https://www.sciencealert.com/antarcticas-ocean-is-mysteriously-getting-saltier-spelling-end-to-sea-ice

02 July 2025, By A. Silvano, The Conversation
https://www.sciencealert.com/antarcticas-ocean-is-mysteriously-getting-saltier-spelling-end-to-sea-ice

Sea ice will have a harder time forming in saltier waters.

 (Ray Hems/Getty Images)

The ocean around Antarctica is rapidly getting saltier at the same time as sea ice is retreating at a record pace. Since 2015, the frozen continent has lost sea ice similar to the size of Greenland.

That ice hasn't returned, marking the largest global environmental change during the past decade.

This finding caught us off guard – melting ice typically makes the ocean fresher. But new satellite data shows the opposite is happening, and that's a big problem.

Saltier water at the ocean surface behaves differently than fresher seawater by drawing up heat from the deep ocean and making it harder for sea ice to regrow.

The loss of Antarctic sea ice has global consequences. Less sea ice means less habitat for penguins and other ice-dwelling species. More of the heat stored in the ocean is released into the atmosphere when ice melts, increasing the number and intensity of storms and accelerating global warming.

This brings heatwaves on land and melts even more of the Antarctic ice sheet, which raises sea levels globally.

Our new study has revealed that the Southern Ocean is changing, but in a different way to what we expected. We may have passed a tipping point and entered a new state defined by persistent sea ice decline, sustained by a newly discovered feedback loop.

The Southern Ocean surrounds Antarctica, which is fringed by sea ice. (NASA)

A surprising discovery

Monitoring the Southern Ocean is no small task. It's one of the most remote and stormy places on Earth, and is covered in darkness for several months a year.

Thanks to new European Space Agency satellites and underwater robots which stay below the ocean surface measuring temperature and salinity, we can now observe what is happening in real time.

Our team at the University of Southampton worked with colleagues at the Barcelona Expert Centre and the European Space Agency to develop new algorithms to track ocean surface conditions in polar regions from satellites. By combining satellite observations with data from underwater robots, we built a 15-year picture of changes in ocean salinity, temperature and sea ice.

What we found was astonishing. Around 2015, surface salinity in the Southern Ocean began rising sharply – just as sea ice extent started to crash.

This reversal was completely unexpected. For decades, the surface had been getting fresher and colder, helping sea ice expand.

The annual summer minimum extent of Antarctic sea ice dropped precipitously in 2015.

 (NOAA Climate.gov/National Snow and Ice Data Center)




To understand why this matters, it helps to think of the Southern Ocean as a series of layers.

Normally, the cold, fresh surface water sits on top of warmer, saltier water deep below. This layering (or stratification, as scientists call it) traps heat in the ocean depths, keeping surface waters cool and helping sea ice to form.

Saltier water is denser and therefore heavier. So, when surface waters become saltier, they sink more readily, stirring the ocean's layers and allowing heat from the deep to rise.

This upward heat flux can melt sea ice from below, even during winter, making it harder for ice to reform. This vertical circulation also draws up more salt from deeper layers, reinforcing the cycle.

A powerful feedback loop is created: more salinity brings more heat to the surface, which melts more ice, which then allows more heat to be absorbed from the Sun.

My colleagues and I saw these processes first hand in 2016-2017 with the return of the Maud Rise polynya, which is a gaping hole in the sea ice that is nearly four times the size of Wales and last appeared in the 1970s.

What happens in Antarctica doesn't stay there

Losing Antarctic sea ice is a planetary problem. Sea ice acts like a giant mirror reflecting sunlight back into space. Without it, more energy stays in the Earth system, speeding up global warming, intensifying storms and driving sea level rise in coastal cities worldwide.

Wildlife also suffers. Emperor penguins rely on sea ice to breed and raise their chicks. Tiny krill – shrimp-like crustaceans which form the foundation of the Antarctic food chain as food for whales and seals – feed on algae that grow beneath the ice. Without that ice, entire ecosystems start to unravel.

What's happening at the bottom of the world is rippling outward, reshaping weather systems, ocean currents and life on land and sea.

Feedback loops are accelerating the loss of Antarctic sea ice.

 (University of Southampton)




Antarctica is no longer the stable, frozen continent we once believed it to be. It is changing rapidly, and in ways that current climate models didn't foresee. Until recently, those models assumed a warming world would increase precipitation and ice-melting, freshening surface waters and helping keep Antarctic sea ice relatively stable. That assumption no longer holds.

Our findings show that the salinity of surface water is rising, the ocean's layered structure is breaking down and sea ice is declining faster than expected. If we don't update our scientific models, we risk being caught off guard by changes we could have prepared for.

Indeed, the ultimate driver of the 2015 salinity increase remains uncertain, underscoring the need for scientists to revise their perspective on the Antarctic system and highlighting the urgency of further research.

We need to keep watching, yet ongoing satellite and ocean monitoring is threatened by funding cuts. This research offers us an early warning signal, a planetary thermometer and a strategic tool for tracking a rapidly shifting climate. Without accurate, continuous data, it will be impossible to adapt to the changes in store.

The Life of Earth

https://chuckincardinal.blogspot.com/

Late-Night Cheese May Fuel Nightmares – New Study Explains How

BY FRONTIERS, JULY 2, 2025

https://scitechdaily.com/late-night-cheese-may-fuel-nightmares-new-study-explains-how/

Eating cheese before bed might do more than upset your stomach — it could be hijacking your dreams. Scientists found a strong connection between dairy, sleep quality, and nightmare frequency. 

Credit: SciTechDaily.com

New research reveals a surprisingly creepy link between nightmares and dairy, especially for those with lactose intolerance.

