Art, peanuts and Dick Van Dyke: ageing well at Christmas

 I try to see lots of museums when I travel, next up.

Heading to Italy April 21-30 with Michigan Public Radio;3 nights at the Cardinal Hotel St. Peter in Rome;4 nights at Hotel Mary, Sorrento Coast; 1 night at Isola Sara Rome Airport Hotel.
Pompei and Naples here I come. The tiles in Pompeii probably qualify as original art

Art, peanuts and Dick Van Dyke: ageing well at Christmas

And all of a sudden – it’s almost Christmas! Another year of ageing well, for us all, we hope. The festive photo of Annabel and I above shows us flanking a Christmas tree decorated by our friend, artist Amy Robson. She handmade the dolls that decorate the tree. Making by hand, crafting in any form, is one of the greatest gifts we can give ourselves. Working with your hands lights up an extraordinary number of neural circuits at once: the combination of fine motor control, spatial feedback, decision making and flow builds cognitive reserve, protecting the brain long-term. 2026 will be the year I make something. Just not sure what yet. I’d gladly welcome your suggestions in the comments below.

The joy of art

Talking of art, if getting out and about to an art gallery is on your to-do list over the festive period, then you’ll also be reducing stress. Research by Kings College London, part-sponsored by the Art Fund, compared the physiological impact of viewing original artworks in a gallery, versus looking at reprints in a non-gallery setting.

Pro-inflammatory cytokines IL-6 and TNF-α, which are linked to stress and chronic disease,  dropped by 30% and 28% respectively for those viewing original art, with no change observed in the reproduction group. This suggests art has a potential calming effect on the body’s inflammatory responses.  I would also suggest that there’s something so uplifting about being in an art gallery – the light, the space, the calm – that must also lower stress, don’t you think?

A few other longevity-focussed stories which have crossed my desk this year, but not yet made it onto the blog:

Superagers

We know that there are an elite group of older people known as ‘superagers’: people 80 and up who have the same memory function as someone 20 to 30 years younger.  And we know that loneliness impacts cognitive function long term. So it’s not a huge surprise that superagers view social relationships as vitally important. A 25-year study by Northwestern University found this was the unifying factor among superagers – more so than diet, exercise regime or other lifestyle choices.

People with greater social connection(I have massive social connections.) experience less chronic stress, which elevates cortisol – which, in turn, leads to inflammation. That, in turn, could damage brain cells and even increase dementia risk.

The most super of agers

Talking of super-agers – or should that be supercalifragilisticexpialidocious-agers – the ineffable Dick Van Dyke turned 100 this month. He’s published a book detailing his 100 rules to living to 100. The headlines: he goes to the gym three times a week, dances, takes five lumps of sugar in his coffee, enjoys a power nap and sings every day. Sounds like a recipe for a good, long life (except, maybe, the sugar).

Peanuts

With Christmas, comes feasting, and all manner of treats. Don’t hold back from grabbing a handful of peanuts: research from The Netherlands published earlier this month linked two servings of them to improvements in both brain vascular function and verbal memory. The study focussed on skin-roasted peanuts – not the salted or dry-roasted kind – and found that eating two servings a day increased blood flow to the brain. Peanuts are rich in polyphenols and antioxidants. Berries and dark chocolate also contain these nutrients, so enjoy those this Christmas too.

Annabel on the radio

Annabel and I bonded over our love of books and reading, so it was a joy to hear her on BBC Radio 4’s  A Good Read, talking about one of her favourite books, The Living Mountain by Nan Shepherd. If you have access to BBC Sounds, you can listen there. Annabel’s episode was the last in the current series. And I can vouch that The Living Mountain is indeed a good read.

