Japanese astronaut to command space station in March

Japanese astronaut Koichi Wakata is seen on a monitor during a training exercise in a cetrifuge at the Star City space centre outside Moscow, August 9, 2013.

Credit: Reuters/Sergei Remezov

By Irene Klotz

CAPE CANAVERAL, Florida | Wed Aug 28, 2013 5:58pm EDT

CAPE CANAVERAL, Florida (Reuters) - The first Japanese astronaut to live aboard the International Space Station is preparing for a return flight, this time to serve as commander, officials said on Wednesday.

Koichi Wakata of the Japan Aerospace Exploration Agency, or JAXA, is due to leave in November with a pair of veteran astronauts from the United States and Russia.

Wakata, 50, is expected to take command of the orbital research outpost in March, marking the first time a Japanese astronaut will lead a human space mission.

"It means a lot to Japan to have its own representative to command the International Space Station," Wakata told a news conference broadcast from the Johnson Space Center in Houston.

"It's a big milestone for Japan ... to have this experience," he said.

In 2009, Wakata became the first astronaut from Japan to live aboard the $100 billion research laboratory that flies about 250 miles above Earth.

Japan, one of 15 nations participating in the project, provided the station's largest and most elaborate laboratory, named Kibo, as well as cargo resupply ships.

Wakata, who was part of two missions on NASA's now-retired space shuttles, is training for his fourth flight along with NASA astronaut Rick Mastracchio and Russian cosmonaut Mikhail Tyurin, both 53.

Mastracchio, a veteran of three shuttle missions and one of NASA's most experienced spacewalkers, will be making his first long-duration flight. Tyurin will be living aboard the station for a third time.

Command of the station typically rotates between a U.S. astronaut and Russian cosmonaut. In 2009, Belgium astronaut Frank De Winne became the first European to command the station. Canada's first commander, Chris Hadfield, was in charge from March until May.

Wakata, a native of Saitama, Japan, holds a bachelor's degree in aeronautical engineering, a master's in applied mechanics and a doctorate in aerospace engineering from Kyushu University. Before being selected as an astronaut in 1992, he worked as an aircraft structural engineer for Japan Airlines.

Wakata's first two spaceflights, in January 1996 and October 2000, were aboard NASA space shuttles. He was Japan's first live-aboard space station resident from March to July 2009. Upon returning to the station in November, Wakata will serve as a flight engineer before taking over command in March.

(Reporting by Tom Brown,; Editing by Stacey Joyce)

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Scientists discover key to normal memory lapses in seniors

By Sharon Begley

NEW YORK | Wed Aug 28, 2013 2:24pm EDT

NEW YORK (Reuters) - Scientists have good news for all the older adults who occasionally forget why they walked into a room - and panic that they are getting Alzheimer's disease.

Not only is age-related memory loss a syndrome in its own right and completely unrelated to that dread disease, but unlike Alzheimer's it may be reversible or even preventable, researchers led by a Nobel laureate said in a study published on Wednesday.

Using human brains that had been donated to science as well as the brains of lab mice, the study for the first time pinpointed the molecular defects that cause cognitive aging.

In an unusual ray of hope for a field that has had almost nothing to offer older adults whose memory is failing, the study's authors conclude that drugs, foods or even behaviors might be identified that affect those molecular mechanisms, helping to restore memory.

Any such interventions would represent a significant advance over the paltry offerings science has come up with so far to prevent memory decline, such as advice to keep cognitively active and healthy - which helps some people, but not all, and has only a flimsy scientific foundation. By identifying the "where did I park the car?" molecule, the discovery could also kick-start the mostly moribund efforts to develop drugs to slow or roll back the memory lapses that accompany normal aging.

"This is a lovely set of studies," said Molly Wagster of the National Institute on Aging, an expert on normal age-related memory decline who was not involved in the new study. "They provide clues to the underlying mechanism of age-related memory decline and will, hopefully, move us down the road toward targeted therapeutics."