In a survey of over 1,000 students, scientists found that people who consumed dairy products like cheese before bed were more likely to experience unsettling dreams, possibly due to gut discomfort disrupting sleep. The findings suggest that what’s in your stomach might be influencing what happens in your dreams — and that late-night snacks could be fueling more than just cravings.

Dairy Intake and Disturbed Dreams

Eating too much dairy might be doing more than upsetting your stomach, it could be disturbing your sleep. In a new study, researchers found a strong connection between nightmares and lactose intolerance. The likely culprit? Gastrointestinal discomfort like gas or bloating may be sneaking into your dreams and disrupting restful sleep.

Dr. Tore Nielsen of Université de Montréal, lead author of the study published in Frontiers in Psychology, explained, “Nightmare severity is robustly associated with lactose intolerance and other food allergies. These new findings imply that changing eating habits for people with some food sensitivities could alleviate nightmares. They could also explain why people so often blame dairy for bad dreams!”

A Curious Link Between Food and Dreams

To explore the link between diet and sleep, researchers surveyed 1,082 students at MacEwan University. Participants answered questions about their sleep patterns, dream experiences, overall health, and eating habits.

Roughly a third of students reported frequent nightmares. Women were more likely to experience poor sleep, remember their dreams, and report food intolerances or allergies. Around 40 percent of participants believed certain foods or eating late affected their sleep, and 25 percent said specific foods seemed to make their sleep worse.

The results also showed that students who ate less healthy diets tended to have more unpleasant dreams and were less likely to remember them.

While it’s long been a popular belief that food can influence dreams, scientific evidence has been limited. This new study helps fill that gap. “We are routinely asked whether food affects dreaming — especially by journalists on food-centric holidays,” said Nielsen. “Now we have some answers.”

Dairy, Sweets, and Nightmare Triggers

Most participants who blamed their bad sleep on food thought sweets, spicy foods, or dairy were responsible. Only a comparatively small proportion — 5.5% of respondents — felt that what they ate affected the tone of their dreams, but many of these people said they thought sweets or dairy made their dreams more disturbing or bizarre.

When the authors compared reports of food intolerances to reports of bad dreams and poor sleep, they found that lactose intolerance was associated with gastrointestinal symptoms, nightmares, and low sleep quality. It’s possible that eating dairy activates gastrointestinal disturbance, and the resulting discomfort affects people’s dreams and the quality of their rest.

Gut Discomfort Hijacks REM

“Nightmares are worse for lactose-intolerant people who suffer severe gastrointestinal symptoms and whose sleep is disrupted,” said Nielsen. “This makes sense, because we know that other bodily sensations can affect dreaming. Nightmares can be very disruptive, especially if they occur often, because they tend to awaken people from sleep in a dysphoric state. They might also produce sleep avoidance behaviors. Both symptoms can rob you of restful sleep.”

This could also explain why fewer participants reported a link between their food and their dreams than in a previous study by Nielsen and his colleague, Dr. Russell Powell of MacEwan University, conducted eleven years earlier on a similar population. Improved awareness of food intolerances could mean that the students in the present study ate fewer foods likely to activate their intolerances and affect their sleep. If this is the case, then simple dietary interventions could potentially help people improve their sleep and overall health.

Unraveling Diet–Dream Mysteries

However, besides the robust link between lactose intolerance and nightmares, it’s not clear how the relationship between sleep and diet works. It’s possible that people sleep less well because they eat less well, but it’s also possible that people don’t eat well because they don’t sleep well, or that another factor influences both sleep and diet. Further research will be needed to confirm these links and identify the underlying mechanisms.

“We need to study more people of different ages, from different walks of life, and with different dietary habits to determine if our results are truly generalizable to the larger population,” said Nielsen. “Experimental studies are also needed to determine if people can truly detect the effects of specific foods on dreams. We would like to run a study in which we ask people to ingest cheese products versus some control food before sleep to see if this alters their sleep or dreams.”

The Life of Earth

https://chuckincardinal.blogspot.com/

Oldest and most complete ancient Egyptian human genome ever sequenced reveals ties to Mesopotamia

By P. Thaler published July 2, 2025

https://www.livescience.com/archaeology/ancient-egyptians/oldest-and-most-complete-ancient-egyptian-human-genome-ever-sequenced-reveals-ties-to-mesopotamia

Rock-cut tombs housed the burial of an Egyptian man who lived during the Old Kingdom nearly 5,000 years ago.

 (Image credit: Garstang Museum of Archaeology, University of Liverpool)

Scientists have sequenced the oldest and most complete genome from ancient Egypt — and the DNA reveals that a man who lived 5,000 years ago had roots in both Mesopotamia and North Africa, a new study finds.

The man — who lived during the Old Kingdom in the third millennium B.C., just a few centuries after Upper and Lower Egypt unified into one empire — provides researchers with a rare glimpse into the genetic roots of ancient Egyptians.

The individual's body was first recovered from a tomb in Nuwayrat, in Upper Egypt, in 1902 and now reveals new information about the genetic makeup of early Egyptians. Prior to this analysis, only three ancient Egyptian genomes had been sequenced, and all were partial.

"I was very surprised" by the success of the sequencing, study co-author Pontus Skoglund, who studies ancient DNA at The Francis Crick Institute in the U.K., said at a news conference Tuesday (July 1), before the paper's publication. "It was a long shot that it would work, as it is with many of these individuals."

An old potter

Radiocarbon dating found that the man had lived around 2855 to 2570 B.C., during the Old Kingdom, a period known for its stability, innovation, and the construction of the step pyramid and the Great Pyramid of Giza, according to a statement.

He was buried in a ceramic pot within a rock-cut tomb and was preserved well enough that two DNA extracts from the roots of his teeth could be sequenced. Researchers compared his genome against a library of thousands of known DNA samples.

