Using CRISPR to fix disease-causing mutations in embryos, changing the way scientists think about Alzheimer’s disease and should you be worried about mad cow disease?
(Nature, 9/20/2017, Heidi Ledford)
Gene-edited human embryos have offered a glimpse into the earliest stages of development, while hinting at the role of a pivotal protein that guides embryo growth. The first-of-its-kind study stands in contrast to previous research that attempted to fix disease-causing mutations in human embryos, in the hope of eventually preventing genetic disorders. Whereas those studies raised concerns over potential ‘designer babies’, the latest paper describes basic research that aims to understand human embryo development and causes of miscarriage. The study relied on CRISPR–Cas9, a gene-editing system that can make precise changes to DNA in the genome. In this case, researchers harnessed CRISPR–Cas9 to disrupt the production of a protein called OCT4 that is important for embryo development.
(Science, 9/20/2017, Emily Underwood)
A new study published in the journal Nature has uncovered a new role for a gene known to be key in the development of Alzheimer’s disease: apolipoprotein E (ApoE). This newly gained understanding gives researchers a novel therapeutic target, which, they hope, will soon enable them to cure the condition. People with Alzheimer’s disease die with brains riddled by both amyloid plaques and intracellular tau “tangles.” Yet the evidence linking tau to ApoE4 has been indirect and circumstantial. This new study took genetically engineered mice that produce a version of tau found in the brains of people with a neurodegenerative disease similar to Alzheimer’s, and cross-bred them with strains expressing ApoE4 or the two other main human variants of ApoE: E2 and E3. They also crossed the tau mice with mice in which its ApoE had been disabled. When the team examined brain tissue in the four resulting strains, all the mice carrying the human variants of ApoE had tau tangles and neurodegeneration, with the most profound tissue loss in E4 mice. In the taumaking mice with no ApoE gene, however, there was little or no neuronal death.
(LabRoots, 9/22/2017, Xuan Pham)
Next week, we’ll be speaking at the Charles River World Congress on Animal Models in Drug Discovery & Development about our quest to prevent prion disease. Prion diseases made headlines in the mid-1980s through the 1990s as the cause of mad cow disease. The epidemic hit the United Kingdom the hardest, infecting over 180,000 cattle. Subsequently, 4.4 million cattle were sacrificed in the attempt to eradicate the disease from the food chain to humans. The event led to drastic changes to how cattle can be fed and how cattle parts should be properly handled, which played a crucial part in controlling the disease. Given the stringent guidelines on cattle raising, the risk that a steak is tainted with prion seems to be very slim.
—Compiled by Social Media Specialist Jillian Scola