Astronauts for Crew-11 fly into KSC ahead of upcoming launch
NASA astronauts Zena Cardman and Mike Fincke, JAXA (Japan Aerospace Exploration Agency) astronaut Kimiya Yui and Roscosmos cosmonaut Oleg Platonov, the quartet for SpaceX's Crew-11 mission to the International Space Station, flew into the former space shuttle landing site at KSC after noon under the searing sun as temperatures on the tarmac climbed into the 90s.
'Sorry for the heat, but it's Florida in the summertime,' said veteran Fincke, who kept cracking jokes and even made bunny ears behind Platonov's head during a photo as the crewmates talked to media.
They're slated to lift off as early as 12:09 p.m. Thursday from KSC's Launch Pad 39-A atop a Falcon 9 rocket riding in the Crew Dragon Endeavour.
'We've been training together for over a year now and we are ready to fly,' said Cardman, who is making her first spaceflight. 'As a first-time flyer, this is the first moment when it's really starting to feel real.'
They expect at least a six-month stay on board the space station where they will relieve the four members of Crew-10 on board since March.
In addition to the two NASA flights this year, SpaceX has flown a private polar orbital mission Fram2 in March and the private Axiom Space Ax-4 mission to the space station last month.
The launch is one shy of the five human spaceflight missions from Florida seen in 2024, although it would equal the number of people launching with 16 in space. Both last year's Boeing Starliner CFT mission and the Crew-9 mission only flew up with two crew each instead of four. That was because Crew-9 became the ride home for Starliner astronauts after NASA opted to send Boeing's beleaguered spacecraft home minus crew over safety concerns — and they ultimately had to be ferried home by SpaceX.
NASA astronaut Michael Fincke talks about how he started to bald after going to space causing laughter from Crew-11 crewmate and JAXA astronaut Kimiya Yui after they arrived to Kennedy Space Center on Saturday, July 26, 2025 ahead of their planned launch this week to the International Space Station. (Richard Tribou/Orlando Sentinel) NASA astronaut and pilot Michael Fincke gives a handoff wave to Crew-11 crewmate JAXA astronaut Kimiya Yu as NASA astronaut and commander Zena Cardman, left, and Roscosmos cosmonaut Oleg Platonov, right, look on after they arrived to Kennedy Space Center on Saturday, July 26, 2025 ahead of their planned launch this week to the International Space Station. (Richard Tribou/Orlando Sentinel) NASA astronaut and pilot Michael Fincke cracks a joke causing JAXA astronaut Kimiya Yui to break into laughter after they and their fellow Crew-11 crewmates, NASA astronaut and commander Zena Cardman and Roscosmos cosmonaut Oleg Platonov, arrived to Kennedy Space Center on Saturday, July 26, 2025 ahead of their planned launch this week to the International Space Station. (Richard Tribou/Orlando Sentinel) The four members of Crew-11 arrive to Kennedy Space Center on Saturday, July 26, 2025 ahead of their planned launch this week to the International Space Station. From left to right are NASA astronaut and commander Zena Cardman, NASA astronaut and pilot Michael Fincke, JAXA astronaut Kimiya Yui and Roscosmos cosmonaut Oleg Platonov along with his translator. (Richard Tribou/Orlando Sentinel) The four members of Crew-11 arrive to Kennedy Space Center on Saturday, July 26, 2025 ahead of their planned launch this week to the International Space Station. From left to right are NASA astronaut and commander Zena Cardman, NASA astronaut and pilot Michael Fincke, JAXA astronaut Kimiya Yui and Roscosmos cosmonaut Oleg Platonov along with his translator. (Richard Tribou/Orlando Sentinel) Show Caption1 of 6NASA astronaut Michael Fincke, right, raises some bunny ears behind the head Roscosmos cosmonaut Oleg Platonov while posing for photos with their Crew-11 crewmates, NASA astronaut Zena Cardman and JAXA astronaut Kimiya Yui, after arriving at Kennedy Space Center on Saturday, July 26, 2025 ahead of their planned launch this week to the International Space Station. (Richard Tribou/Orlando Sentinel)Expand
Endeavour is making a record sixth trip to space, the first of SpaceX's fleet of five Crew Dragons to hit that mark as NASA looks to stretch their utility beyond the original five flights for which they have been certified.