A bonus workshop on nutrition for better brain health

I’m running a bonus workshop to help you create Your 2026 Brain Food Plan on January 15th . It’s for everyone who has my course, Feed Your Brain Better. The course is digital so you can buy and access any time. It costs £37 – approx $49. The free bonus workshop is designed to help you stay consistent with nutrition for better brain health in 2026 – especially when things get busy – and will be on Zoom. Details of how to join the course – and the workshop – here

Christmas recipes from the archive

Of course, it wouldn’t be Christmas without some recipes from the Age Well archive. Here are a few of our festive favourites:

Christmas nuts

Griddled Brussel sprouts with parmesan

Spiced parsnip soup – warming and hearty

Vegetable tartlets for Christmas dinner  

Christmas granola

Beautiful-on-the-inside Christmas cake

Wishing you a very happy and healthy festive season

Susan

Responsiveness to exoskeleton loading during bimanual reaching is associated with corticospinal tract integrity in stroke.

It would be nice if you told us if it worked towards recovery or not! But you do word salad quite well, not that that gets survivors recovered!

 Responsiveness to exoskeleton loading during bimanual reaching is associated with corticospinal tract integrity in stroke.

NARIC Accession Number: J94484. What's this?
Author(s): Brunfeldt, Alexander T., Bregman, Barbara S., Lum, Peter S..
Publication Year: 2024.
Abstract: Study investigated whether reducing the muscular cost discrepancy between the limbs in chronic stroke survivors would result in their increasing use of their more-impaired arm during bimanual reaching. Fourteen stroke participants performed a bimanual shared cursor reaching task in virtual reality while exoskeletons decreased the effective weight of the more-impaired arm and increased the effective weight of the less-impaired arm. The relative contribution (RC) was calculated as the primary measure of the kinematic relationship between the arms and the muscle contribution (MC) was calculated as the primary measure of the dynamic relationship between the arms from the biceps and deltoids. The corticospinal tract lesion load (wCSTLL) was calculated in a subset of 10 participants. Exoskeleton loading did not change RC or MC at the group level, but significant individual differences emerged. Participants with little overlap between the lesion and corticospinal tract responded to loading by decreasing muscle activity in the more-impaired arm relative to the less-impaired arm. The change in deltoid MC was associated with smaller wCSTLL; there was no such relationship for biceps MC. This study provides evidence that corticospinal tract integrity is a critical feature that determines one's ability to respond to upper-extremity exoskeleton loading.
Descriptor Terms: BIOENGINEERING, BODY MOVEMENT, COMPUTER APPLICATIONS, ELECTROPHYSIOLOGY, IMAGING, LIMBS, MOTOR SKILLS, REHABILITATION TECHNOLOGY, ROBOTICS, STROKE, TASK ANALYSIS.


Can this document be ordered through NARIC's document delivery service*?: Request Information.
Get this Document: https://www.frontiersin.org/journals/neuroscience/articles/10.3389/fnins.2024.1348103/full.

Low Hemoglobin Levels Linked to Higher Dementia Risk

 When I donate blood every two months I'm usually good, but just to make sure a couple days before I start taking a few iron pills. 

Low Hemoglobin Levels Linked to Higher Dementia Risk

Key Takeaways

• Lower hemoglobin levels were linked with higher dementia risk over 9 years of follow-up.
• Anemia was associated with elevated Alzheimer's blood biomarkers including p-tau217 and neurofilament light chain.
• Dementia risk was highest when anemia coexisted with abnormal Alzheimer's biomarkers.

Lower hemoglobin levels were associated with progressively higher dementia risk and elevated blood concentrations of Alzheimer's disease biomarkers, data from a Swedish cohort study suggested.

In a study of 2,300 older adults without dementia, anemia was cross-sectionally associated with higher levels of serum phosphorylated tau 217 (p-tau 217; β=0.22), neurofilament light chain (NfL; β=0.25) and glial fibrillary acidic protein (GFAP; β=0.08), reported Martina Valletta, MD, of the Karolinska Institute in Stockholm, and co-authors.

Anemia was longitudinally associated with a higher risk of incident dementia over a mean follow-up of 9 years (HR 1.66, 95% CI 1.21-2.28), Valletta and colleagues reported in JAMA Network Open.

The highest dementia risk occurred when anemia and elevated biomarkers coexisted, the researchers said. For older adults with low hemoglobin and high NfL, for example, the HR was 3.64 (95% CI 2.39-5.56).