Eventually, they found that most of the man's genome could be traced to North African Neolithic ancestry, according to the study, which was published in the journal Nature Wednesday (July 2). About 20% of his DNA was linked to the eastern Fertile Crescent, including ancient Mesopotamia and its neighboring regions.

(Image credit: Garstang Museum of Archaeology, University of Liverpool)

The facial reconstruction of the Egyptian man whose genome can be traced to ancient Mesopotamia.

(Image credit: Garstang Museum of Archaeology, University of Liverpool)
Remains were buried in a pottery coffin in Nuwayrat, in Upper Egypt, in 1902.

(Image credit: Morez, A. (2025). Nature.)

Scientists analyzed the genome of an ancient individual found in Nuwayrat (red dot), about 165 miles (265 kilometers) south of Cairo. It's rare to find preserved human DNA from ancient Egypt, but another individual's DNA from Abusir el-Meleq (purple diamond) from the Third Intermediate Period (circa 1070 to 713 B.C.) was previously sequenced.

This body was uniquely well preserved compared with those of other ancient Egyptians, which often degrade due to the high temperatures of the region. "The pot burial, in combination with the rock-cut tomb into which the pot burial was placed, provided a stable environment" that likely helped preserve the DNA, study co-author Linus Girdland-Flink, an archaeologist at the University of Aberdeen in the U.K., explained at the news conference.

The man's remains provide clues about his life in ancient Egypt nearly 5,000 years ago. He lived to between 44 and 64 years old, which would have been considered an advanced age for his time. The high degree of osteoporosis and arthritis suggests he was on the higher end of that age bracket, study co-author Joel Irish, a bioarchaeologist at Liverpool John Moores University in the U.K., said at the conference.

The man's ceramic-pot burial and rock tomb point to an elevated social status, which contrasts with the many signs of hard physical labor on his remains. Irish found evidence that the man had held his hands out and sat for extended periods of time — a clue that he may have been a potter.

Ancient Egypt's genetic roots

Because most of the man's genetic ancestry is linked to North Africa, it's likely that "at least part of the Egyptian population mainly emerged from local population," study first author Adeline Morez Jacobs, a biological anthropologist at the University of Padua in Italy, said at the conference.

More notably, the link to Mesopotamia "was quite interesting because we actually know from archaeology that the Egyptian and the eastern Fertile Crescent cultures influenced each other for millennia," she said. It was already known that the groups shared goods, domesticated plants and animals, writing systems and farming practices, but this genome is evidence that the populations intermixed more deeply.

However, Morez Jacobs cautioned that this man's DNA may not represent the broader Egyptian population of his time. "We need to remember, this is a single individual," she said. "We didn't capture the full diversity of the population."

The birth of modern Man

https://chuckincardinal.blogspot.com/

An Entire Civilization Might Be Buried Under the Sahara

Michael Button, July 1, 2025

https://www.youtube.com/watch?v=j6jkBmRBR7U

For nearly 9,000 years, the Sahara had one of the most stable and hospitable climates on Earth. It may have been one of the best places to live on the entire planet. 

We think of the Sahara as a vast, lifeless desert — a sea of sand stretching from horizon to horizon. But not too long ago, it was the exact opposite. The Sahara was green. Lush. Alive. 

Despite its vast size, over 9 million square kilometers, only a tiny fraction of it has been archaeologically surveyed, let alone excavated. Some estimates suggest that less than 1% of the Sahara has been properly explored using modern archaeological methods. So isn’t it at least plausible that we’re missing something? That perhaps an entire civilisation — or even multiple civilisations — once thrived here, only to be erased by time and sand?

 If an advanced culture did once exist here, climate collapse could have buried its remains under dunes that stretch for hundreds of miles. Stone structures, cities, even inscriptions—preserved, but hidden.

https://www.youtube.com/watch?v=j6jkBmRBR7U

The birth of modern Man

https://chuckincardinal.blogspot.com/

Microbe 'Flavors' Tell Octopuses Which Babies Deserve Their Care

02 July 2025, By J. COCKERILL

https://www.sciencealert.com/microbe-flavors-tell-octopuses-which-babies-deserve-their-care

A two-spot octopus broods its eggs off Anacapa Island in California.

 (Douglas Klug/Getty Images)

Octopuses can taste with their arms, and a new study reveals that specifically, they're tasting chemical cues from microbes that grow on the surface of objects like dead crabs and living octopus eggs. These 'flavors', it turns out, can signal which prey is worth pursuing, or which egg isn't going to make it.

Octopus arms bristle with neurons that inform these fascinating animals' behaviors, sometimes even independently of their brains. Sensory receptors in their arms enable them to 'taste by touch', which is essential to how they decide what to nurture, what to hunt, and what isn't worth their time.

That's important information for these opportunistic hunters, who forage mainly at night and in shadowy crevices.

"If a microbial strain could activate a receptor, then it could generate a neural signal that tells the octopus: This is something I care about," says Harvard University biochemist Rebecka Sepela, who led the research.

"The microbiome is acting almost like a chemical translator. It integrates environmental signals – like changes in temperature or nutrient levels – and outputs molecules that inform the octopus how to behave."

Proving this to be the case was an ambitious mission. The team isolated 295 different strains of bacteria from 'biologically meaningful' surfaces in the natural environments of wild-caught California two-spot octopuses (Octopus bimaculoides). Those meaningful surfaces included food and family: the shells of fiddler crabs (Leptuca pugilator), and egg casings of the octopus's own offspring.

A) A two-spot octopus alongside the two 'biologically meaningful' surfaces of its life: crab (food) and egg cases (offspring).

 B) Scanning electron microscope images of the bacteria on each surface. 

C) Bacterial composition of each surface, by phylum. 

