logo
‘Nasa is being savaged' — budget cuts and politics put space exploration in jeopardy

‘Nasa is being savaged' — budget cuts and politics put space exploration in jeopardy

Times2 days ago

I t put a man on the moon, sent a rover to Mars and unlocked some of the greatest secrets of the universe. But for all Nasa's past achievements, team spirit is in the doldrums.
'It's not a happy time to work at Nasa right now,' said Casey Dreier, chief of space policy for The Planetary Society. 'There's very low morale and a huge amount of uncertainty.'
The agency has been thrust into chaos by President Trump's proposed budget cuts, his rift with his former ally Elon Musk, and a U-turn on the nomination of Jared Isaacman as Nasa administrator.
It should have been a time for optimism. Nasa is preparing to put humans back on the lunar surface for the first time since 1972 — and this time it was to be no fleeting trip. It was to include moonbases and research stations in which astronauts would live and work, and a permanent space station orbiting the moon called the Lunar Gateway.

Orange background

Try Our AI Features

Explore what Daily8 AI can do for you:

Comments

No comments yet...

Related Articles

INmune Bio's Alzheimer's drug falls short of mid-stage study goal, shares tumble
INmune Bio's Alzheimer's drug falls short of mid-stage study goal, shares tumble

Reuters

time2 hours ago

  • Reuters

INmune Bio's Alzheimer's drug falls short of mid-stage study goal, shares tumble

June 30 (Reuters) - INmune Bio (INMB.O), opens new tab said on Monday its experimental Alzheimer's drug failed to improve cognitive functions in patients with early stages of the mind-robbing disease in a mid-stage study, sending its shares plunging nearly 63% in premarket trading. The drug, XPro, is designed to target and inhibit inflammatory signals associated with a type of protein called tumor necrosis factor without suppressing the immune system. The study enrolled 208 patients with mild Alzheimer's disease (AD), or mild cognitive impairment, an early sign of the disease, who were randomly chosen to receive a weekly subcutaneous injection of XPro or a placebo for 24 weeks. The drug was safe and well-tolerated, the company said, with injection site reactions the most common adverse event.

Researchers pinpoint diet followed by millions that may ward off dementia
Researchers pinpoint diet followed by millions that may ward off dementia

Daily Mail​

time2 hours ago

  • Daily Mail​

Researchers pinpoint diet followed by millions that may ward off dementia

Cutting back on carbohydrates could potentially stave off Alzheimer's, researchers suggested today. Calling the strategy a 'powerful tool for combatting dementia', they showed reducing the amount of blood sugar in the brain via diet could slash the number of harmful proteins that trigger dementia symptoms. Carbohydrates are converted to a type of sugar called glycogen, which is a form of energy that's used by the brain to function. While a small amount is needed, the California-based researchers discovered that an excess can bind to a toxic protein in the brain called tau, stopping it from breaking down. Significant clumps of this protein, as well as another—amyloid—can form plaques and tangles—and this is thought to be behind the symptoms of Alzheimer's, the leading cause of dementia. The latest experiments found high levels of enzymes that break down glycogen in the brain could help destroy the build-up of tau. And eating fewer carbohydrates, the researchers, said was an effective way to increase the presence of this enzyme. Professor Pankaj Kapahi, an expert in metabolism and brain ageing at the Buck Institute for Research on Ageing in California and study co-author, said the team may have uncovered a new 'therapeutic strategy' to tackle dementia early-on. He added: 'As we continue to age as a society, findings like these offer hope that better understanding our brain's hidden sugar code could unlock powerful tools for combating dementia.' In the new study on fruit flies, the scientists found when glycogen can't be broken down, brain cells lose an essential mechanism for managing oxidative stress that ultimately kills them. But, by restoring the activity of an enzyme called glycogen phosphorylase (GlyP)—which triggers glycogen breakdown—they could reduce this damage. Writing in the journal Nature Metabolism, they said that by restricting certain foods that are converted to glycogen such as carbohydrates, GlyP activity is 'enhanced' and sugar levels in the brain reduced. Professor Pankaj Kapahi also said: 'This work could explain why GLP-1 drugs, now widely used for weight loss, show promise against dementia, potentially by mimicking dietary restriction.' Slimming injections, known medically as GLP-1 drugs, have ushered in a new era in the war on obesity. The treatment spurs weight loss by mimicking the actions of a hormone released in the gut after eating—GLP-1. As well as telling the pancreas to make more insulin, the GLP-1 hormone feeds back to the brain and makes us feel full—stopping patients from over-eating. The team hopes that by raising awareness of risk factors—which change as we age—people can take steps to reduce their chances of getting the disease. It comes as a landmark study last July suggested almost half of all Alzheimer's cases could be prevented by tackling 14 lifestyle factors from childhood. World-leading experts found two new risk factors—high cholesterol and suffering vision loss—were, combined, behind almost one in ten dementia cases globally. They join 12 existing factors, ranging from genetics to smoking status, that experts have identified as increasing the risk a person would suffer dementia. Experts claimed the study, published in the prestigious journal The Lancet, provided more hope than 'ever before' that the memory-robbing disorder that blights the lives of millions can be tackled. Recent analysis by the Alzheimer's Society estimates the overall annual cost of the dementia to the UK is £42billion a year, with families bearing the brunt. An ageing population means these costs—which include lost earnings of unpaid carers—are set to soar to £90billion in the next 15 years. Alzheimer's Disease is the most common form of dementia and affects 982,000 people in the UK. Memory problems, thinking and reasoning difficulties and language problems are common early symptoms of the condition, which then worsen over time. Alzheimer's Research UK analysis found 74,261 people died from dementia in 2022 compared with 69,178 a year earlier, making it the country's biggest killer.

