by Fred Pearce, New, August 16, 2007, SOME climate tipping points may already have been passed, and others may be closer than we thought, it emerged this week. Runaway loss of Arctic sea ice may now be inevitable. Even more worrying, and very likely, is the collapse of the giant Greenland ice sheet. So said Tim Lenton of the University of East Anglia, UK, speaking on Monday at a meeting on complexity in nature, organised by the British Antarctic Survey in Cambridge.

Lenton warned the meeting that global warming might trigger tipping points that could cause runaway warming or catastrophic sea-level rise. The risks are far greater than suggested in the current IPCC report, he says.

Yet climate modellers are in a quandary. As models get better and forecasts more alarming, their confidence in the detail of their predictions is evaporating.

The IPCC says the Greenland ice sheet will take at least 1000 years to melt. But Lenton’s group – whose members include John Schellnhuber, the chief scientist on climate change at the recent G8 meeting in Germany – says the sheet could break up within 300 years, raising sea levels by 7 metres. This would flood hundreds of millions of people or more out of their homes. “We are close to being committed to a collapse of the Greenland ice sheet,” Lenton says. “But we don’t think we have passed the tipping point yet.” The calculations show the Greenland collapse could be triggered by temperatures 1 °C warmer than today’s, of which 0.7 °C is already “in the pipeline”, held up by time lags in the system.

Lenton’s study has identified eight dangerous tipping points that could be passed this century. Several could have a cascade effect, with each triggering the next, he says.

The tipping points include a collapse of a global ocean circulation system known as the thermohaline circulation. Besides shutting down the Gulf Stream, this could also “switch off” the Asian monsoon and warm the Southern Ocean, perhaps destabilising the West Antarctica ice sheet. This would cause a further 7-metre rise in sea levels. Likewise, warming may cause a near-permanent El Niño in the Pacific, which would hasten a runaway burning of the Amazon rainforest and its disappearance by mid-century.

The existence of potential climate-change tipping points should dramatically alter economists’ assessments of how much climate change we should prevent, said Lenton. The trouble is, the discovery of tipping points has also unmasked growing uncertainty about the reliability of conventional climate models.

At the Cambridge meeting Lenny Smith, a statistician at the London School of Economics, warned about the “naive realism” of current climate modelling. “Our models are being over-interpreted and misinterpreted,” he said. “They are getting better; I don’t want to trash them per se. But as we change our predictions, how do we maintain the credibility of the science?” Over-interpretation of models is already leading to poor financial decision-making, Smith says. “We need to drop the pretence that they are nearly perfect.”

He singled out for criticism the British government’s UK Climate Impacts Programme and Met Office. He accused both of making detailed climate projections for regions of the UK when global climate models disagree strongly about how climate change will affect the British Isles.

Smith is co-author, with Dave Stainforth of the Tyndall Centre for Climate Change Research in Oxford, of a paper published this week on confidence and uncertainty in climate predictions (Philosophical Transactions of the Royal Society A, DOI: 10.1098/rsta.2007.2074). It is one of several papers on the shortfalls of current climate models.

Some authors say modellers should drop single predictions and instead offer probabilities of different climate futures. But Smith and Stainforth say this approach could be “misleading to the users of climate science in wider society”. Borrowing a phrase from former US defence secretary Donald Rumsfeld, Smith told his Cambridge audience that there were “too many unknown unknowns” for such probabilities to be useful.

Policy-makers, he said, “think we know much more than we actually know. We need to be more open about our uncertainties.” Meanwhile, the tipping points loom.

DEAD EYE. White specks are dying nerve cells in retinas of rats with glaucoma. The retina at bottom was treated with three drugs that inhibit amyloid-beta production. Black lines are blood vessels.
L. Guo, Cordeiro

by Nathan Seppa

Aug 11, 2007, – A protein fragment that litters the brains of people with Alzheimer’s disease may also bear responsibility for some of the vision loss in glaucoma, a new study in rats shows.

Glaucoma patients typically have abnormal fluid pressure within the eye, but it remains unknown how this stress kills the nerve cells at the back of the retina. While there is no cure for glaucoma, easing eye pressure with drugs or surgery helps prevent vision loss in many patients.

Some glaucoma patients, however, experience vision loss even with normal eye pressure, indicating that other factors are sometimes involved.

The new research suggests that one hidden assailant is amyloid-beta, the same protein fragment that accumulates in the brains of Alzheimer’s patients. An earlier rodent study of glaucoma had found the substance in the animals’ eyes, but other evidence of amyloid-beta in glaucoma is scarce.

In the new study, ophthalmologist M. Francesca Cordeiro of University College London and her colleagues induced glaucoma in 60 rats by injecting saline into the animals’ eyes. Within weeks, amyloid-beta deposits showed up in dying retinal-nerve cells.

The researchers then gave another round of eye injections to some of the rats. In one eye, the animals received a synthetic antibody that absorbs amyloid-beta. The other eye got a placebo.

After 3 weeks, the medicated eyes showed only one-fourth as much retinal-cell death as did the untreated eyes, the researchers report in an upcoming Proceedings of the National Academy of Sciences. The effect remained 13 weeks later.

Next, the scientists repeated the experiment on other rats with glaucoma, this time using a cocktail that included the antibody and two other drugs with anti–amyloid-beta effects: a dye called Congo red and an enzyme deactivator called beta-secretase inhibitor. The triple combination worked even better than the antibody alone, reducing cell death by 84 percent.

“This offers a novel hypothesis and very intriguing results with the potential for therapeutic impact on a devastating, blinding disease,” says psychiatrist Lee E. Goldstein of Harvard Medical School and the Brigham and Women’s Hospital in Boston. It remains unclear, though, whether amyloid-beta is similarly involved in human glaucoma and, if so, whether it’s a perpetrator of the disease or a bystander. “The jury is still out,” says Goldstein.

Researchers are currently testing an amyloid-beta antibody as a drug in a large trial of Alzheimer’s patients, but Congo red and beta-secretase inhibitor haven’t entered that stage of Alzheimer’s testing, Cordeiro says. She says she’s hopeful that scientists will assess the triple combination in glaucoma patients within 2 or 3 years.

“One of the problems I have as a glaucoma doctor is that there are no other real treatments out there, other than reducing pressure in the eye,” she says.