(Sepela et al., Cell, 2025)

"Those microbes produce molecules that allow the octopus to tell the difference," Sepela says. "Microbes are chemical factories. They constantly take in environmental cues and produce molecules that reflect their surroundings."

The shells of living crabs, for instance, are surprisingly sterile, while those of decaying crabs are quickly colonized by a dense tapestry of bacteria.

Octopus egg casings tended to by a mother octopus have a curated balance of microbes, but when discarded, this is thrown off by an overgrowth of spiral-shaped bacteria.

The screening – in which Sepela's team painstakingly tested how octopus sensory receptors reacted to each of the nearly 300 strains – revealed that just a few of these microbes, found on decaying prey or unhealthy eggs, activated the octopuses' receptors.

Octopuses can 'taste' their environment through touch, enabling them to sense bacterial signals.

 (Sepela et al., Cell, 2025)

To test these signals in action, octopuses who were actively brooding a clutch of eggs were given a collection of egg mimics, some marred with the spiral bacteria. The octopuses tended to these false eggs for a while, except for those bacterially marked as 'bad eggs', which were quickly discarded.

The researchers were even able to identify which specific molecules the octopuses responded to. This chemical 'language' is enabled by molecules that, despite the submarine environment, are not readily washed away from the surface on which they are formed.

While the research focuses on octopuses, Sepela and her colleagues believe this sort of chemical signaling may apply to many other kinds of microbiomes; even our own.

"This might seem like a very specific case… but what we're seeing is actually a general rule about how organisms sense microbiomes," says Harvard cell physiologist Nicholas Bellono.

"Across life, evolution, and organ systems, microbes are essential – and this study shows another example of how deeply they influence physiology and behavior."

The Life of Earth

https://chuckincardinal.blogspot.com/

They Just Discovered A New Type Of Orca… And It’s Unlike Anything Ever Seen

Incredible Stories, July 1, 2025

https://www.youtube.com/watch?v=tp1InhD_JS8

We thought we knew orcas—majestic, intelligent, apex predators of the sea. But it turns out, we were only scratching the surface. 

Scientists have just discovered a new type of orca, and it’s unlike anything ever seen before. This isn’t just a behavioral quirk or a rare variation—it’s a discovery that could rewrite the species map entirely.

 What if the ocean’s most iconic predator has been hiding a secret evolution in plain sight? Let’s dive in, because the truth about these orcas is stranger—and more thrilling—than fiction.

https://www.youtube.com/watch?v=tp1InhD_JS8

The Life of Earth

https://chuckincardinal.blogspot.com/

Bold Plan to DNA Test All Babies in UK Poses Serious Risks, Experts Warn

01 July 2025, By L. STROPPA & E. WILSON, THE CONVERSATION

https://www.sciencealert.com/bold-plan-to-dna-test-all-babies-in-uk-poses-serious-risks-experts-warn

The current heel-prick test checks for nine rare genetic conditions. 

(Petri Oeschger/Getty Images)

By 2030, every baby born in the UK could have their entire genome sequenced under a new NHS initiative to "predict and prevent illness". This would dramatically expand the current heel-prick test, which checks for nine rare genetic conditions, into a far more extensive screen of hundreds of potential risks.

On the surface, the idea sounds like an obvious win for public health: spot problems early, intervene sooner and save lives. But genetic testing on this scale carries real risks, especially if the results are misunderstood or poorly communicated.

The new plan builds on a recent NHS pilot study that sequenced the genomes of 100,000 newborns in England to identify more than 200 genetic conditions. However, these tests don't provide clear cut answers. They don't offer a diagnosis or certainty, just an estimate of risk.

A genetic result might suggest a child has a higher (or lower) probability of developing a certain disease later in life. But risk is not prediction. If parents, or even clinicians, misinterpret that nuance, the consequences could be serious.

Some families may come to see a child flagged as "at risk" as a patient-in-waiting. In extreme cases, they may treat a probability as a certainty; assuming, for instance, that a child "has the gene" and will inevitably become ill. That assumption could reshape how children are raised, how they're treated and how they could see themselves.

https://www.youtube.com/watch?v=KnqPJHOW3yI

Alarming language

This isn't speculation. Research shows that while some people understand risk scores accurately, many struggle with statistical information.

Words like "high risk" or "likely" are interpreted differently by different people and often more seriously than intended. Even trained doctors can overestimate what a positive test result means. When it comes to genomics, the line between "you might get sick" and "you will get sick" can blur quickly.

UK policymakers haven't helped this confusion. Government messaging refers to "diagnosis before symptoms even occur" and "leapfrogging disease." But this language overpromises what genomic data can do and downplays its uncertainty.

When testing is indiscriminate and communication unclear, the fallout can be wide ranging. Children identified as "high risk" may undergo years of monitoring, unnecessary medical appointments, or even treatment for diseases they never develop.

In some cases, this leads to physical harms, from unnecessary medications to procedures with side effects. In others, the damage is psychological: shaping a child's identity around an anticipated future of illness. These psychological effects can be lasting. Being told you're likely to develop a condition like dementia may influence how a person plans their life, even if that illness never materialises.

https://www.youtube.com/watch?v=O7iMttNVQfQ&t=1s

False positives

There are also broader issues with applying this kind of screening to everyone. Risk based testing works best when it's targeted; for example, among those with symptoms or a strong family history.

But in the general population, where most people are healthy, false positives can far outnumber accurate results. Even well designed tests can produce misleading outcomes when applied at scale.

This is a well-known statistical effect, discussed during the COVID pandemic. In populations where a disease is rare, even highly accurate tests produce more false positives than true ones. If DNA screening is rolled out universally, many families will be told their child is at risk when they are not.

These false positives can lead to a cascade of further tests, stress and unnecessary clinical interventions; all of which consume time and resources and may cause real harm.

