Brain Aging - Smart Parkinson's DBS - Idiosyncratic Pain - Ant Neuropeptides

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Jul 16, 2025, 7:54:52 AMJul 16

https://www.sciencenews.org/article/protein-brain-diseases-blood-parkinsons

Protein signatures may one day tell brain diseases apart before symptoms

By Tina Hesman Saey

A large-scale study of proteins in blood and cerebrospinal fluid could pave the way for improved blood tests to diagnose multiple brain diseases — and potential early warning signs of disease risk — researchers report July 15 in several papers in Nature Medicine and Nature Aging.

Proteins do much of the work to keep cells and bodies working. Trouble with these building blocks can spell disease; protein misfolding, for instance, links many brain diseases.

The results, drawn from samples from 18,645 people, reveal biochemical fingerprints of neurodegenerative disorders such as Alzheimer’s, Parkinson’s, frontotemporal dementia and amyotrophic lateral sclerosis, or ALS. These tests could also help identify disease subtypes and track progression before symptoms emerge.

Such well-validated and robust results are “more likely to ultimately translate into something that’s medically actionable,” says Andrew Saykin, director of the Indiana Alzheimer’s Disease Research Center in Indianapolis, which contributed samples to the effort.

In one key finding, researchers discovered that individuals carrying a form of the APOE gene called APOE4 — the biggest genetic risk factor for developing Alzheimer’s — share a blood signature regardless of diagnosis. That signature appeared not only in people with Alzheimer’s but also in those with other brain diseases or no neurodegeneration at all, neuroscientist Caitlin Finney and colleagues report in Nature Medicine. The APOE4 protein signature involves proteins that respond to infection and inflammation, hinting at how the variant predisposes carriers to brain diseases. It also suggests that the APOE4 protein may be involved in the early stages of multiple diseases.

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https://www.sciencenews.org/article/organ-age-predict-health-lifespan

Organ age, not just your birthday, may determine your health risks

By Celina Zhao

You could be 45 on paper but 60 in your kidneys.

Turns out, your organs have birthdays of their own — and how well they’re faring may set the pace for your health, researchers report July 9 in Nature Medicine. Using data from nearly 45,000 people, scientists developed a blood-based test to estimate the biological age of 11 organs, providing a measure of how healthy or worn down each organ is. When a person has an organ substantially “older” than their actual age, disease risks tied to that organ surge. Conversely, extremely youthful brains and immune systems are linked to living longer, the results suggest.

“The fact that [the researchers] can create an organ age using proteins — and use it to predict diseases that you would expect to be predicted from that organ — is quite amazing,” says Sarah Harris, a molecular biologist at the University of Edinburgh who was not involved in the study.

Aging is far from a uniform process; each organ follows its own clock of decline. One way to track this hidden timeline, previously discovered by Stanford neurology researchers Hamilton Oh and Tony Wyss-Coray, is through the thousands of proteins coursing through our blood. Some unmistakably originate in the liver, while others can be traced to the lungs. Analyzing these proteins can reveal clues about how each organ is holding up.

In the new study, the team zeroed in on thousands of patients from the UK Biobank, a long-term database tracking the health of individuals ages 40 to 70 for up to 17 years. By assessing proteins in the blood, the team determined the average protein signature for, say, a 40-year-old liver or 70-year-old arteries.

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https://www.nature.com/articles/d41586-025-02196-4

Smart brain-zapping implants could revolutionize Parkinson’s treatment

Sally Adee

Keith Krehbiel lived with Parkinson’s disease for nearly 25 years before agreeing to try a brain implant that might alleviate his symptoms. He had long been reluctant to submit to the surgery. “It was a big move,” he says. But by 2020, his symptoms had become so severe that he grudgingly agreed to go ahead.