Cardman was originally tapped as commander for the Crew-9 mission, but as a rookie, she was bumped in favor of another member of that crew with flight experience. She is now back for Crew-11 as its commander.
She becomes the last of 12 NASA astronauts from the 2017 class known as The Turtles to make it space.
'In spaceflight, the journey is often nonlinear. It's just a privilege to be here with this crew, especially. I have the privilege of overlapping with one of my classmates, Jonny Kim, who's currently on board as a member of Expedition 73. I also have the privilege of flying with Kimiya Yui, whose patch has a turtle on it. And so that makes him an honorary turtle in my heart.'
Fincke was also reassigned from what was supposed to be Starliner's first operational crew mission, Starliner-1, but shifted to this SpaceX mission as Boeing and NASA continue to work on Starliner's issues. He is making his fourth trip to space having made trips on Soyuz in 2004 and 2008 as well as the penultimate flight of the Space Shuttle Program, STS-134, on Space Shuttle Endeavour in 2011.
'It's been a really interesting journey watching brand new spaceships be built,' Fincke said. 'I'm very proud of our teams, both SpaceX and Boeing, to what they built together and really proud to actually finally fly on a commercial crew spacecraft.'
Japan's Yui also was training for a Starliner flight, but is now headed for his second trip to space — having been on a Soyuz mission in 2015.
'My last mission was 10 years ago, so I'm very much looking forward to going back to my home,' he said.
Platonov joins Cardman as the second rookie on this mission.
The four will be on board when the station reaches a milestone on Nov. 2, which will signify 25 years of continuous occupation. They will be part of Expeditions 73 and 74 along with the three members on board that flew up on a Soyuz.
'I'm personally looking forward to going back up to the space station. I helped build it, and now I get to see it in its full maturity with six other crewmates,' Fincke said.
NASA looks to decommission the station after 2030.
'I know it's coming near its time, but this is something that I think that humans should just really remember of all the cool things we can do when we work together constructively,' Fincke said.
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35 minutes ago
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Scientists say it may be possible to protect aging brains from Alzheimer's with an old remedy — lithium
In a major new finding almost a decade in the making, researchers at Harvard Medical School say they've found a key that may unlock many of the mysteries of Alzheimer's disease and brain aging — the humble metal lithium. Lithium is best known to medicine as a mood stabilizer given to people who have bipolar disorder and depression. It was approved by the US Food and Drug Administration in 1970, but it was used by doctors to treat mood disorders for nearly a century beforehand. Now, for the first time, researchers have shown that lithium is naturally present in the body in tiny amounts and that cells require it to function normally — much like vitamin C or iron. It also appears to play a critical role in maintaining brain health. In a series of experiments reported Wednesday in the journal Nature, researchers at Harvard and Rush universities found that depleting lithium in the diet of normal mice caused their brains to develop inflammation and changes associated with accelerated aging. In mice that were specially bred to develop the same kinds of brain changes as humans with Alzheimer's disease, a low-lithium diet revved the buildup of sticky proteins that form plaques and tangles in the brains that are hallmarks of the disease. It also sped up memory loss. Maintaining normal lithium levels in mice as they aged, however, protected them from brain changes associated with Alzheimer's. If further research supports the findings, it could open the door to new treatments and diagnostic tests for Alzheimer's, which affects an estimated 6.7 million older adults in the United States, according to the US Centers for Disease Control and Prevention. The research provides a unifying theory that helps explain so many of the puzzle pieces scientists have been trying to fit together for decades. 'It is a potential candidate for a common mechanism leading to the multisystem degeneration of the brain that precedes dementia,' said Dr. Bruce Yankner, a professor of genetics at Harvard Medical School, who led the study. 'It will take a lot more science to determine whether this is a common pathway… or one of several pathways,' to Alzheimer's, he added. 