These findings suggested that anemia may interact with neuropathologic processes, potentially accelerating dementia development, Valletta and co-authors noted.

"Dementia risk was particularly high when anemia co-occurred with high levels of blood biomarkers reflecting Alzheimer's disease pathology, neurodegeneration, and glial activation. This suggests a biological interplay between anemia and neuropathology, in which low hemoglobin may not only contribute to neuropathology but also reduce the brain's resilience to it," the researchers wrote.

"Taken together, our findings suggest anemia is a clinically relevant factor in the context of dementia risk stratification and is possibly a modifiable target in dementia prevention strategies," they added.

A causal role of anemia in dementia etiology could have substantial public health implications, observed Frank Wolters, MD, PhD, of Erasmus MC-University Medical Center in Rotterdam, the Netherlands.

"Anemia is present in 25% of the global population, with the highest prevalence in countries that are expected to have the steepest increases in dementia incidence," Wolters wrote in an accompanying editorial.

The biomarker-level observations in the Swedish study "provide novel evidence that connects hemoglobin directly to Alzheimer's disease," he noted. "Although the cross-sectional design in this respect did not allow for formal mediation analyses, results point at least toward a joint role of Alzheimer's pathology and anemia, in line with earlier observations linking hemoglobin to plasma amyloid-beta," he pointed out.

To move findings from observation to effective intervention, "mechanistic insight is mandatory," Wolters emphasized. "Such insights could come from observational studies on anemia and its causes, including use of repeated measures of hemoglobin and emulated target trials, as well as from small physiological trials," he added.

Valletta and colleagues studied participants in the Swedish National Study on Aging and Care in Kungsholmen (SNAC-K), a longitudinal population-based study. Participants enrolled from 2001 to 2004 were followed up every 3 or 6 years according to age through 2019.

The analysis included 2,282 dementia-free participants with a median age of 72.2 years; 61.6% were female. Analyses were adjusted for age cohort, sex, educational level, chronic kidney disease, heart disease, cerebrovascular disease, cancer, underweight, iron and vitamin supplement intake, and interleukin-6 levels.

Hemoglobin level was measured at baseline, and anemia was defined according to World Health Organization criteria as a blood hemoglobin level of 12 g/dL or less for women and 13 g/dL or less for men. A total of 199 participants had anemia.

Alzheimer's biomarkers were measured in blood samples taken at baseline. Incident dementia was diagnosed based on DSM-IV criteria. Over a mean follow-up of 9.3 years, 362 participants (15.9%) developed dementia.

"In a previous study by our group, anemia emerged as one of the chronic conditions most significantly associated with elevated levels of Alzheimer's disease blood biomarkers. Expanding that evidence, in this study we also included p-tau217, currently regarded as the most specific blood biomarker for Alzheimer's disease, and we observed that all biomarker levels tended to be higher as hemoglobin levels declined, following a nonlinear dose-response association," Valletta and colleagues noted.

"These findings suggest a more nuanced relation between hemoglobin levels, Alzheimer's disease blood biomarkers, and dementia beyond the definition of anemia itself," they wrote.

The study had several limitations, the researchers acknowledged. Hemoglobin levels ranged from 8.2 to 17.6 g/dL, and most anemia cases were normocytic, limiting analysis of more extreme values and other anemia subtypes. Alzheimer's biomarkers were measured in serum, which typically produces lower concentrations than plasma. Blood biomarkers also were available only at baseline.

Judy George covers neurology and neuroscience news for MedPage Today, writing about brain aging, Alzheimer’s, dementia, MS, rare diseases, epilepsy, autism, headache, stroke, Parkinson’s, ALS, concussion, CTE, sleep, pain, and more. Connect:

Disclosures

SNAC-K data collection was supported by the Swedish Research Council and by the Swedish Ministry of Health and Social Affairs. The study also received support from Stiftelsen Sigurd och Elsa Goljes minne, Hjärnfonden, the Gamla Tjänarinnor Foundation, and Svenska Läkaresällskapet.