About 40 percent of Americans age 85 and older say they experience some memory loss, a 2009 survey by the Pew Research Center found, as did 27 percent of those 75 to 84 and 20 percent of those ages 65 to 74.

BRAIN BANK

The researchers began with eight brains from the New York Brain Bank at Columbia University donated by people aged 33 to 88 who were free of brain disease when they died. They extracted two structures in the hippocampus, a vital cog in the brain's memory machinery: the dentate gyrus, a boomerang-shaped region whose function declines with age but is not affected by Alzheimer's, and the entorhinal cortex, which is largely unaffected by aging but is where Alzheimer's first takes hold, killing neurons.

The scientists then measured which genes had been active in each structure, and found one suspicious difference: 17 genes in the dentate gyrus became more active, or less, as the age of the brain increased.

The most significant change was that the gene for a protein called RbAp48 had essentially retired: The gene's activity tailed off dramatically the older a brain got. As a result, old brains had about half the RbAp48 of young brains, the scientists report online in the journal Science Translational Medicine.

The scientists then sampled 10 more healthy human brains, ranging from 41 to 89 years at the time of death. Once again, the amount of RbAp48 protein declined with age in the dentate gyrus. They next confirmed that RbAp48 protein was also less abundant in the dentate gyrus of old mice compared to young ones.

For the final step, the scientists had to nail down whether the missing protein caused age-related memory loss. They genetically engineered mice whose RbAp48 genes were disabled. Result: The young mice had memories as poor as animals four times their age (the mouse equivalent of late middle age), and they had terrible trouble navigating a water maze or differentiating objects they had seen before from novel ones.

Crucially, the scientists also did the reverse experiment, engineering mice so their brains had extra doses of RbAp48. The mice's memories returned to the flower of youth.

"With RbAp48, we were able to reverse age-related memory loss in the mice," said Columbia's Dr Eric Kandel, who shared the 2000 Nobel Prize in medicine for discoveries of the molecular basis of memory and led the research. "Unlike in Alzheimer's, there is no significant cell death in age-related memory loss, which gives us hope it can be prevented or reversed."

Exactly how RbAp48 does that is not clear. The protein acts as a sort of genetic master key: By causing chromosomes to loosen their hold on the molecular spool they are wound around like thread, it allows genes to be turned on. Among the activated genes, Kandel explained, are those involved in forming memories.

The emerging picture is that levels of RbAp48 decline with age, allowing chromosomes to maintain a death grip on their spools. Memory genes remain dormant, and you can't remember that you promised your spouse you would make dinner.

The researchers plan to see what social and dietary factors might boost RbAp48 in mice, said Kandel, who will be 84 in November. Pharmaceuticals, nutraceuticals, physical and cognitive exercise are all candidates, said Columbia's Dr Scott Small, co-senior author of the study.

Testing such interventions in mice should be more useful to humans than tests of drugs for Alzheimer's, he said. RbAp48 "is different," Small said. "Alzheimer's does not occur naturally in the mouse. Here, we've caused age-related memory loss in the mouse, and we've shown it to be relevant to human aging."

(Reporting by Sharon Begley; Editing by Julie Steenhuysen and Prudence Crowther)

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Insight: Research renaissance offers new ways out of depression

1 of 3. Prozac medicine is seen at a pharmacy in Los Angeles, California, in this October 18, 2010 file photo.

Credit: Reuters/Lucy Nicholson/Files

By Kate Kelland, Health and Science Correspondent

LONDON | Mon Sep 9, 2013 6:53am EDT

LONDON (Reuters)- As Susan sits chatting to a nurse in a London clinic, a light tapping sound by her head signals that parts of her brain are being zapped by thousands of tiny electro-magnetic pulses from a machine plugged into the wall.

The 50 year-old doctor is among growing ranks of people with so-called treatment-resistant depression, and after 21 years fighting a disorder that destroyed her ability to work and at times made her want to "opt out of life", this is a last resort.

Until recently, Susan and others like her had effectively reached the end of the road with depression treatments, having tied the best drugs medical science had to offer, engaged in hours of therapy, and tried cocktails of both.