'The data are very intriguing.' In an editorial published in Nature, Dr. Ashley Bush, a neuroscientist who directs the Melbourne Dementia Research Center at the University of Melbourne in Australia, said the researchers 'present compelling evidence that lithium does in fact have a physiological role and that normal aging might impair the regulation of lithium levels in the brain.' He was not involved in the study. Close examination of human and animal brain tissues, along with genetic investigations in the study, found the mechanism that appears to be at play: Beta amyloid plaques — the sticky deposits that gum up the brains of Alzheimer's patients — bind to lithium and hold it, including the type that's normally present in the body, as well as the commonly prescribed form. This binding depletes lithium available for nearby cells, including important scavengers known as microglia. When the brain is healthy and functioning normally, microglia are waste managers, clearing away beta amyloid before it can accumulate and can cause harm. In the team's experiments, microglia from the brains of lithium-deficient mice showed a reduced ability to sweep away and break down beta amyloid. Yankner believes this creates a downward spiral. The accumulation of beta amyloid soaks up more and more lithium, further crippling the brain's ability to clear it away. He and his colleagues tested different lithium compounds and found one — lithium orotate — that doesn't bind to amyloid beta. When they gave lithium orotate to mice with signs of Alzheimer's in their brains, these changes reversed: Beta amyloid plaques and tangles of tau that were choking the memory centers of the brain were reduced. Mice treated with lithium were once again able to navigate mazes and learn to identify new objects, whereas those who got placebos showed no change in their memory and thinking deficits. In its natural form, lithium is an element, a soft, silvery-white metal that readily combines with other elements to form compounds and salts. It's naturally present in the environment, including in food and water. Scientists have never fully known how it works to improve mood — only that it does. The original formula for 7Up soda included lithium — it was called 7Up Lithiated Lemon Soda — and touted as a hangover cure and mood lifter 'for hospital or home use.' Some hot springs known to contain mineral water brimming with lithium became sought out wellness destinations for their curative powers. Still, people who take prescription doses of lithium — which were much higher than the doses used in the new study — can sometimes develop thyroid or kidney toxicity. Tests of the mice given low doses of lithium orotate showed no signs of damage. That's encouraging, Yankner said, but it doesn't mean people should try to take lithium supplements on their own. 'A mouse is not a human. Nobody should take anything based just on mouse studies,' Yankner said. 'The lithium treatment data we have is in mice, and it needs to be replicated in humans. We need to find the right dose in humans,' he added. The normal amounts of lithium in our bodies, and the concentrations given to the mice, are small — about 1,000 times lower than doses given to treat bipolar disorder, Yankner notes. Yankner said he hoped toxicity trials of lithium salts would start soon. Neither he nor any of his co-authors have a financial interest in the outcome of the research, he said. The National Institutes of Health was the major funder of the study, along with grants from private foundations. 'NIH support was absolutely critical for this work,' Yankner said. The new research corroborates earlier studies hinting that lithium might be important for Alzheimer's. A large Danish study published in 2017 found people with higher levels of lithium in their drinking water were less likely to be diagnosed with dementia compared with those whose tap water contained naturally lower lithium levels. Another large study published in 2022 from the United Kingdom found that people prescribed lithium were about half as likely has those in a control group to be diagnosed with Alzheimer's, suggesting a protective effect of the drug. But lithium's use in psychiatry caused it to become type cast as therapeutic, Yankner said. No one realized it might be important to the body's normal physiology. That happened in part because the amounts of lithium that typically circulate in the body are so small, they couldn't be quantified until recently. Yankner and his team had to adapt new technology to measure it. In the first stage of the research, the scientists tested the brain tissue and blood of older patients collected by the brain bank at Rush University for trace levels of 27 metals. Some of the patients had no history of memory trouble, while others had early memory decline and pronounced Alzheimer's. While there was no change in the levels of most metals they measured, lithium was an exception. Lithium levels were consistently lower in patients with mild cognitive impairment or Alzheimer's compared to those with normal brain function. The brains of patients Alzheimer's disease also showed increased levels of zinc and decreased levels of copper, something scientists had observed before. Consistently finding lower lithium levels in the brains of people with memory loss amounted to a smoking gun, Yankner said. 