How old cells might be harming our hearts, Zika’s bewildering impact in Latin America, solving the riddle of snake feet with CRISPR.
(Washington Post, 10/25/16, Dom Phillips and Nick Miroff)
Much to the bewilderment of scientists tracking this mosquito-borne virus in Latin America, infections are in the millions yet the epidemic has not produced the wave of congenital deformities initially feared by public health authorities. According to the latest U.N. figures, of the 2,175 babies born in the past year with undersized heads or other congenital neurological damage linked to Zika, more than 75 percent have been clustered in a single region: northeastern Brazil. Scientists now suspect that the presence of another mosquito-borne virus like chikungunya or dengue may be to blame for the cases of microcephaly, or that environmental, genetic or immunological factors combined with Zika put mothers in Northern Brazil at greater risk.
(Scientific American, 10/27/16, Ryan Mandelbaum)
What does CRISPR have to do with snake evolution? Scientists have used CRISPR to explain how snakes might have lost their legs. Hoping to understand how and why evolution shaped the snake as it did—and what happened to its genome when it stopped walking—a team from Lawrence Berkeley National Laboratory have used the gene-editing system to produce the same change in mice. Their results of this fascinating experiment appeared recently in Cell.
(Science, 10/27/16, Mitch Leslie)
Findings released this week suggest that worn out cells known as senescent cells, which accumulate as we age, may be contributing to atherosclerosis, the buildup of fatty plaques in our arteries that can spur heart attacks and strokes. A study led by cancer biologist Jan van Deursen of the Mayo Clinic in Minnesota revealed that deleting these senescent cells from mice increase their life spans by up to 20% and improved their health. The findings were published this week in Science. Van Deursen’s team used mice that had been genetically engineered to kill off many of their senescent cells in response to a particular drug. The researchers let the mice chow down on a fat-rich diet for 3 months and dosed some of them with the drug. Several types of senescent cells lurk inside plaques, but the researchers’ results suggest that the wrongdoers that promote atherosclerosis are foam cells, a type of immune cell that has settled down in the artery lining and begun feasting on fats.
(GEN, 10/27/16, Gai Ayalon)
Most of the efforts to-date to develop disease-modifying therapies for Alzheimer’s disease have focused on targeting the formation of amyloid plaques and/or attempting to clear them. But the pendulum lately has been shifting toward the study of neurofibrillary tangles (NFTs) that form when a protein known as tau aggregates inside neurons. Although NFTs accumulate inside neurons, research suggests that soluble species of tau can spread from cell to cell via the extracellular space. This provides an opportunity for antibodies to bind free-floating tau before it has a chance to enter a nearby neuron. Genentech scientist Gai Ayalon describes some of the ongoing research being conducted by the California pharmaceutical company.
—Stories compiled by Senior Scientific Writer Regina McEnery