Stroke Recovery - Air Pollution & Dementia - Parkinson's Helmet - Whole Brain Decisions
Breedlove, S
https://www.nytimes.com/2025/09/04/science/neuroscience-brain-injury-pill.html
A Pill to Heal the Brain Could Revolutionize Neuroscience
By Rachel E. Gross
The first thing Debra McVean did when she woke up at the hospital in March 2024 was try to get to the bathroom. But her left arm wouldn’t move; neither would her left leg. She was paralyzed all along her left side.
She had suffered a stroke, her doctor soon explained. A few nights before, a blood clot had lodged in an artery in her neck, choking off oxygen to her brain cells. Now an M.R.I. showed a dark spot in her brain, an eerie absence directly behind her right eye. What that meant for her prognosis, however, the doctor couldn’t say.
“Something’s missing there, but you don’t know what,” Ms. McVean’s husband, Ian, recalled recently. “And you don’t know how that will affect her recovery. It’s that uncertainty, it eats away at you.”
With a brain injury, unlike a broken bone, there is no clear road to recovery. Nor are there medical tools or therapies to help guide the brain toward healing. All doctors can do is encourage patients to work hard in rehab, and hope.
That is why, for decades, the medical attitude toward survivors of brain injury has been largely one of neurological “nihilism,” said Dr. Fernando Testai, a neurologist at the University of Illinois, Chicago, and the editor in chief of the Journal of Stroke and Cerebrovascular Diseases. Stroke, he said, “was often seen as a disease of ‘diagnose and adios.’”
That may be about to change. A few days after Ms. McVean woke up in the Foothills Medical Center in Calgary, she was told about a clinical trial for a pill that could help the brain recover from a stroke or traumatic injury, called Maraviroc. Given her level of physical disability, she was a good candidate for the study.
She hesitated. The pills were large — horse pills, she called them. But she knew the study could help others, and there was a 50 percent chance that she would get a drug that could help her, too.
© 2025 The New York Times Company
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https://www.nature.com/articles/d41586-025-02844-9
Air pollution directly linked to increased dementia risk
Rachel Fieldhouse
An analysis of 56 million people has shown that exposure to air pollution increases the risk of developing a particular form of dementia, the third most common type after Alzheimer’s disease and vascular dementia.
The study, published in Science on 4 September1, suggests that there is a clear link between long-term exposure to PM2.5 — airborne particles that are smaller than 2.5 micrometres in diameter — and the development of dementia in people with Lewy body dementia or Parkinson’s disease.
The study found that PM2.5 exposure does not necessarily induce Lewy body dementia, but “accelerates the development,” in people who are already genetically predisposed to it, says Hui Chen, a clinician–neuroscientist at the University of Technology Sydney in Australia.
PM2.5 exposure
Lewy body dementia is an umbrella term for two different types of dementia: Parkinson’s disease with dementia, and dementia with Lewy bodies. In both cases, dementia is caused by the build-up of α-synuclein (αSyn) proteins into clumps, called Lewy bodies, in the brain’s nerve cells, which cause the cells to stop working and eventually die. Studies have suggested that long-term exposure to air pollution from car-exhaust, wildfires and factory fumes, is linked with increased risks of developing neurodegenerative illnesses, including Parkinson's disease with dementia2.
Study co-author Xiaobo Mao, who researches neurodegenerative conditions at Johns Hopkins University in Baltimore, Maryland, says he and his colleagues wanted to determine if PM2.5 exposure also influenced the risk of developing Lewy body dementia. They analysed 2000–2014 hospital-admissions data from 56.5 million people with Lewy body dementia and Parkinson’s disease with or without dementia. The data served to identify people with severe neurological diseases.
© 2025 Springer Nature Limited
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Ultrasound ‘helmet’ could treat Parkinson’s non-invasively
Ivana Drobnjak O'Brien
An ultrasound “helmet” offers potential new ways for treating neurological conditions without surgery or other invasive procedures, a study has shown.