This issue already affects adult testing. For example, Alzheimer's tests that measure early changes in the brain work well in memory clinics, where patients already show symptoms. But when these same tests are used on the general population, where most people are healthy, they produce false positives in up to two-thirds of cases.

If genetic screening in newborns is rolled out in the same way, it could lead to similar problems: mislabelling healthy children as sick, and causing unnecessary worry and follow-up tests.

So what's the solution? It's not to abandon genetic testing altogether – far from it. When used carefully, genomic data can offer real benefits, particularly for patients with symptoms or in research settings. But if we're going to roll this out to every newborn, the surrounding infrastructure needs to be robust.

That includes:  Clear, consistent communication: Risk scores must be explained in ways that emphasise uncertainty, not oversold as definitive predictions.

Support for parents:   For consent to be truly informed, parents need help understanding that a genetic flag is not a diagnosis – and that many people with elevated risk never go on to develop the condition.

Training for clinicians:   Many doctors still lack the tools to interpret and explain genetic information accurately and responsibly.

A national network of genetic counsellors are essential for supporting families through testing and interpretation. But current numbers in the UK fall far short of what universal newborn screening would require.

Genomic data holds great promise. But using it as a blanket tool for all newborns demands caution, clarity, and investment in communication and care. Without these safeguards, we risk turning healthy babies into patients-in-waiting.

The birth of modern Man

https://chuckincardinal.blogspot.com/

Alzheimer's Might Not Actually Be a Brain Disease, Says Expert

01 July 2025, By D. WEAVER, THE CONVERSATION

https://www.sciencealert.com/alzheimers-might-not-actually-be-a-brain-disease-says-expert

(Westend61/Getty Images)

The pursuit of a cure for Alzheimer's disease is becoming an increasingly competitive and contentious quest with recent years witnessing several important controversies.

In July 2022, Science magazine reported that a key 2006 research paper, published in the prestigious journal Nature, which identified a subtype of brain protein called beta-amyloid as the cause of Alzheimer's, may have been based on fabricated data.

One year earlier, in June 2021, the US Food and Drug Administration had approved aducanumab, an antibody-targeting beta-amyloid, as a treatment for Alzheimer's, even though the data supporting its use were incomplete and contradictory.

Some physicians believe aducanumab never should have been approved, while others maintain it should be given a chance.

With millions of people needing an effective treatment, why are researchers still fumbling in this quest for a cure for what is arguably one of the most important diseases confronting humankind?

Illustration of beta-amyloid plaques (yellow) amongst neurons. 

(Science Photo Library/Canva)

Escaping the beta-amyloid rut

For years, scientists have been focused on trying to come up with new treatments for Alzheimer's by preventing the formation of brain-damaging clumps of this mysterious protein called beta-amyloid.

In fact, we scientists have arguably got ourselves into a bit of an intellectual rut concentrating almost exclusively on this approach, often neglecting or even ignoring other possible explanations.

Regrettably, this dedication to studying the abnormal protein clumps has not translated into a useful drug or therapy. The need for a new "out-of-the-clump" way of thinking about Alzheimer's is emerging as a top priority in brain science.

My laboratory at the Krembil Brain Institute, part of the University Health Network in Toronto, is devising a new theory of Alzheimer's disease.

Based on our past 30 years of research, we no longer think of Alzheimer's as primarily a disease of the brain. Rather, we believe that Alzheimer's is principally a disorder of the immune system within the brain.

The immune system, found in every organ in the body, is a collection of cells and molecules that work in harmony to help repair injuries and protect from foreign invaders.

When a person trips and falls, the immune system helps to mend the damaged tissues. When someone experiences a viral or bacterial infection, the immune system helps in the fight against these microbial invaders.

The exact same processes are present in the brain. When there is head trauma, the brain's immune system kicks into gear to help repair. When bacteria are present in the brain, the immune system is there to fight back.

White blood cells of the immune system activated to fight a bacterial infection. Green shows expression of molecules in their surfaces, and orange shows synthesis of molecules inside the cells.

 (Dlumen/Canva)

Alzheimer's as autoimmune disease

We believe that beta-amyloid is not an abnormally produced protein, but rather is a normally occurring molecule that is part of the brain's immune system. It is supposed to be there.

When brain trauma occurs or when bacteria are present in the brain, beta-amyloid is a key contributor to the brain's comprehensive immune response. And this is where the problem begins.

Because of striking similarities between the fat molecules that make up both the membranes of bacteria and the membranes of brain cells, beta-amyloid cannot tell the difference between invading bacteria and host brain cells, and mistakenly attacks the very brain cells it is supposed to be protecting.

This leads to a chronic, progressive loss of brain cell function, which ultimately culminates in dementia – all because our body's immune system cannot differentiate between bacteria and brain cells.

When regarded as a misdirected attack by the brain's immune system on the very organ it is supposed to be defending, Alzheimer's disease emerges as an autoimmune disease.

There are many types of autoimmune diseases, such as rheumatoid arthritis, in which autoantibodies play a crucial role in the development of the disease, and for which steroid-based therapies can be effective. But these therapies will not work against Alzheimer's disease.

The brain is a very special and distinctive organ, recognized as the most complex structure in the Universe.

Alzheimer's is arguably one of the most important diseases confronting humankind. 

(Robert Kneschke/Canva)



In our model of Alzheimer's, beta-amyloid helps to protect and bolster our immune system, but unfortunately, it also plays a central role in the autoimmune process that, we believe, may lead to the development of Alzheimer's.

Though drugs conventionally used in the treatment of autoimmune diseases may not work against Alzheimer's, we strongly believe that targeting other immune-regulating pathways in the brain will lead us to new and effective treatment approaches for the disease.