Gene discovery may lead to ‘exercise pill' for Alzheimer's patients
Gene discovery may lead to ‘exercise pill' for Alzheimer's patients

The Independent

time3 hours ago

  • The Independent

Gene discovery may lead to ‘exercise pill' for Alzheimer's patients

Scientists have identified specific brain cells which respond most to exercise, an advance that could lead to a pill to boost the benefits Alzheimer's patients receive from exercise. The study, published in the journal Nature Neuroscience, reveals further insights into the connection between exercise and the brain and can point to future drug targets. 'While we've long known that exercise helps protect the brain, we didn't fully understand which cells were responsible or how it worked at a molecular level,' said study co-author Christiane D. Wrann from Mass General Brigham in the US. 'Now, we have a detailed map of how exercise impacts each major cell type in the memory centre of the brain in Alzheimer's disease,' Dr Wrann said. In the study, scientists focused on the brain's hippocampus – a key region for memory and learning that is damaged early in Alzheimer's disease. Using cutting-edge technology to peer into the molecules inside individual cell nuclei, researchers looked at the gene activity in single cells for an in-depth understanding of diseases like Alzheimer's. They used a common mouse model for Alzheimer's disease, which ran on wheels for the benefit of improved memory compared to the sedentary rodents. Researchers then analysed the individual cells in the brain of these mice. They found that the rodents running on wheels had changed activity in Alzheimer's disease-associated microglia cells, which are located throughout the brain and spinal cord. Scientists also found altered activity linked to exercise in a specific cell type called Oligodendrocyte progenitor cells, which are linked to blood vessels in the brain. They probed even further to find that a gene named Atpif1 was an important regulator in creating new nerve cells in the brain. 'That we were able to modulate newborn neurons using our new target genes set underscores the promise our study,' said study lead author Joana Da Rocha. Researchers then validated their discoveries in a large dataset of human Alzheimer's brain tissue, finding striking similarities. 'This work not only sheds light on how exercise benefits the brain but also uncovers potential cell-specific targets for future Alzheimer's therapies,' said Nathan Tucker, another author of the study. 'Together, these data present a comprehensive resource for understanding the molecular mediators of neuroprotection by exercise in Alzheimer's disease,' scientists wrote.

DOWNLOAD THE APP

Get Started Now: Download the App

Ready to dive into a world of global content with local flavor? Download Daily8 app today from your preferred app store and start exploring.
app-storeplay-store