Brains & Aging - Alzheimer's & ALS Genes - Eavesdropping Curlews - Tasting Bacteria

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Jun 18, 2025, 6:59:39 AMJun 18

https://www.nature.com/articles/d41586-025-01886-3

How your brain controls ageing — and why zombie cells could be key

Diana Kwon

There might be a paradox in the biology of ageing. As humans grow older, their metabolisms tend to slow, they lose muscle mass and they burn many fewer calories. But certain cells in older people appear to do the exact opposite — they consume more energy than when they were young.

These potential energy hogs are senescent cells, older cells that have stopped dividing and no longer perform the essential functions that they used to. Because they seem idle, biologists had assumed that zombie-like senescent cells use less energy than their younger, actively replicating counterparts, says Martin Picard, a psychobiologist at Columbia University in New York City.

But in 2022, Gabriel Sturm, a former graduate student of Picard’s, painstakingly observed the life course of human skin cells cultured in a dish1 and, in findings that have not yet been published in full, found that cells that had stopped dividing had a metabolic rate about double that of younger cells.

For Picard and his colleagues, the energetic mismatch wasn’t a paradox at all: ageing cells accumulate energetically costly forms of damage, such as alterations in DNA, and they initiate pro-inflammatory signalling. How that corresponds with the relatively low energy expenditure for ageing organisms is still unclear, but the researchers hypothesize that this tension might be an important driver of many of the negative effects of growing old, and that the brain might be playing a key part as mediator2. As some cells get older and require more energy, the brain reacts by stripping resources from other biological processes, which ultimately results in outward signs of ageing, such as greying hair or a reduction in muscle mass (see ‘Energy management and ageing’).

Picard and his colleagues call this concept the ‘brain–body energy-conservation model’. And although many parts of the hypothesis are still untested, scientists are working to decipher the precise mechanisms that connect the brain to processes associated with ageing, such as senescence, inflammation and the shortening of telomeres — the stretches of repetitive DNA that cap the ends of chromosomes and protect them.

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https://www.thetransmitter.org/alzheimers-disease/everything-everywhere-all-at-once-inside-the-chaos-of-alzheimers-disease/

Everything, everywhere, all at once: Inside the chaos of Alzheimer’s disease

By Michael A. Yassa

For nearly three decades, Alzheimer’s disease has been framed as a story about amyloid: A toxic protein builds up, forms plaques, kills neurons and slowly robs people of their memories and identity. The simplicity of this “amyloid cascade hypothesis” gave us targets, tools and a sense of purpose. It felt like a clean story. Almost too clean.

We spent decades chasing it, developing dozens of animal models and pouring billions into anti-amyloid therapies, most of which failed. The few that made it to market offer only modest benefits, often with serious side effects. Whenever I think about this, I can’t help but picture Will Ferrell’s Buddy the Elf, in the movie “Elf,” confronting the mall Santa: “You sit on a throne of lies.” Not because anyone meant to mislead people (though maybe some did). But because we wanted so badly for the story to be true.

So what happened? This should have worked … right?

I would argue it was never going to work because we have been thinking about Alzheimer’s the wrong way. For decades, we have treated it as a single disease with a single straight line from amyloid to dementia. But what if that’s not how it works? What if Alzheimer’s only looks like one disease because we keep trying to force it into a single narrative? If that’s the case, then the search for a single cause—and a single cure—was always destined to fail.

”What if Alzheimer’s only looks like one disease because we keep trying to force it into a single narrative? If that’s the case, then the search for a single cause—and a single cure—was always destined to fail.

Real progress, I believe, requires two major shifts in how we think. First, we have to let go of our obsession with amyloid.

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https://knowablemagazine.org/content/article/health-disease/2025/awakened-viral-jumping-genes-role-in-alzheimers-als

How rogue jumping genes can spur Alzheimer’s, ALS

By Amber Dance

Back in 2008, neurovirologist Renée Douville observed something weird in the brains of people who’d died of the movement disorder ALS: virus proteins.

But these people hadn’t caught any known virus.

Instead, ancient genes originally from viruses, and still lurking within these patients’ chromosomes, had awakened and started churning out viral proteins.

Our genomes are littered with scraps of long-lost viruses, the descendants of viral infections often from millions of years ago. Most of these once-foreign DNA bits are a type called retrotransposons; they make up more than 40 percent of the human genome.

Pie chart shows that retrotransposons make up nearly half the human genome.

Our genomes are riddled with DNA from ancient viral infections known as jumping genes. The majority of these are retrotransposons, which copy themselves via RNA intermediates; a smaller portion are cut-and-paste DNA transposons.

Many retrotransposons seem to be harmless, most of the time. But Douville and others are pursuing the possibility that some reawakened retrotransposons may do serious damage: They can degrade nerve cells and fire up inflammation and may underlie some instances of Alzheimer’s disease and ALS (amyotrophic lateral sclerosis, or Lou Gehrig’s disease).

The theory linking retrotransposons to neurodegenerative diseases — conditions in which nerve cells decline or die — is still developing; even its proponents, while optimistic, are cautious. “It’s not yet the consensus view,” says Josh Dubnau, a neurobiologist at the Renaissance School of Medicine at Stony Brook University in New York. And retrotransposons can’t explain all cases of neurodegeneration.