Other theories of the disease

In addition to this autoimmune theory of Alzheimer's, many other new and varied theories are beginning to appear. For example, some scientists believe that Alzheimer's is a disease of tiny cellular structures called mitochondria – the energy factories in every brain cell.

Mitochondria convert oxygen from the air we breathe and glucose from the food we eat into the energy required for remembering and thinking.

Some maintain that it is the end-result of a particular brain infection, with bacteria from the mouth often being suggested as the culprit. Still others suggest that the disease may arise from an abnormal handling of metals within the brain, possibly zinc, copper, or iron.

It is gratifying to see new thinking about this age-old disease. Dementia currently affects more than 50 million people worldwide, with a new diagnosis being made every three seconds.

Often, people living with Alzheimer's disease are unable to recognize their own children or even their spouse of more than 50 years.

Alzheimer's is a public health crisis in need of innovative ideas and fresh directions.

Often, people living with Alzheimer's disease are unable to recognize their own children.

 (akurtz/Canva)



For the well-being of the people and families living with dementia, and for the socioeconomic impact on our already stressed health-care system coping with the ever-escalating costs and demands of dementia, we need a better understanding of Alzheimer's, its causes, and what we can do to treat it and to help the people and families who are living with it.

The birth of modern Man

https://chuckincardinal.blogspot.com/

Scientists discover never-before-seen part of human cells — and it looks like a snowman wearing a scarf

By Christoph Schwaiger published June 30, 2025

https://www.livescience.com/health/scientists-discover-never-before-seen-part-of-human-cells-and-it-looks-like-a-snowman-wearing-a-scarf

The green and orange structures in this image are hemifusomes, newly discovered organelles that may represent a previously unrecognized pathway for recycling in human cells. 

(Image credit: Courtesy UVA Health)

Scientists say they captured 3D images of a new organelle they're calling a "hemifusome," which may be a recycling center in human cells.

A new organelle has been discovered in human cells — and scientists call it a "hemifusome."

Like the full-size organs in our bodies, the organelles within cells are specialized structures that carry out specific functions. While observing filaments that maintain the shape of cells, Seham Ebrahim, an assistant professor at the University of Virginia, and her team noticed a new structure that was consistently appearing in the 3D images they were making.

What at first seemed like an artifact in the images turned out to be a new organelle that may be involved in sorting, recycling and discarding proteins within human cells. Ebrahim likened the hemifusome's shape to that of a snowman wearing a scarf; picture a small head attached to a larger body, with a thin border separating the two ends.

The organelle is around 100 nanometers in diameter, less than half the size of even a small mitochondrion, the famous powerhouse of the cell.

The scientists were able to observe the hemifusomes because they used a method called cryo-electron tomography (cryo-ET) to generate their images. This technique involved rapidly freezing cells from four lab-raised cell lines to preserve as much of their structures as possible, making it possible to create clear, 3D images.

"It's like a snapshot in time without any kind of chemical or any kind of stain," Ebrahim told Live Science. Using this imaging technique, they could look inside cells in a "very native state," as if they were glass balls, she said.

In their paper, published in the journal Nature Communications in May, the researchers wrote that the harsh processing steps that other imaging techniques subject cells to likely prevented hemifusomes from being observed earlier. In addition, with other techniques that use imaging to study the traffic unfolding in a living cell, the organelle was probably too small to be seen, appearing at most as a blur, Ebrahim added.

Ebrahim and her colleagues were looking at a configuration of vesicles they had never observed before. Vesicles are balloon-like structures used to transport things like proteins and hormones within and between cells. The new study revealed two vesicles fused together with a two-layer barrier of fat between them.

"Even from a biophysics perspective, it's a breakthrough," Ebrahim said, "because biophysically, people have always predicted, or theorized, that vesicles can exist in this hemifused state … but this was the first time that it has actually been seen in a living cell." This observation inspired the name hemifusome, since hemifusion refers to the partial merger of two bilayers.

This cryo-electron tomography image (left) 

and two corresponding schematics (center and right) highlight the distinctive structure of a hemifusome, where two vesicle membranes connect through a hemifusion diaphragm. 

(Image credit: Courtesy UVA Health)

Ebrahim argues that hemifusomes can be classified as organelles because they are self-contained functional units within a cell, as opposed to "fleeting" structures that temporarily appear as membranes form and split. In the paper, she wrote that it's unlikely hemifusomes are artifacts of cryo-ET.

Ebrahim's findings "suggest that the hemifusomes they visualize are genuine cellular intermediates, not freezing-induced distortions," said Yi-Wei Chang, an assistant professor of biochemistry and biophysics at the University of Pennsylvania Perelman School of Medicine who was not involved in the work.

Once the role and function of hemifusomes have been confirmed through further studies, they may be recognized as their own class of intermediate structures that fulfill part of fusion processes in mammalian cells, Chang told Live Science in an email.

With their current work, the researchers can confirm that the hemifusome exists, but they have yet to determine the organelle's exact role, its life cycle or its composition. Ebrahim hypothesizes that hemifusomes are precursors to certain types of vesicles. She believes hemifusomes may play a crucial role in the recycling or disposal of cellular membranes, which is important for preventing the buildup of stuff in cells that could gum up their operations if allowed to accumulate.

The researchers wrote that understanding more about how hemifusomes work could also unlock new insight into how diseases such as Alzheimer's manifest. Alzheimer's disease is linked to the improper clearance of abnormal protein plaques in the brain, which leads to buildup over time.

"Without cryo-electron tomography, we would have missed this discovery," Ebrahim said, adding that "there's probably a whole world out there that we still have to find."

The Life of Earth

https://chuckincardinal.blogspot.com/

Your Cell's Powerhouses Are Secretly Helping Fight Bacteria, Study Finds

27 June 2025, By A. MONTEITH, THE CONVERSATION

https://www.sciencealert.com/your-cells-powerhouses-are-secretly-helping-fight-bacteria-study-finds

Mitochondria (red) are organelles found in most cells.

