Lab talk: Alzheimer's, El Niño, the universe and cancer
We ask four researchers to tell us about the recent papers that have excited them the most.
A coffee a day to keep Alzheimer’s away?
The brains of patients with Alzheimer’s disease look abnormal. The spaces between the brain cells get clogged by deposits of a protein called amyloid. Meanwhile within the cells a protein called tau gets daubed with phosphate and ends up in a tangled mess. The greater the phosphorylation, the greater the tangling and the worse the disease.
In this study, genetically modified mice that produce abnormal tau and develop Alzheimer’s disease were treated with a trace doses of caffeine – no more than in a cup of coffee. Their tau protein showed less phosphorylation and they had less memory loss than untreated peers. They also showed less oxidative stress and inflammation.
The study highlights the possibility that your daily cup of coffee may help protect against the progression of Alzheimer’s disease.
Paper: Beneficial effects of caffeine in a transgenic model of Alzheimer’s disease-like tau pathology.
Neurobiology of Aging, 2014, DOI: 10.1016/j.neurobiolaging.2014.03.027
El Niño events great and not so small
El Niño events originate in the tropical Pacific Ocean every three to seven years, triggered by warming of the ocean waters in the east that change the wind patterns. But every 20 years or so, the Pacific throws up a really big one, bringing intense rainfall to South America and very dry weather to Australia. The last extreme El Niño formed in 1997 causing an estimated 23,000 deaths, primarily through catastrophic floods, and billions of dollars of damage.
Will extreme El Niño events be more frequent as the world warms? This paper gives a convincing forecast. The researchers simulated El Niño conditions in a number of models, delving deeper into the interplay between ocean and atmosphere, and a clear picture emerges: extreme El Niño events will double in frequency in the coming century.
A new El Niño event is currently brewing in the Pacific. We’ll have to watch for a few more months to find out if it’s the “biggy” we are due.
Paper: Increasing frequency of extreme El Niño events due to greenhouse warming.
Nature Climate Change, 2014, vol 4, pp111-116
Stargazing in a virtual universe
The universe is a complicated place. It’s filled with dark matter, gas, dust, stars, and supermassive black holes, all mixed together in the cosmic web. But if we have a good understanding of the physical laws governing the evolution of the universe, in theory, we should be able to reproduce the overall layout of the cosmos in a computer.
This desire to test our cosmic calculations drives numerical simulations toward ever-greater complexity. The newest, swankiest simulation to show up on the scene is called Illustris, and it has produced a simulated universe almost indistinguishable from what we see in the sky, indicating that the input physics is on the right track.
The key advance with Illustris is its ability to reproduce a plausible assortment of spiral and elliptical galaxies. While there are still some kinks to be worked out, it’s another step forward in the quest for a synthetic cosmos.
Paper: Properties of galaxies reproduced by a hydrodynamic simulation.
Nature, 2014, vol 509, pp177-182
Hunting down aggressive cancer cells
Combatting glioblastoma, the most common deadly brain tumour of adults, is usually a losing battle. Even after a combination of surgery, chemotherapy and radiotherapy, the tumour is so aggressive, any surviving cells rapidly spread again through the brain.
This new report helps explain what gives the glioblastoma cells their winning edge. It turns out that tumour spread is driven by a small subset of cells that reseed the tumour. The cells carry four genes altered to match those that are often found in stem cells – cells that can reseed organs.
Knowing these four genes drive the tumour cells could help patients in two ways. Pathologists will look for them in brain biopsies so they know early on whether they are dealing with a highly aggressive tumour. Second, drug developers can target new drugs to these genes to try and disable them.
Paper: Reconstructing and Reprogramming the Tumor-Propagating Potential of Glioblastoma Stem-like Cells.
Cell, 2014, vol 157, pp580-594