But a renaissance in research into depression prompted by some remarkable results with highly experimental treatments has changed the way neuroscientists see the disorder and is offering hope for patients who had feared there was nowhere left to go.

Their drive to find an answer has taken neuroscientists to uncharted waters - researching everything from psychedelic magic mushrooms, to the veterinary tranquilizer ketamine, to magnetic stimulation through the skull, to using electrical implants - a bit like a pacemaker for the brain - to try and reset this complex organ's wiring and engender a more positive outlook.

Their sometimes surprising findings have in turn taught them more about depression - leading to a view of it not as a single mental illness but a range of disorders each with distinct mechanisms, yet all producing similarly debilitating symptoms.

"The thinking about depression has been revitalized," said Helen Mayberg, a neurologist at Emory University in Atlanta in the United States.

"We have a new model for thinking about psychiatric diseases not just as chemical imbalance - that your brain is a just big vat of soup where you can just add a chemical and stir - but where we ask different questions - what's wrong with brain chemistry and what's wrong with brain circuits."

ADD A CHEMICAL AND STIR?

There's little doubt that until this new breath of hope, depression had been going through a bad patch.

Affecting more than 350 million people, depression is ranked by the World Health Organization as the leading cause of disability worldwide. In extreme cases, depressed people kill themselves. Around a million people commit suicide every year, the majority due to unidentified or untreated depression.

Treatment for depression involves either medication or psychotherapy - and often a combination of both. Yet as things stand, as many as half of patients fail to recover on their first medication, and around a third find no lasting benefit from any medication or talking therapy currently available.

High hopes for "wonder" drugs like Prozac, Seroxat and others in their class of selective serotonin reuptake inhibitors (SSRIs) in the 1980s and 1990s were dimmed by studies in the 2000s that showed they helped a proportion of people, but left at least 30 percent of patients little or no better than before.

And as chronically depressed patients move from trying one drug to the next, or one type of therapy to another, their hopes too dim as it becomes clear that failing to get better with each depressive bout in turn also ups their chances of relapse.

For Susan, the battle seemed never ending.

When she was at her lowest, she dreaded each day, says she was "frightened of everything" and overwhelmed even by straightforward tasks like making a meal for her two children.

"I was taking double doses of antidepressants - two types at once - and because I was also very agitated I was on (the sedative) chloral hydrate to help me sleep," she told Reuters.

"So I was on this massive amount of medication, but with no effect whatsoever on my depression. Nothing was working."

Desperate to help patients like Susan, and alarmed by news of some pharmaceutical firms such as GlaxoSmithKline abandoning research and development in depression because it was proving too hard to find new drugs that could turn a profit, doctors began looking for new approaches.

"We often encounter patients who say 'I've tried a million things and nothing seems to be working'," said Rafael Euba, a consultant psychiatrist at the London Psychiatry Centre (LPC)where Susan was treated. "We want to instill a feeling of hope."

ELECTRO-THERAPY

In Susan's case, past experience with a controversial electrical intervention - electro convulsion therapy (ECT) - which she says was what eventually clawed her back from her severe depression 17 years ago, lead her to investigate the latest in electrical treatments - so-called repetitive transcranial magnetic stimulation, or rTMS

Approved by medicines regulators in the United States and in Europe it is a painless treatment that uses electro-magnetic induction to activate an area of the brain that psychiatrists know is involved in the regulation of mood.

Unlike ECT, which gained notoriety in the 1975 American drama film One Flew Over the Cuckoo's Nest, rTMS it does not induce "shock", but is far more targeted, delivering a pulse to neurons in the brain and that makes them fire again.

At the LPC - currently the only place in Britain where patients can get rTMS - a treatment course can be anything from 3 to 6 weeks of half an hour a day, five days a week.

It isn't cheap. The treatment costs 1,500 pounds ($2,300) per week, with the average course lasting four weeks. And some patients also need weekly or fortnightly "maintenance" sessions beyond that.

Patients put on a white fabric cap and the electro-magnetic coil is positioned over the part of the brain that needs help - normally the left dorso-lateral prefrontal cortex, which is a few inches above the temple beneath the skull.