 (U. Manor, NICHD/Flickr/CC BY 2.0)

Mitochondria have primarily been known as the energy-producing components of cells.

But scientists are increasingly discovering that these small organelles do much more than just power cells. They are also involved in immune functions such as controlling inflammation, regulating cell death and responding to infections.

Research from my colleagues and I revealed that mitochondria play another key role in your immune response: sensing bacterial activity and helping neutrophils, a type of white blood cell, trap and kill them.

For the past 16 years, my research has focused on understanding the decisions immune cells make during infection and how the breakdown of these decision-making processes cause disease.

My lab's recent findings shed light on why people with autoimmune diseases such as lupus may struggle to fight infections, revealing a potential link between dysfunctional mitochondria and weakened immune defenses.

The immune system's secret weapons

Neutrophils are the most abundant type of immune cell and serve as the immune system's first responders. One of their key defense mechanisms is releasing neutrophil extracellular traps, or NETs – weblike structures composed of DNA and antimicrobial proteins.

These sticky NETs trap and neutralize invading microbes, preventing their spread in the body.

Neutrophils (yellow) eject a NET (green) to ensnare bacteria (purple). Other cells, such as red blood cells (orange), may also get trapped.

 (CHDENK/Wikimedia Commons, CC BY-SA)



Until recently, scientists believed that NET formation was primarily triggered by cellular stress and damage. However, our study found that mitochondria can detect a specific bacterial byproduct – lactate – and use that signal to initiate NET formation.

Lactate is commonly associated with muscle fatigue in people. But in the context of bacterial infections, it plays a different role. Many bacteria release lactate as part of their own energy production.

My team found that once bacteria are engulfed by a compartment of the cell called the phagosome, neutrophils can sense the presence of this lactate.

Mitochondria do so much more than just produce energy. 

(OpenStax, CC BY-SA)

Inside the phagosome, this lactate communicates to the neutrophil that bacteria are present and that the antibacterial processes are not sufficient to kill these pathogens.

When the mitochondria in neutrophil cells detect this lactate, they start signaling for the cell to get rid of the NETs that have entrapped bacteria. Once the bacteria are released outside the cell, other immune cells can kill them.

When we blocked the mitochondria's ability to sense lactate, neutrophils failed to produce NETs effectively. This meant bacteria were more likely to escape capture and proliferate, showing how crucial this mechanism is to immune defense. This process highlights an intricate dialogue between the bacteria's metabolism and the host cell's energy machinery.

Here, a neutrophil engulfs MRSA bacteria (green).

What makes this finding surprising is that the mitochondria within cells are able to detect bacteria trapped in phagosomes, even though the microbes are enclosed in a separate space. Somehow, mitochondrial sensors can pick up cues from within these compartments – an impressive feat of cellular coordination.

Targeting mitochondria to fight infections

Our study is part of a growing field called immunometabolism, which explores how metabolism and immune function are deeply intertwined. Rather than viewing cellular metabolism as strictly a means to generate energy, researchers are now recognizing it as a central driver of immune decisions.

Mitochondria sit at the heart of this interaction. Their ability to sense, respond to and even shape the metabolic environment of a cell gives them a critical role in determining how and when immune responses are deployed.

For example, our findings provide a key reason why patients with a chronic autoimmune disease called systemic lupus erythematosus often suffer from recurrent infections.

Mitochondria in the neutrophils of lupus patients fail to sense bacterial lactate properly. As a result, NET production was significantly reduced. This mitochondrial dysfunction could explain why lupus patients are more vulnerable to bacterial infections – even though their immune systems are constantly activated due to the disease.

This observation points to mitochondria's central role in balancing immune responses. It connects two seemingly unrelated issues: immune overactivity, as seen in lupus, and immune weakness like increased susceptibility to infection.

When mitochondria work correctly, they help neutrophils mount an effective, targeted attack on bacteria. But when mitochondria are impaired, this system breaks down.

Neutrophils unable to effectively produce NETs may contribute to the development of lupus.
(Luz Blanco/National Institute of Arthritis and Musculoskeletal and Skin Diseases via Flickr, CC BY-NC-SA)



Our discovery that mitochondria can sense bacterial lactate to trigger NET formation opens up new possibilities for treating infections. For instance, drugs that enhance mitochondrial sensing could boost NET production in people with weakened immune systems.

On the flip side, for conditions where NETs contribute to tissue damage – such as in severe COVID-19 or autoimmune diseases – it might be beneficial to limit this response.

Additionally, our study raises the question of whether other immune cells use similar mechanisms to sense microbial metabolites, and whether other bacterial byproducts might serve as immune signals.

Understanding these pathways in more detail could lead to new treatments that modulate immune responses more precisely, reducing collateral damage while preserving antimicrobial defenses.

Mitochondria are not just the powerhouses of the cell – they are the immune system's watchtowers, alert to even the faintest metabolic signals of bacterial invaders.

As researchers' understanding of their roles expands, so too does our appreciation for the complexity – and adaptability – of our cellular defenses.

The Life of Earth

https://chuckincardinal.blogspot.com/

Ruins of Ancient Temple Belonged to Mysterious Pre-Inca Civilization

30 June 2025, By J. COCKERILL

https://www.sciencealert.com/ruins-of-ancient-temple-belonged-to-mysterious-pre-inca-civilization

A digital reconstruction of the ancient temple. 

(José Capriles/Penn State/CC BY-NC-ND 4.0)

Before the rise of the Incas, a civilization known as Tiwakanu ruled the Andes, and archaeologists have uncovered a massive temple left behind by this enigmatic society.