'At first, frankly, we were skeptical of the result because it wasn't expected,' said Yankner. But it held up even when they checked samples from other brain banks at Massachusetts General Hospital, Duke and Washington universities. 'We wanted to know whether this drop in lithium was biologically meaningful, so we devised an experimental protocol where we could take lithium selectively out of the diet of mice and see what happens,' Yankner said. When they fed the mice a low-lithium diet, simply dropping their natural levels by 50%, their brains rapidly developed features of Alzheimer's. 'The neurons started to degenerate. The immune cells in the brain went wild in terms of increased inflammation and worse maintenance function of the neurons around them, and it looked more like an advanced Alzheimer patient,' Yankner said. The team also found the gene expression profiles of lithium-deficient mice and people who had Alzheimer's disease looked very similar. The researchers then started to look at how this drop in lithium might occur. Yankner said in the earliest stages there's a decrease in the uptake of lithium in the brain from the blood. They don't yet know exactly how or why it happens, but it's likely to be from a variety of things including reduced dietary intake, as well as genetic and environmental factors. The major source of lithium for most people is their diet. Some of the foods that have the most lithium are leafy green vegetables, nuts, legumes and some spices like turmeric and cumin. Some mineral waters are also rich sources. In other words, Yankner said, a lot of the foods that have already proven to be healthy and reduce a person's risk of dementia may be beneficial because of their lithium content. 'You know, oftentimes one finds in science that things may have an effect, and you think you know exactly why, but then subsequently turn out to be completely wrong about why,' he said.
CNN
35 minutes ago
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Scientists say it may be possible to protect aging brains from Alzheimer's with an old remedy — lithium
Chronic diseases Dementia Getting olderFacebookTweetLink Follow In a major new finding almost a decade in the making, researchers at Harvard Medical School say they've found a key that may unlock many of the mysteries of Alzheimer's disease and brain aging — the humble metal lithium. Lithium is best known to medicine as a mood stabilizer given to people who have bipolar disorder and depression. It was approved by the US Food and Drug Administration in 1970, but it was used by doctors to treat mood disorders for nearly a century beforehand. Now, for the first time, researchers have shown that lithium is naturally present in the body in tiny amounts and that cells require it to function normally — much like vitamin C or iron. It also appears to play a critical role in maintaining brain health. In a series of experiments reported Wednesday in the journal Nature, researchers at Harvard and Rush universities found that depleting lithium in the diet of normal mice caused their brains to develop inflammation and changes associated with accelerated aging. In mice that were specially bred to develop the same kinds of brain changes as humans with Alzheimer's disease, a low-lithium diet revved the buildup of sticky proteins that form plaques and tangles in the brains that are hallmarks of the disease. It also sped up memory loss. Maintaining normal lithium levels in mice as they aged, however, protected them from brain changes associated with Alzheimer's. If further research supports the findings, it could open the door to new treatments and diagnostic tests for Alzheimer's, which affects an estimated 6.7 million older adults in the United States, according to the US Centers for Disease Control and Prevention. The research provides a unifying theory that helps explain so many of the puzzle pieces scientists have been trying to fit together for decades. 'It is a potential candidate for a common mechanism leading to the multisystem degeneration of the brain that precedes dementia,' said Dr. Bruce Yankner, a professor of genetics at Harvard Medical School, who led the study. 'It will take a lot more science to determine whether this is a common pathway… or one of several pathways,' to Alzheimer's, he added. 