The device can target brain regions 1,000 times smaller than ultrasound can, and could replace existing approaches such as deep brain stimulation (DBS) in treating Parkinson’s disease. It also holds potential for conditions such as depression, Tourette syndrome, chronic pain, Alzheimer’s and addiction.
Unlike DBS, which requires a highly invasive procedure in which electrodes are implanted deep in the brain to deliver electrical pulses, using ultrasound sends mechanical pulses into the brain.
But no one had managed to create an approach capable of delivering them precisely enough to make a meaningful impact until now.
A study published in Nature Communications introduces a breakthrough system that can hit brain regions 30 times smaller than previous deep-brain ultrasound devices could.
“It is a head helmet with 256 sources that fits inside an MRI scanner,” said the author and participant Ioana Grigoras, of Oxford University. “It is chunky and claustrophobic putting it on the head at first, but then you get comfortable.”
Current DBS methods used on Parkinson’s patients use hard metal frames that are screwed into the head to hold them down.
To test the system, the researchers applied it to seven volunteers, directing ultrasound waves to a tiny region the size of a grain of rice in the lateral geniculate nucleus (LGN), the key pathway for visual information that comes from the eyes to the brain.
“The waves reached their target with remarkable accuracy,” the senior author Prof Charlotte Stagg of Oxford University said. “That alone was extraordinary, and no one has done it before.”
Follow-up experiments showed that modulating the LGN produced lasting effects in the visual cortex, reducing its activity. “The equivalent in patients with Parkinson’s would be targeting a motor control region and seeing tremors disappear,” she added.
© 2025 Guardian News & Media Limite
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Everything everywhere all at once: Decision-making signals engage entire brain
By Claudia López Lloreda
The process of making a decision engages neurons across the entire brain, according to a new mouse dataset created by an international collaboration.
“Many, many areas are recruited even for what are arguably rather simple decisions,” says Anne Churchland, professor of neurobiology at University of California, Los Angeles and one of the founding members of the collaboration, called the International Brain Laboratory (IBL).
The canonical model suggests that the activity underlying vision-dependent decisions goes from the visual thalamus to the primary visual cortex and association areas, and then possibly to the frontal cortex, Churchland says. But the new findings suggest that “maybe there’s more parallel processing and less of a straightforward circuit than we thought.”
Churchland and other scientists established the IBL in 2017 out of frustration with small-scale studies of decision-making that analyzed only one or two brain regions at a time. The IBL aimed to study how the brain integrates information and makes a decision at scale. “We came together as a large group with the realization that a large team effort could be transformative in these questions that had been kind of stymieing all of us,” Churchland says.
After years of standardizing their methods and instrumentation across the 12 participating labs, the IBL team constructed a brain-wide map of neural activity in mice as they complete a decision-making task. That map, published today in Nature, reveals that the activity associated with choices and motor actions shows up widely across the brain. The same is true for the activity underlying decisions based on prior knowledge, according to a companion paper by the same team, also published today in Nature.
© 2025 Simons Foundation
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'One and done' dose of LSD keeps anxiety at bay
Jon Hamilton
A rigorous new study finds that a single dose of LSD can ease anxiety and depression for months.
The study involved 198 adults with generalized anxiety disorder, or GAD, a disabling form of anxiety that affects about 1 in 10 people over the course of a year.
Participants who got lower doses of LSD (25 or 50 micrograms) did no better than those who got a placebo. But people who received higher doses (100 or 200 micrograms) responded quickly, a team reports in the Journal of the American Medical Association.
"By the next day, they were showing strong improvements," says Dr. David Feifel of Kadima Neuropsychiatry Institute in San Diego, one of the 22 centers that participated in the study. "And those improvements held out all the way to the end of the study, which was 12 weeks."
But it's unclear whether some of the improvement was related to non-drug factors like the sensory environment in which people were treated, says Robin Carhart-Harris, a psychedelics researcher at the University of California, San Francisco who was not involved in the study.