Valletta had no disclosures. Co-authors reported relationships with the Swedish Research Council, the Karolinska Institutet Strategic Research Area in Epidemiology and Biostatistics, and the Margaretha af Ugglas' Foundation.

Wolters reported no conflicts of interest.

Primary Source

JAMA Network Open

Source Reference: Valletta M, et al "Anemia and blood biomarkers of Alzheimer disease in dementia development" JAMA Netw Open 2026; DOI: 10.1001/jamanetworkopen.2026.4029.

Secondary Source

JAMA Network Open

Source Reference: Wolters FJ "Hemoglobin and anemia in dementia prevention -- the new face of a familiar protein" JAMA Netw Open 2026; DOI: 10.1001/jamanetworkopen.2026.7758.

Your vitamin D levels in midlife could shape your brain decades later

 Since I just exited midlife at 70, I'll just have to use coffee as dementia prevention. Hopefully I did enough outside activities to build a substantial base.

Your vitamin D levels in midlife could shape your brain decades later

Date:

April 7, 2026

Source:

American Academy of Neurology

Summary:

Vitamin D levels in midlife may play a bigger role in long-term brain health than previously thought. In a study following nearly 800 people over 16 years, those with higher vitamin D levels in their 30s and 40s had lower levels of tau protein later on, a key marker linked to dementia.

People with higher levels of vitamin D in midlife may have lower levels of tau protein in the brain years later, according to a study published April 1, 2026, in Neurology Open Access, an official journal of the American Academy of Neurology. Tau is a protein closely linked to dementia.

The researchers note that the findings show a relationship, not proof that vitamin D directly reduces tau levels or lowers the risk of dementia.

"These results suggests that higher vitamin D levels in midlife may offer protection against developing these tau deposits in the brain and that low vitamin D levels could potentially be a risk factor that could be modified and treated to reduce the risk of dementia," said study author Martin David Mulligan, MB BCh BAO, of the University of Galway in Ireland. "Of course, these results need to be further tested with additional studies."

The study followed 793 adults who were an average of 39 years old and free of dementia at the beginning. Researchers measured each participant's blood vitamin D level at the start of the study.

About 16 years later, participants underwent brain scans to evaluate levels of tau and amyloid beta proteins, both of which are considered biomarkers of Alzheimer's disease. A vitamin D level above 30 nanograms per milliliter (ng/mL) was classified as high, while levels below that threshold were considered low.

Overall, 34% of participants had low vitamin D levels, and only 5% reported taking vitamin D supplements.

Higher Vitamin D Linked to Lower Tau Protein

After accounting for factors such as age, sex and symptoms of depression, the researchers found that higher vitamin D levels were associated with lower levels of tau protein years later.

However, vitamin D levels were not linked to the amount of amyloid beta protein in the brain.

"These results are promising, as they suggest an association between higher Vitamin D levels in early middle-age and lower tau burden on average 16 years later," Mulligan said. "Mid-life is a time where risk factor modification can have a greater impact."

Study Limitations and Need for Further Research

One limitation of the study is that vitamin D levels were measured only once rather than tracked over time.

Highlights:

• People with higher vitamin D levels in midlife had lower levels of tau protein later on, a key marker linked to Alzheimer's disease
• The study shows a link, but it does not prove that vitamin D directly reduces dementia risk
• Researchers found no connection between vitamin D levels and amyloid beta, another Alzheimer's biomarker
• Further research is needed to confirm these findings and better understand the role of vitamin D in brain health

 Long-Term Study Tracks Vitamin D and Brain Biomarkers

The study followed 793 adults who were an average of 39 years old and free of dementia at the beginning. Researchers measured each participant's blood vitamin D level at the start of the study.

About 16 years later, participants underwent brain scans to evaluate levels of tau and amyloid beta proteins, both of which are considered biomarkers of Alzheimer's disease. A vitamin D level above 30 nanograms per milliliter (ng/mL) was classified as high, while levels below that threshold were considered low.