Deep-brain stimulation involves inserting thin wires through two small holes in the skull into a region of the brain associated with movement. The hope is that by delivering electrical pulses to the region, the implant can normalize aberrant brain activity and reduce symptoms. Since the devices were first approved almost three decades ago, some 200,000 people have had them fitted to help calm the tremors and rigidity caused by Parkinson’s disease. But about 40,000 of those who received devices made after 2020 got them with a special feature that has largely not yet been turned on. The devices can read brain waves and then adapt and tailor the rhythm of their output, in much the same way as a pacemaker monitors and corrects the heart’s electrical rhythms, says Helen Bronte-Stewart, a neurologist at Stanford University in California.

Bronte-Stewart received approval to start a clinical trial of this new technology, known as adaptive deep-brain stimulation (aDBS), the same week that Krehbiel was preparing for surgery. He recalls the phone call in which she asked him if he wanted to be her first participant: “I said, ‘Boy, do I!’”

Five years on, the results of this 68-person trial, called ADAPT-PD, are under review for publication. Although the exact details are still under wraps, they were convincing enough to earn approval for the technology earlier this year from both US and European regulators.

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https://www.theguardian.com/australia-news/2025/jul/14/the-fascinating-science-of-pain-and-why-everyone-feels-it-differently

The fascinating science of pain – and why everyone feels it differently

By Celina Ribeiro

Some say it was John Sattler’s own fault. The lead-up to the 1970 rugby league grand final had been tense; the team he led, the South Sydney Rabbitohs, had lost the 1969 final. Here was an opportunity for redemption. The Rabbitohs were not about to let glory slip through their fingers again.

Soon after the starting whistle, Sattler went in for a tackle. As he untangled – in a move not uncommon in the sport at the time – he gave the Manly Sea Eagles’ John Bucknall a clip on the ear.

Seconds later – just three minutes into the game – the towering second rower returned favour with force: Bucknall’s mighty right arm bore down on Sattler, breaking his jaw in three places and tearing his skin; he would later need eight stitches. When his teammate Bob McCarthy turned to check on him, he saw his captain spurting blood, his jaw hanging low. Forty years later Sattler would recall that moment. One thought raged in his shattered head: “I have never felt pain like this in my life.”

But he played on. Tackling heaving muscular players as they advanced. Being tackled in turn, around the head, as he pushed forward. All the while he could feel his jaw in pieces.

At half-time the Rabbitohs were leading. In the locker room, Sattler warned his teammates, “Don’t play me out of this grand final.”

McCarthy told him, “Mate, you’ve got to go off.”

He refused. “I’m staying.”

Sattler played the whole game. The remaining 77 minutes. At the end, he gave a speech and ran a lap of honour. The Rabbitohs had won. The back page of the next day’s Sunday Mirror screamed “BROKEN JAW HERO”.

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https://www.thetransmitter.org/social-behavior/neuropeptides-reprogram-social-roles-in-leafcutter-ants/

Neuropeptides reprogram social roles in leafcutter ants

By Shaena Montanari

Leafcutter ants’ roles can be reprogrammed by manipulating two neuropeptides, according to a new study. These ants are known for their rigorous division of labor in a caste system, with groups performing roles ranging from cutting leaves to nest defense to tending the fungus that is their food source.

Despite physical differences among the ants—the heads of the nest defender ants can be five times the size of the fungal carers’ heads, for instance—it’s still possible to “pharmacologically reprogram them to assume some of the roles that typically other castes assume,” indicating behavioral flexibility, says Daniel Kronauer, professor at Rockefeller University, who was not involved in the work.

The researchers induced the behavioral changes by first using RNA sequencing to uncover target neuropeptides and then manipulating neuropeptide levels in the ants. The study was published in June in Cell.

The work illustrates the close relationship between neuropeptides and behavior, says Shelley Berger, professor of cell and developmental biology at the University of Pennsylvania and principal investigator of the study. Defender ants are “so big and awkward and clumsy,” she says, but after a certain neuropeptide level is lowered, the ant becomes a “nurse tending to the brood.”

The study shows the “importance of neuropeptides as these molecular controllers of incredibly complex” behavioral traits, says Zoe Donaldson, professor of behavioral neuroscience at the University of Colorado Boulder, who was not involved in the study. “I think it’s a really elegant demonstration of just how powerful they are.”