'The data are very intriguing.' In an editorial published in Nature, Dr. Ashley Bush, a neuroscientist who directs the Melbourne Dementia Research Center at the University of Melbourne in Australia, said the researchers 'present compelling evidence that lithium does in fact have a physiological role and that normal aging might impair the regulation of lithium levels in the brain.' He was not involved in the study. Close examination of human and animal brain tissues, along with genetic investigations in the study, found the mechanism that appears to be at play: Beta amyloid plaques — the sticky deposits that gum up the brains of Alzheimer's patients — bind to lithium and hold it, including the type that's normally present in the body, as well as the commonly prescribed form. This binding depletes lithium available for nearby cells, including important scavengers known as microglia. When the brain is healthy and functioning normally, microglia are waste managers, clearing away beta amyloid before it can accumulate and can cause harm. In the team's experiments, microglia from the brains of lithium-deficient mice showed a reduced ability to sweep away and break down beta amyloid. Yankner believes this creates a downward spiral. The accumulation of beta amyloid soaks up more and more lithium, further crippling the brain's ability to clear it away. He and his colleagues tested different lithium compounds and found one — lithium orotate — that doesn't bind to amyloid beta. When they gave lithium orotate to mice with signs of Alzheimer's in their brains, these changes reversed: Beta amyloid plaques and tangles of tau that were choking the memory centers of the brain were reduced. Mice treated with lithium were once again able to navigate mazes and learn to identify new objects, whereas those who got placebos showed no change in their memory and thinking deficits. In its natural form, lithium is an element, a soft, silvery-white metal that readily combines with other elements to form compounds and salts. It's naturally present in the environment, including in food and water. Scientists have never fully known how it works to improve mood — only that it does. The original formula for 7Up soda included lithium — it was called 7Up Lithiated Lemon Soda — and touted as a hangover cure and mood lifter 'for hospital or home use.' Some hot springs known to contain mineral water brimming with lithium became sought out wellness destinations for their curative powers. Still, people who take prescription doses of lithium — which were much higher than the doses used in the new study — can sometimes develop thyroid or kidney toxicity. Tests of the mice given low doses of lithium orotate showed no signs of damage. That's encouraging, Yankner said, but it doesn't mean people should try to take lithium supplements on their own. 'A mouse is not a human. Nobody should take anything based just on mouse studies,' Yankner said. 'The lithium treatment data we have is in mice, and it needs to be replicated in humans. We need to find the right dose in humans,' he added. The normal amounts of lithium in our bodies, and the concentrations given to the mice, are small — about 1,000 times lower than doses given to treat bipolar disorder, Yankner notes. Yankner said he hoped toxicity trials of lithium salts would start soon. Neither he nor any of his co-authors have a financial interest in the outcome of the research, he said. The National Institutes of Health was the major funder of the study, along with grants from private foundations. 'NIH support was absolutely critical for this work,' Yankner said. The new research corroborates earlier studies hinting that lithium might be important for Alzheimer's. A large Danish study published in 2017 found people with higher levels of lithium in their drinking water were less likely to be diagnosed with dementia compared with those whose tap water contained naturally lower lithium levels. Another large study published in 2022 from the United Kingdom found that people prescribed lithium were about half as likely has those in a control group to be diagnosed with Alzheimer's, suggesting a protective effect of the drug. But lithium's use in psychiatry caused it to become type cast as therapeutic, Yankner said. No one realized it might be important to the body's normal physiology. That happened in part because the amounts of lithium that typically circulate in the body are so small, they couldn't be quantified until recently. Yankner and his team had to adapt new technology to measure it. In the first stage of the research, the scientists tested the brain tissue and blood of older patients collected by the brain bank at Rush University for trace levels of 27 metals. Some of the patients had no history of memory trouble, while others had early memory decline and pronounced Alzheimer's. While there was no change in the levels of most metals they measured, lithium was an exception. Lithium levels were consistently lower in patients with mild cognitive impairment or Alzheimer's compared to those with normal brain function. The brains of patients Alzheimer's disease also showed increased levels of zinc and decreased levels of copper, something scientists had observed before. Consistently finding lower lithium levels in the brains of people with memory loss amounted to a smoking gun, Yankner said. 