"The safety looks good, the tolerability looks good," he says, "but where is the depth of information about the way you delivered this product?"
Carhart-Harris, like many scientists who study psychedelics, believes that successful treatment is more likely if a person has the right mindset when beginning a trip and if the trip occurs in a place with the right sensory environment.
"It's characterized by continuous worry, inability to relax, and all the physical manifestations, racing heart rates and sweatiness," Feifel says. It's also frequently accompanied by depression.
Current antidepressant and antianxiety drugs are inadequate for about half of people diagnosed with GAD.
© 2025 npr
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The other end of the weight spectrum: Very thin people
By Ute Eberle
Before weight coach Bella Barnes consults with new clients, she already knows what they’ll say. The women struggle with their weight, naturally. But they don’t want to lose pounds. They want to gain them.
Her clients find themselves too thin, and they’re suffering. “Last week, I signed up a client who wears leggings that have bum pads in them,” says Barnes, who lives in Great Britain. “I’ve had another client recently that, in summer, wears three pairs of leggings just to try and make herself look a bit bigger.”
These women belong to a demographic group that has been widely overlooked. As the world focuses on its billion-plus obese citizens, there remain people at the other end of the spectrum who are skinny, often painfully so, but don’t want to be. Researchers estimate that around 1.9 percent of the population are “constitutionally thin,” with 6.5 million of these people in the United States alone.
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Conceptual illustration shows three dinner plates, two at night with crescent moons are empty, representing a nightly fast, and a third with a sun theme, full of food and representing the benefits of eating during a limited time during the day.
Constitutionally thin individuals often eat as much as their peers and don’t exercise hard. Yet their body mass index is below 18.5 — and sometimes as low as 14, which translates to 72 pounds on a five-foot frame — and they don’t easily gain weight. The condition is “a real enigma,” write the authors of a recent paper in the Annual Review of Nutrition. Constitutional thinness, they say, challenges “basic dogmatic knowledge about energy balance and metabolism.” It is also understudied: Fewer than 50 clinical studies have looked at constitutionally thin people, compared with thousands on unwanted weight gain.
© 2025 Annual Reviews
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https://www.nytimes.com/2025/09/05/science/dr-a-james-hudspeth-dead.html
James Hudspeth, Who Unlocked Mysteries Behind Hearing, Dies at 79
By Jeré Longman
Dr. A. James Hudspeth, a neuroscientist at the Rockefeller University in Manhattan who was pivotal in discovering how sound waves are converted in the inner ear to electrical signals that the brain can perceive as a whisper, a symphony or a thunderclap, died on Aug. 16 at his home in Manhattan. He was 79.
His wife, Dr. Ann Maurine Packard, said the cause was glioblastoma, a brain cancer.
Scientists have long understood how sound waves enter the ear canal and cause the eardrum to vibrate. They have also understood how the vibrations travel through the three small bones of the middle ear, then to the cochlea in the inner ear, a tiny organ about the size of a chickpea that is filled with fluid and is shaped like a snail’s shell.
And they have long known that microscopic receptor cells in the cochlea play a role in the process of hearing. But by the time Dr. Hudspeth began his research in the 1970s, it was still unclear how these cells — known as hair cells (the name derives from tufts of cylindrical, hairlike rods known as stereocilia) — transformed the mechanical vibrations of sound waves into nerve impulses that the brain could interpret as, say, a child crying or a dog barking.
Dr. Hudspeth “provided the major framework” for this understanding, the committee that awarded him and two other scientists (Robert Fettiplace and Christine Petit) the Kavli Prize in Neuroscience for their pioneering work on the processes of hearing wrote in its citation in 2018.
Each cochlea contains about 16,000 hair cells. Atop each cell, 20 to 300 of these rods are gathered in a bundle — the shortest to the tallest — in rows that resemble a staircase or a pipe organ. Hair cells line the cochlea, with each tuned to a narrow frequency range that collectively decodes the broad spectrum of tones in every sound.
© 2025 The New York Times Compan
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