Overall, 34% of participants had low vitamin D levels, and only 5% reported taking vitamin D supplements.

Higher Vitamin D Linked to Lower Tau Protein

After accounting for factors such as age, sex and symptoms of depression, the researchers found that higher vitamin D levels were associated with lower levels of tau protein years later.

However, vitamin D levels were not linked to the amount of amyloid beta protein in the brain.

"These results are promising, as they suggest an association between higher Vitamin D levels in early middle-age and lower tau burden on average 16 years later," Mulligan said. "Mid-life is a time where risk factor modification can have a greater impact."

Study Limitations and Need for Further Research

One limitation of the study is that vitamin D levels were measured only once rather than tracked over time.

Highlights:

• People with higher vitamin D levels in midlife had lower levels of tau protein later on, a key marker linked to Alzheimer's disease
• The study shows a link, but it does not prove that vitamin D directly reduces dementia risk
• Researchers found no connection between vitamin D levels and amyloid beta, another Alzheimer's biomarker
• Further research is needed to confirm these findings and better understand the role of vitamin D in brain health

Cell Death Protein Silently Ages Your Blood

 Is your competent? doctor providing young blood to you to solve this problem? OH NO; DOING NOTHING, LIKE USUAL!

• (young blood 30 posts to June 2014) Ask your doctor, how young and where to get it

Cell Death Protein Silently Ages Your Blood

Summary: As we age, our blood-making factory, the hematopoietic stem cells (HSCs), starts to break down, leading to a weaker immune system and an overproduction of inflammatory myeloid cells. A new study has identified a surprising culprit: a protein called MLKL.

Previously known only for triggering “necroptosis” (programmed cell death), researchers discovered that MLKL has a “non-lethal” side job; it hijacks and damages the mitochondria in stem cells, causing them to age prematurely without actually killing them.

Key Findings

• Hallmarks of Aging: Stress-induced MLKL activation caused HSCs to stop renewing themselves and begin favoring myeloid cells over lymphoid cells (which are needed for a strong immune response).
• The “Delete” Effect: When researchers deleted MLKL, the stem cells maintained their regenerative capacity, produced healthier immune cells, and showed significantly lower DNA damage, even under intense stress or in old age.
• Organelle-Level Control: Most aging research focuses on gene expression (RNA). However, this study found that MLKL drives aging through post-transcriptional mechanisms, meaning it changes the cell’s physical hardware (mitochondria) rather than just its “software” (genes).
• Mitochondrial Protection: Deactivating MLKL effectively preserved the blood system’s health, suggesting that the protein is a central “bottleneck” where various types of age-related stress converge.Source: University of Tokyo

As we age, our ability to maintain healthy blood and a strong immune system gradually declines, largely because hematopoietic stem cells (HSCs), the cells responsible for producing all blood cell types, begin to lose their effectiveness.

Normally, HSCs can both self-renew and generate a balanced mix of blood cells, but over time they produce fewer new cells, favor certain cells such as myeloid cells over lymphoid cells, and struggle to support a robust immune response.

Accumulated cellular damage, shifts in gene activity, ongoing low-level inflammation, and changes in the bone marrow environment, all appear to contribute to this decline. However, the precise mechanisms by which these diverse stresses converge to weaken HSCs have remained unclear.

Researchers from The University of Tokyo, Japan, and St. Jude Children’s Research Hospital, USA, sought to uncover a mechanism explaining how age-related stresses drive HSC functional deterioration, focusing on the receptor-interacting protein kinase 3 (RIPK3)-mixed lineage kinase like (MLKL) signaling axis—a pathway traditionally associated with necroptosis, or programmed cell death.

The study was led by Dr. Masayuki Yamashita, an Assistant Member at St. Jude Children’s Research Hospital, who, at the time of the investigation, was an Assistant Professor at The Institute of Medical Science, The University of Tokyo. The other co-authors include Dr. Atsushi Iwama from The Institute of Medical Science, The University of Tokyo, and Dr. Yuta Yamada from St. Jude Children’s Research Hospital, who was a graduate student at The Institute of Medical Science, The University of Tokyo.