'At first, frankly, we were skeptical of the result because it wasn't expected,' said Yankner. But it held up even when they checked samples from other brain banks at Massachusetts General Hospital, Duke and Washington universities. 'We wanted to know whether this drop in lithium was biologically meaningful, so we devised an experimental protocol where we could take lithium selectively out of the diet of mice and see what happens,' Yankner said. When they fed the mice a low-lithium diet, simply dropping their natural levels by 50%, their brains rapidly developed features of Alzheimer's. 'The neurons started to degenerate. The immune cells in the brain went wild in terms of increased inflammation and worse maintenance function of the neurons around them, and it looked more like an advanced Alzheimer patient,' Yankner said. The team also found the gene expression profiles of lithium-deficient mice and people who had Alzheimer's disease looked very similar. The researchers then started to look at how this drop in lithium might occur. Yankner said in the earliest stages there's a decrease in the uptake of lithium in the brain from the blood. They don't yet know exactly how or why it happens, but it's likely to be from a variety of things including reduced dietary intake, as well as genetic and environmental factors. The major source of lithium for most people is their diet. Some of the foods that have the most lithium are leafy green vegetables, nuts, legumes and some spices like turmeric and cumin. Some mineral waters are also rich sources. In other words, Yankner said, a lot of the foods that have already proven to be healthy and reduce a person's risk of dementia may be beneficial because of their lithium content. 'You know, oftentimes one finds in science that things may have an effect, and you think you know exactly why, but then subsequently turn out to be completely wrong about why,' he said.
Yahoo
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Stranger Things' Star Shares Wild Theory About the Spinoff
Stranger Things' Star Shares Wild Theory About the Spinoff originally appeared on Parade. Even though Stranger Things is coming to an end with the series finale set to premiere on New Year's Eve, Finn Wolfhard still has some ideas regarding what the spinoff series will be about. 'Like David Lynch's Twin Peaks. Sort of an anthology and different tones but similar universe or same universe,' Wolfhard, 22, said in a new interview with Variety published on Tuesday, August 5. 'I think set in different places and all tied together through this mythology of the Upside Down. Don't even talk about Hawkins. Don't have any mention of our characters.' However, before fans get too excited, the Ghostbusters: Afterlife star clarified that no official announcements about a spinoff had been made just yet. '[Stranger Things creators Matt and Ross Duffer] were toying around with ideas in case Netflix wanted them. I'm sure they do, and I'm sure it will happen, but there's nothing official,' he explained. 'I think the coolest way, the way that I would do it, there has to be labs everywhere. If there was one in Hawkins, there's one in Russia. Where else could they be?' RELATED: In 2023, Wolfhard revealed that he had previously been a little too close for comfort in his guess about what the Duffers had planned for a spinoff. 'I was like, 'But if you guys are actually going to do a spin-off, it should be this.' And then I said it and the Duffers looked at each other and looked at me and they were like, 'Could we talk to you for a second?'' he said during an appearance on The Tonight Show With Jimmy Fallon. 'And then they pulled me off and they were like, 'That is the idea. Who told you?' and I was like, 'No one,' and they were like 'What do you mean? You just came up with it?' and I was like, 'Well, no, I just thought that that would be a cool way to expand.' It was really funny and they were like 'Okay, well… don't tell anyone.'' Granted, the Duffers could have easily changed their mind since then, but dedicated Stranger Things fans might want to brush up on their Twin Peaks lore just in case. 🎬 SIGN UP for Parade's Daily newsletter to get the latest pop culture news & celebrity interviews delivered right to your inbox 🎬 Stranger Things' Star Shares Wild Theory About the Spinoff first appeared on Parade on Aug 6, 2025 This story was originally reported by Parade on Aug 6, 2025, where it first appeared. Solve the daily Crossword