Yet evidence is building that they may underlie some cases. Now, after more than a decade of studying this possibility in human brain tissue, fruit flies and mice, researchers are putting their ideas to the ultimate test: clinical trials in people with ALS, Alzheimer’s and related conditions. These trials, which borrow antiretroviral medications from the HIV pharmacopeia, have yielded preliminary but promising results.

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https://www.nytimes.com/2025/06/14/health/texas-psychedelics-ibogaine-veterans.html

Texas OK’s $50 Million for Ibogaine Research

By Andrew Jacobs

When Gov. Greg Abbott of Texas approved legislation this week to spend $50 million in state money researching ibogaine, a powerful psychedelic, he put the spotlight on a promising, still illegal drug that has shown promise in treating opioid addiction, traumatic brain injury and depression.

Interest in ibogaine therapy has surged in recent years, driven in large part by veterans who have had to travel to other countries for the treatment.

The measure, which passed the Texas Legislature with bipartisan support, seeks to leverage an additional $50 million in private investment to fund clinical trials that supporters hope will provide a pathway for ibogaine therapy to win approval from the Food and Drug Administration, a process that could take years.

The legislation directs the state to work with Texas universities and hospitals and tries to ensure that the state retains a financial stake in any revenue from the drug’s development.

“You can’t put a price on a human life, but if this is successful and ibogaine becomes commercialized, it will help people all across the country and provide an incredible return on investment for the people of Texas,” said State Senator Tan Parker, a Republican who sponsored the bill.

The initiative, one of the largest government investments in psychedelic medicine to date, is a watershed moment for a field that continues to gain mainstream acceptance. Regulated psilocybin clinics have opened in Oregon and Colorado, and ketamine has become widely available across the country as a treatment for depression and anxiety.

There have been speed bumps. Last year, the F.D.A. rejected MDMA-assisted therapy for PTSD, the first psychedelic compound to make it through much of the agency’s rigorous drug review process.

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https://www.theguardian.com/science/2025/jun/12/prairie-dog-calls-curlews-predators

Crafty curlews: birds eavesdrop on prairie dog calls to evade predators

Associated Press

Prairie dogs bark to alert each other to the presence of predators, with different cries depending on whether the threat is airborne or approaching by land.

But their warnings also seem to help a vulnerable grassland bird.

Curlews have figured out that if they eavesdrop on alarms from US prairie dog colonies they may get a jump on predators coming for them, too, according to research published on Thursday in the journal Animal Behavior.

“Prairie dogs are on the menu for just about every predator you can think of – golden eagles, red-tailed hawks, foxes, badgers, even large snakes,” said Andy Boyce, a research ecologist in Montana at the Smithsonian’s National Zoo and Conservation Biology Institute. Such animals also gladly snack on grassland nesting birds such as the long-billed curlew, so the birds have adapted.

Previous research has shown birds frequently eavesdrop on other bird species to glean information about food sources or danger, said Georgetown University ornithologist Emily Williams, who was not involved in the study.

But, so far, scientists have documented only a few instances of birds eavesdropping on mammals.

“That doesn’t necessarily mean it’s rare in the wild,” she said, “it just means we haven’t studied it yet.”

Prairie dogs, a type of ground squirrel, live in large colonies with a series of burrows that may stretch for miles underground, especially on the vast US plains. When they hear each other’s barks, they either stand alert watching or dive into their burrows.

“Those little barks are very loud; they can carry quite a long way,” said research co-author Andrew Dreelin, who also works for the Smithsonian.

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https://www.nytimes.com/2025/06/17/science/octopus-arms-microbiome.html

Eight Arms to Taste Your Microbiome

By Sofia Quaglia

When octopuses extend their eight arms into hidden nooks and crannies in search of a meal, they are not just feeling around in the dark for their food. They are tasting their prey, and with even more sensory sophistication than scientists had already imagined.

Researchers reported on Tuesday in the journal Cell that octopus arms are fine-tuned to “eavesdrop into the microbial world,” detecting microbiomes on the surfaces around them and deriving information from them, said Rebecka Sepela, a molecular biologist at Harvard and an author of the new study.

Where octopus eyes cannot see, their arms can go to identify prey and make sense of their surroundings. Scientists knew that those eight arms (not tentacles) sense whether their eggs are healthy or need to be pruned. And the hundreds of suckers on each arm have over 10,000 chemotactile sensory receptors each, working with 500 million neurons to pick up that information and relay it throughout the nervous system.

Yet, what exactly the octopus is tasting by probing and prodding — and how its arms can distinguish, say, a rock from an egg, a healthy egg in its clutch from a sick one or a crab that’s safe to eat from a rotting, toxic one — has long baffled scientists.

What about the surfaces are they perceiving?

For Dr. Sepela, this question was heightened when her team discovered 26 receptors along the octopuses’ arms that didn’t have a known function. She supposed those receptors were tuned only to molecules found on surfaces, rather than those diffused in water.

So she and her colleagues collected swaths of molecules coating healthy and unhealthy crabs and octopus eggs. They grew and cultured the microbes from those surfaces in the lab, then tested 300 microbial strains, one by one, on two of those 26 receptors.

During the screening, only particular microbes could switch open the receptors, and these microbes were more abundant on the decaying crabs and dying eggs than on their healthy counterparts.