Named Palaspata by local Indigenous farmers, the ruined temple is perched on a Bolivian hilltop 215 km (about 134 miles) southeast of the center of the Tiwanaku archaeological site.

The team behind the discovery, led by Jose Capriles from Penn State University, suspects the newly described temple was an important strategic site for the Tiwanaku people, as it's located at the nexus of three main trade routes that connected the society to important ecosystem resources.

There's debate around what brought this civilization's downfall, but we know it was a complex culture built on cosmological religion, politics, and an agropastoral economy that emerged around 110 CE.

"Their society collapsed sometime around 1000 CE and was a ruin by the time the Incas conquered the Andes in the 15th century," Capriles says.

"Remnants of architectural monuments like pyramids, terraced temples, and monoliths [are mostly] distributed in sites around Lake Titicaca and, while we know Tiwanaku's control and influence extended much further, scholars debate how much actual control over distant places it had."

Layers of data enabled the team to create this digital reconstruction of the temple.

(José Capriles/Penn State/CC BY-NC-ND 4.0)




With drone images and photogrammetry, the team built a detailed 3D rendering of the temple's structure and topography.

"Because the features are very faint, we blended various satellite images together," Capriles says.

What remains of the temple indicates a complex measuring 125 by 145 meters (410 by 475 feet), with 15 enclosed areas arranged around a central inner courtyard.

This design is typical of Tiwanaku culture, which left behind many other temple ruins featuring sunken courts surrounded by rectangular rooms and stone-lined terrace platforms, mostly around the southern end of Lake Titicaca.

"The modules range in size between 358 and 595 m2 [3,853–6,405 ft²] and could have contained additional rooms and divisions," Capriles and team report.

"The main entrance of the temple faces west in alignment with the solar equinox. Currently, a local trail crosses the building, intersecting its western and northern walls."

The temple is littered with fragments of its inhabitants' lives, including pieces of ceramic keru cups, flared bowls, jars, and incense burners.

Fragments of keru cups – used for drinking chicha, a traditional maize beer, during agricultural feasts and celebrations – suggest the temple was used as a central hub for trade. 

(José Capriles/Penn State/CC BY-NC-ND 4.0)



"[Objects] with Tiwanaku iconography are common, but some sherds of Yampara, Tupuraya, Mojocoya, and other decorative styles are also present and suggest interaction with the inter-Andean valleys," the team writes.

They also found a few fragments of black-on-red Carangas pottery, pieces of camel bone, and some fragments of turquoise stone along with an Oliva peruviana seashell – evidence of connections to the Atacama Desert and the Pacific Ocean.

Religion played an important role in the politics and economics of Tiwanaku society, and in the Andes, sites like this were often built not only for spiritual practice, but also as a means of expanding societies and exerting control over the surrounding resources.

As one of the only terraced platform sites found beyond the lake basin, and one of the farthest from it, Palaspata would have connected Tiwanaku with the Central Altiplano and the inter-Andean valleys of Cochabamba.

Map showing archaeological sites associated with Tiwanaku occupations.

 (Capriles et al., Antiquity, 2025)

"Most economic and political transactions had to be mediated through divinity, because that would be a common language that would facilitate various individuals cooperating," says Capriles.

"With more insight into the past of this ancient site, we get a window into how people managed cooperation, and how we can materially see evidence of political and economic control."

The birth of modern Man

https://chuckincardinal.blogspot.com/

Scientists Uncover New Concerns About Billion-Dollar Heart Drug

BY BMJ GROUP, JUNE 29, 2025

https://scitechdaily.com/scientists-uncover-new-concerns-about-billion-dollar-heart-drug/

New findings suggest serious data issues behind a major heart drug’s approval, reigniting concern over its decade-long use.

 Credit: Stock

An investigation has uncovered evidence of significant misreporting, raising new concerns about the approval and long-term use of ticagrelor over the past decade.

In a follow-up investigation into the multibillion-dollar drug ticagrelor, The BMJ has identified new concerns, this time focusing on key platelet studies that supported the drug’s approval by the FDA.

For over ten years, ticagrelor (sold as Brilinta in the US and Brilique in Europe) has been recommended for patients with acute coronary syndrome, a group of conditions involving a sudden reduction in blood flow to the heart.

In December, The BMJ reported serious issues with data integrity in the landmark PLATO clinical trial, which played a central role in ticagrelor’s global approval. The findings raised doubts about the drug’s claimed benefits over less expensive alternatives.

Concerns resurface as generics enter the market

Now, with generic versions of the drug expected to launch this year, The BMJ has broadened its investigation to examine two key platelet studies that AstraZeneca cited as evidence of ticagrelor’s effectiveness in treating acute coronary syndrome.

It finds that the “primary endpoint” results (the trial’s key measurement) for both clinical trials were inaccurately reported in the leading cardiology journal Circulation, and reveals that more than 60 of 282 readings from platelet machines used in the trials were not present in US Food and Drug Administration (FDA) datasets.

What’s more, one active trial investigator never became a study author, while one author told The BMJ he was not involved in the trial, and most investigators, including the principal investigator, were unreachable or declined to be interviewed.

Expert criticism and lack of transparency

Victor Serebruany, an adjunct faculty member at Johns Hopkins University and ticagrelor’s most renowned critic, told The BMJ that “there are episodes of skyrocketing rebound and profound platelet inhibition after ticagrelor making patients prone to thrombosis or bleeding. If doctors had known what happened in these trials, they would never have started using ticagrelor.”

Circulation and AstraZeneca did not respond to a request for comment.

Serebruany added: “It’s been obvious for years that there is something wrong with the data. That the FDA’s leadership could look past all these problems—on top of the many problems their own reviewers identified and are now being discovered by The BMJ—is unconscionable. We all need to know how and why that happened.”

The birth of modern Man

https://chuckincardinal.blogspot.com/