"Unlike with other psychiatric treatments, patients tend to find this experience quite pleasant," said Euba. "All you get is a slight tingling on the scalp - and some people like that because it's a physical sensation that something is happening."

Although they are from a controlled trial and show only a snapshot of the couple of dozen patients treated and monitored at one clinic, Euba's results so far have been striking.

Of 24 patients with depression ranging from mild to severe who received rTMS at the LPC, 18 of them - or 75 percent - got completely well and were classed as being in remission. Two more responded to treatment but did not get completely well, and only four - 17 percent - did not respond.

DEEP BRAIN STIMULATION

Mayberg and her colleagues in the United States had also been intrigued by the potential for electrical stimulation to ease severe depression, but they went in deeper.

After the success of using deep brain stimulation (DBS) devices made by firms such as Medtronic to treat tremors in patients with Parkinson's disease, her team conducted a trial using them in a small number of patients who'd had depression for decades and had not been helped by numerous different drugs.

Electrical stimulation devices were implanted into the brains of patients with severe depression and bipolar disorder.

"In this treatment the stimulation continues all the time - they implant the "pacemaker" and leave it switched on for years - and only sometimes they have to change the battery," said Jonathan Roiser, a reader in cognitive neuroscience at University College London.

According to study results published in the Archives of General Psychiatry journal last year, the number of patients who had responded to treatment after two years was very high - at 92 percent - and the proportion who were completely well and in remission from their depression was 58 percent.

For psychiatrists more used to seeing patients fail again and again to get better on any kind of treatment, these results were unheard-of. "It was a remarkable finding," says Roiser.

Yet it's not just the brain's wiring that is getting more attention. Chemistry, too has thrown up some exciting results.

Researchers who looked, for example, at the veterinary tranquilizer ketamine - or "Special K" as it is called as a party drug - found that in some patients with depression it dramatically reduced their symptoms, sometimes within hours - and kept their mood stable for several weeks after treatment.

Inspired by these uplifting findings, several drug firms, including Roche, AstraZeneca and Johnson & Johnson's Janssen unit, are in the early or mid stages of developing ketamine derivatives into what they hope will become successful new antidepressants.

DEFINE SUBTYPES AND TREAT ACCORDINGLY

Experts say the success these new and some still experimental treatments for depression emphasizes the re-thinking of it as not one but a cluster of disorders.

"We now have this increasingly influential model of what is causing mental health problems like depression - one focused on the brain circuits," said Roiser.

"We've learnt a lot about how these circuits operate, what kind of cognitive tasks they are involved in, how they interact and how they are connected to each other."

More evidence of this came in a recent study in the Journal of the American Medical Association in which researchers found that brain scans of depressed patients could help predict whether they would be more likely to respond to treatment with anti-depressant drugs or with psychotherapy.

The study focused on a part of the brain known as the insula, which plays a role in influencing emotions.

It found that in patients whose scans showed their insula consumed an excess of glucose, psychotherapy was more likely to help. In patients whose insula were less active, consuming less glucose, antidepressants were more successful.

"Our gut tells us there are subtypes (of depression), and this shows that if you look the brain, you should define the biology and treat accordingly - just as we do in other branches of medicine (like cancer or diabetes)," said Mayberg.

Far from being defeated by the emergence of depression as a more complex a disorder than first assumed, scientists say the renaissance in research is based in confidence that deeper knowledge will ensure new and better treatments can be found.

Roiser confesses to feeling "extremely excited and optimistic" about the future of treating mental illnesses.

"We're in a movement away from the traditional psychological and biological explanations for depression - which look increasingly outdated and simplistic - and we're in the middle of specifying these disorders in terms of their underlying brain circuits," he said. "That's a much better position than we were in 20 years ago."

