causing, the condition. A clever use of gene therapy is to commandeer liver cells to step in for the pancreatic beta cells that autoimmunity destroys.
—Compiled by Senior Scientific Writer Regina McEnery