Almost all species of ants live in colonies, but leafcutter ants (Atta cephalotes) have a particularly intricate labor division, says study investigator Karl Glastad, assistant professor of biology at the University of Rochester. He and Berger previously explored hormonal controls of social behavior in Florida carpenter ants, which have two worker subtypes, but leafcutter ants are a “really elaborated version” of that species, Glastad says.

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https://www.nature.com/articles/d41586-025-02237-y

One potent gene raises risk of Alzheimer’s, Parkinson’s and other brain diseases

Smriti Mallapaty

A gene variant known to increase the risk of Alzheimer’s disease also makes people vulnerable to a host of other age-related brain disorders, from Parkinson’s disease to motor neuron disease. The gene variant, a version of apolipoprotein E called APOE ε4, produces a distinct set of proteins that contribute to chronic inflammation, finds an analysis1 using the largest proteomics database for neurodegenerative disease.

Neurodegenerative diseases affect more than 57 million people worldwide. Researchers know that people who carry the APOE ε4 variant have an increased risk of developing late-onset Alzheimer’s disease, but studies are beginning to implicate this version, or allele, of APOE in other neurodegenerative diseases.

Caitlin Finney and Artur Shvetcov, who study neurodegenerative diseases at the Westmead Institute for Medical Research in Sydney, Australia, and their colleagues wanted to better understand how this genetic risk factor contributes to disease. They took advantage of a newly established proteomics database that allowed them to look beyond individual diseases, says Finney.

The Global Neurodegeneration Proteomics Consortium (GNPC) data set2 includes samples from more than 18,600 individuals, mainly of European ancestry, including many with Alzheimer’s, Parkinson’s, a form of motor neuron disease called amyotrophic lateral sclerosis (ALS) and types of dementia, as well as individuals without neurological disorders. The consortia collected around 250 million measurements of proteins found in the blood and cerebrospinal fluid, which surrounds the brain and spinal cord, taken at some two dozen clinics across the United States and Europe. “It’s one of the most powerful databases that we have available for proteomics right now,” says Maryam Shoai, a bioinformatician at University College London.

Predicting risk

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https://www.nytimes.com/2025/07/16/health/meth-addiction-treatment-contingency-management.html

Upended by Meth, Some Communities Are Paying Users to Quit

By Jan Hoffman

Jamie Mains showed up for her checkup so high that there was no point in pretending otherwise. At least she wasn’t shooting fentanyl again; medication was suppressing those cravings. Now it was methamphetamine that manacled her, keeping her from eating, sleeping, thinking straight. Still, she could not stop injecting.

“Give me something that’s going to help me with this,” she begged her doctor.

“There is nothing,” the doctor replied.

Overcoming meth addiction has become one of the biggest challenges of the national drug crisis. Fentanyl deaths have been dropping, in part because of medications that can reverse overdoses and curb the urge to use opioids. But no such prescriptions exist for meth, which works differently on the brain.

In recent years, meth, a highly addictive stimulant, has been spreading aggressively across the country, rattling communities and increasingly involved in overdoses. Lacking a medical treatment, a growing number of clinics are trying a startlingly different strategy: To induce patients to stop using meth, they pay them.

The approach has been around for decades, but most clinics were uneasy about adopting it because of its bluntly transactional nature. Patients typically come in twice a week for a urine drug screen. If they test negative, they are immediately handed a small reward: a modest store voucher, a prize or debit card cash. The longer they abstain from use, the greater the rewards, with a typical cumulative value of nearly $600. The programs, which usually last three to six months, operate on the principle of positive reinforcement, with incentives intended to encourage repetition of desired behavior — somewhat like a parent who permits a child to stay up late as a reward for good grades.

Research shows that the approach, known in addiction treatment as “contingency management,” or CM, produces better outcomes for stimulant addiction than counseling or cognitive behavioral therapy. Follow-up studies of patients a year after they successfully completed programs show that about half remained stimulant-free.