($1 = 0.6398 British pounds)

(Reporting and writing by Kate Kelland; Editing by Peter Graff)

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Glitch resolved, NASA probe on its way to the moon

1 of 2. The small car-sized Lunar Atmosphere and Dust Environment Explorer (LADEE) is a robotic mission that will orbit the moon to gather detailed information about the structure and composition of the thin lunar atmosphere and determine whether dust is being lofted into the lunar sky is pictured at NASA's Wallops Flight Facility on Wallops Island, Virginia September 5, 2013.

Credit: Reuters/NASA/Handout via Reuters

By Irene Klotz

CAPE CANAVERAL, Florida | Sun Sep 8, 2013 4:28pm EDT

CAPE CANAVERAL, Florida (Reuters) - Engineers have resolved a minor glitch with a new NASA robotic lunar probe, which blasted off Friday night for the first leg of a 30-day trip to the moon.

Shortly after the Lunar Atmosphere and Dust Environment Explorer, or LADEE, spacecraft separated from its Minotaur 5 launch vehicle, its positioning system shut down due to what appeared to be a high electrical current.

Engineers quickly determined there was no problem with the reaction wheels, which are needed to steer and stabilize the spacecraft. Rather, the glitch involved a fault protection system designed to safeguard the wheels.

"The limits that caused the powering off of the wheels soon after activation were disabled, and reaction wheel fault protection has been selectively re-enabled," NASA wrote in a statement posted on its website.

Engineers will assess how to manage the fault protection system, added project manager Butler Hine, with NASA's Ames Research Center in Moffett Field, California.

LADEE blasted off aboard the Minotaur 5 rocket, which was making its debut flight, at 11:27 p.m. EDT/0327 GMT on Saturday from the Mid-Atlantic Regional Spaceport at NASA's Wallops Flight Facility on Wallops Island, Virginia.

The rocket, made up of three decommissioned intercontinental ballistic missile motors and two commercial boosters, deposited LADEE into a highly elliptical orbit stretching as far as 170,000 miles from Earth. During its third pass around the planet, LADEE will be in position to fire its braking rocket and slip into lunar orbit.

A 30-day checkout of the probe's science instruments will follow. Engineers also will test a prototype two-way optical laser communications system that NASA is developing for use on future space probes.

LADEE's main mission is to analyze the thin shell of gases enveloping the lunar surface, a tenuous atmosphere known as an exosphere. It also will look for signs that the lunar dust rising off the surface.

Scientists believe the dust may be the cause of a strange glow on the lunar horizon spotted by the Apollo astronauts and NASA's 1960s-era Ranger robotic probes.

LADEE was the first deep-space probe to fly from the Wallops Island spaceport. On September 17, Orbital Sciences Corp. (NYSE: ORB) is scheduled to launch its Antares rocket and Cygnus cargo capsule on a trial run to the International Space Station for NASA.

The station, a project of 15 countries, flies about 250 miles above Earth.

(Reporting by Irene Klotz)

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Baseball-sized meteor blows up over Alabama

By Irene Klotz

CAPE CANAVERAL, Florida | Tue Sep 10, 2013 4:02pm EDT

CAPE CANAVERAL, Florida (Reuters) - A baseball-sized meteor blasted over the southeastern United States on Monday night, creating a bright streak of light, a sonic boom and a ruckus on Twitter, officials said on Tuesday.

The meteor appeared at 9:18 p.m. EDT over Alabama, traveling at about 76,000 mph. It exploded 25 miles above Woodstock, Alabama, located about 30 miles from Birmingham.

"Objects of this size hit the Earth's atmosphere on a daily basis, but this one happened near Birmingham, which is a fairly decently sized city and lot of people saw it," Bill Cooke, head of NASA's Meteoroid Environment Office at the Marshall Space Flight Center in Huntsville, Alabama, told Reuters.

Many of the more than 180 eyewitness reports came from people attending a Mumford & Sons concert in Birmingham.

"This one wasn't at 2 in the morning, so a lot of people were out and about," Cooke said.

"I saw what I first thought was a falling star and then it turned bright green," an observer from Anniston, Alabama, posted on the American Meteor Society website.

"I saw it near Dallas Highway in Marietta, (Georgia), near the National Battlefield," wrote another witness. "At first, I thought it was an errant firework, but it was bigger, neon green, came straight down and then disappeared."