Explaining the motivation behind the study, Dr. Yamashita says, “We discovered an unexpected phenotype in HSCs of MLKL-knockout mice repeatedly treated with 5-fluorouracil, where aging-associated functional changes were markedly attenuated despite no detectable difference in HSC death, prompting us to investigate whether this pathway might induce functional changes beyond cell death.”

This observation shifted the research focus toward a non-lethal role of MLKL—a concept later highlighted in their study, published in Volume 17 of the journal Nature Communications on April 6, 2026.

To investigate this, the team employed a combination of genetic mouse models, stress treatments, and functional assays. They used wild-type, MLKL-deficient, and RIPK3-deficient mice, along with specialized reporter mice capable of detecting MLKL activation through a Förster resonance energy transfer-based biosensor.

Mice were exposed to stressors mimicking aging, including inflammation, replication stress, and oncogenic stress. HSC function was then assessed primarily through bone marrow transplantation, which measures the ability of stem cells to regenerate the blood system.

Complementary analyses included flow cytometry, ex vivo expansion, RNA-seq, assay for transposase-accessible chromatin-seq, high-resolution microscopy, metabolic assays, and mitochondrial analyses, enabling a detailed understanding of how non-lethal MLKL activation impairs HSC function at molecular, cellular, and organelle levels.The results revealed a novel, non-necroptotic role for MLKL in HSC aging. While MLKL is typically linked to cell death, its activation in HSCs did not increase cell death or reduce cell numbers. Instead, stress-induced MLKL activation was transient and localized to mitochondria, where it caused direct damage, reducing membrane potential, altering mitochondrial structure, and impairing energy production.

These changes led HSCs to exhibit hallmark features of aging, such as diminished self-renewal, reduced lymphoid differentiation, and a shift toward myeloid-biased output.

Crucially, deletion or inactivation of MLKL significantly alleviated these defects. MLKL-deficient HSCs maintained regenerative capacity, produced healthier immune cells, displayed lower DNA damage, and preserved mitochondrial function, even under stress or in aged animals.

Interestingly, these improvements occurred without substantial changes in gene expression or chromatin accessibility, suggesting that MLKL drives HSC aging primarily through post-transcriptional and organelle-level mechanisms, rather than through transcriptional regulation or inflammation.

These findings have broad implications for understanding aging and potential therapies. By linking diverse stress signals to mitochondrial dysfunction via MLKL, the study identifies a common pathway underlying HSC aging.

Dr. Yamashita emphasizes, “In the longer term, this research could lead to therapies that preserve the function of hematopoietic stem cells, ultimately improving recovery and long-term health for patients undergoing chemotherapy, radiation, or transplantation. By revealing how non-lethal activation of cell-death pathways drives stem cell aging, these findings may inspire new classes of mitochondrial-protective or necroptosis-modulating drugs.”

In conclusion, this study uncovers a previously unrecognized role of MLKL as a non-lethal regulator of stem cell aging. Rather than inducing cell death, MLKL acts as a stress-responsive factor that damages mitochondria and drives functional decline in HSCs. These insights not only redefine the role of necroptosis-related proteins but also open new avenues for understanding and potentially intervening in the aging of the hematopoietic system.

Key Questions Answered:

Q: If this protein is supposed to kill cells, why doesn’t it kill the stem cells?

A: This is the most shocking part of the study. In stem cells, the MLKL signal is “transient”, it turns on just long enough to damage the mitochondria but stops before it can blow up the cell membrane. It’s the biological equivalent of a burglar who breaks into your house just to break your appliances instead of stealing the whole house.

Q: Does this mean we can “cure” a weak immune system in the elderly?

A: It provides a specific target. By developing “necroptosis-modulating” drugs that block MLKL, doctors could potentially keep a patient’s blood “younger,” helping them recover faster from chemotherapy or age-related immune decline.

Q: Is this only relevant to blood cells?

