How mutations made Ebola more lethal, electron microscopes in living color and encouraging findings for a dreaded disease.
(Scientific American, 11/2/16, Simon Makin)
An experimental drug designed to inhibit the β-amyloid plaques that form in the brains of Alzheimer’s patients passed two key hurdles recently. In findings published this week in Science Translational Medicine, researchers from Merck reported that a drug called verubecestat blocked the buildup of amyloid beta in both animals and people without apparent signs of toxicity. These results helped propel testing to full-blown clinical trials, making verubecestat the first so-called BACE1 (beta-site amyloid precursor protein Cleaving Enzyme 1) inhibitor to reach phase III trials.
(New York Times, 11/3/16, Carl Zimmer)
Cities on the move, a poor public health system and unsafe burial practices all contributed to the Ebola outbreak that killed 11,318 people in West Africa two years ago. But it turns out these factors don’t entirely explain the ferocity of the virus. In separate studies, two teams of virologists concluded that a genetic mutation may have made Ebola more deadly by improving the virus’s ability to enter human cells. Patients who were infected with the mutated version of Ebola were significantly more likely to die. The studies appeared here and here in this week’s issue of the journal Cell.
(Science, 11/3/16, Rachael Lallensack)
Electron microscopes are powerful machines, but in one aspect at least they were a bit “last century.” That all changed recently when an effort led by scientists at the University of California-San Diego finally succeeded in taking the first color images with this device. The findings were published this week in Cell Chemical Biology. The new advance—15 years in the making—uses three different kinds of rare earth metals called lanthanides layered one-by-one over cells on a microscope slide.
—Compiled by Senior Scientific Writer Regina McEnery