Scientists calculated the meteor's orbit and determined that it came from an unknown comet. It exploded so low in Earth's atmosphere that it triggered a sonic boom.

The meteor was too bright to be picked up by NASA's All-sky Fireball Network, which tracks meteors brighter than Venus with 12 cameras in the eastern United States and New Mexico but whose parameters are set to screen out things like lightning.

The network did detect nearly two dozen other meteors on Monday night, including five that are part of the little-known annual Epsilon Perseids meteor shower, which peaks in early- to mid-September.

Sky watchers also are on the lookout for Comet ISON, which is due to pass by Mars this month and by Earth in November.

The comet, which was discovered last September by a pair of amateur astronomers in Russia, is expected to pass relatively close to the sun on November 28. As it approaches, heat from the sun vaporizes ice in the comet's body, creating a bright tail.

But so far, Comet ISON hasn't brightened as much as astronomers had predicted.

"People are no longer thinking it is going to be visible in daylight," Cooke said.

(Editing by Jane Sutton and Phil Berlowitz)

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Mouse body clock study offers clues to possible jet lag cure

LONDON | Thu Aug 29, 2013 12:22pm EDT

LONDON (Reuters) - Scientists have found a genetic mechanism in mice that hampers their body clock's ability to adjust to changes in patterns of light and dark, and say their results could someday lead to the development of drugs to combat jet lag.

Researchers from Britain's Oxford University and from the Swiss drug firm Roche used mice to analyze patterns of genes in an area of the brain called the suprachiasmatic nuclei (SCN) - which in mammals pulls every cell in the body into the same biological rhythm.

They found that one molecule, called SIK1, is key to how the mice responded to changes in light cycles.

When the scientists blocked the activity of SIK1, the mice recovered faster from disturbances in their daily light and dark cycle that had been designed to induce a form of mouse jet lag.

If the corresponding mechanism can be found and similarly blocked in humans, jet lag may become a thing of the past, the researchers said in their study, published online in the journal Cell on Thursday.

"We're still several years away from a cure for jet lag, but understanding the mechanisms that generate and regulate our circadian clock gives us targets to develop drugs to help bring our bodies in tune with the solar cycle," said Russell Foster, director of Oxford's sleep and circadian neuroscience institute.

He said such drugs could also have broader potential value, including for people with mental illnesses where sleep disturbances are common.

(Reporting by Kate Kelland; Editing by Sonya Hepinstall)

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NASA's Mars rover spies solar eclipse

Phobos, the larger of Mars' two moons, is pictured in the midst of an annular eclipse of the sun on August 17, 2013 in this combination of three handout photographs taken three seconds apart by NASA's Curiosity rover from the surface of Mars.

Credit: Reuters/NASA/Handout via Reuters

By Irene Klotz

CAPE CANAVERAL, Florida | Thu Aug 29, 2013 12:49pm EDT

CAPE CANAVERAL, Florida (Reuters) - NASA's Mars rover Curiosity turned its cameras skyward to snap pictures of the planet's moon, Phobos, passing in front of the sun, images released on Thursday show.

Curiosity landed on Mars in August 2012 for a two-year mission to determine if the planet most like Earth in the solar system has, or ever had, the chemical ingredients for life. It struck pay dirt in its first analysis of powder drilled out from inside a once water-soaked piece of bedrock.

The rover is now enroute to its primary hunting ground, a three-mile (5-km) high mountain of layered sediment called Mount Sharp. It paused on August 17 to snap pictures of Mars' larger moon, Phobos, making a dash in front of the sun. NASA released three pictures, taken three seconds apart, of the eclipse, taken with the rover's telephoto lens.

"This one is by far the most detailed image of any Martian lunar transit ever taken. It was even closer to the sun's center than predicted, so we learned something," Curiosity scientist Mark Lemmon of Texas A&M University said in a statement.

Curiosity is scheduled to moonlight as an astronomer again in September and October when it tries to catch a glimpse of the approaching Comet ISON.

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