A: While this study focused on blood, many other types of stem cells (like those in the brain or skin) also age via mitochondrial failure. Researchers suspect this “non-lethal” role for death proteins might be a universal mechanism for aging across the whole body.

Editorial Notes:

• This article was edited by a Neuroscience News editor.
• Journal paper reviewed in full.
• Additional context added by our staff.

About this genetics and aging research news

Author: Project Coordination Office
Source: University of Tokyo
Contact: Project Coordination Office – University of Tokyo
Image: The image is credited to Neuroscience News

Call for more investment in vital rehabilitation for stroke survivors

 This is just calling for more of the failed status quo. STATUS QUO OF ONLY 10% FULL RECOVERY IS MASSIVE FAILURE! Ask for the correct solution: 100% recovery protocols! Your stroke medical 'professionals' will pooh pooh it and say it can't be done! BOLLOCKS,  have them contact me for remedial education(OC1Dean@gmail.com)

You don't need any medical training to see that stroke rehab is a complete shitshow!

And in the end they only talk of providing 'care' NOT RECOVERY! I'd fire anyone settling for 'care' and you should too! A lot of dead wood needs to be removed in stroke; start with your 'professionals' if they have nothing for 100% recovery!

Call for more investment in vital rehabilitation for stroke survivors

Video at link

ITV Meridian's Richard Slee reports from Highcliffe in Dorset

---

A man from Dorset who suffered a stroke is backing calls for more investment in vital rehabilitation after a new survey reveals that most regions are seriously underfunded and understaffed.

David Stadelman, 73, who lives in Highcliffe near Bournemouth, had a stroke two years ago.

He credits the excellent care(NOT RECOVERY!) he received and ongoing therapy for his good recovery, but he wants every patient to have that same benefit.

"The rehabilitation that I received started very quickly after I had the stroke," David said.

"People called physiotherapists came along with the view of getting me home.

"Gradually I realised that there was a future to be had."

David has continued with his recovery by joining an exercise classCredit: ITV Meridian

David is now fit enough to drive himself to a local heart health group.

The Chartered Society of Physiotherapy claims that community stroke services have on average 26% fewer physiotherapists than recommended, and Acute Stroke teams are down by 15% which is leaving some people with avoidable disabilities.The government says it accepts it is failing many patients, but is committed to reducing the number of people who die from heart disease and strokes by a quarter over the next ten years.

In a statement a spokesperson said: 'We're rolling out specialist stroke rehabilitation in people's homes, so more people can get the right care(NOT RECOVERY!) without having to rely on hospital stays."

The $129 Device Used in 100+ Hospitals for Neurological Rehab Is Now Available to Every Patient Training at Home

 No clue. Ask your competent? doctor for an evaluation. No knowledge IS GROUNDS FOR IMMEDIATE FIRING!

The $129 Device Used in 100+ Hospitals for Neurological Rehab Is Now Available to Every Patient Training at Home

From the Cage to the Clinic: How a Training Tool Built for Fighters Became Standard Equipment in 100+ Hospitals

I built it for fighters,” Brad said. “Then a physical therapist called me and said, ‘Do you know what you actually made?’ That changed everything.”

— Brad Evans

SALT LAKE CITY, UT, UNITED STATES, April 17, 2026 /EINPresswire.com/ — Every year, millions of patients use reaction training equipment in hospital rehabilitation programs for Parkinson’s disease, stroke recovery, vestibular disorders, and traumatic brain injury. The devices they train on typically cost thousands of dollars and remain locked inside clinical settings. The coordination training that helps them recover stays behind when they go home.

Jukestir, a patented 3D reactive neurotraining device invented by Utah high school teacher Brad, is closing that gap. Priced at $129, the device is now used in more than 100 hospitals and rehabilitation facilities for neurological training — and is simultaneously available to any consumer through Amazon, where it holds 100 reviews at a 4.5-star rating.

Unlike conventional 2D light-based reaction systems that present stimuli on flat surfaces, Jukestir moves unpredictably through three-dimensional space, requiring users to track, react, and coordinate full-body movement in real time. The result is adaptive decision-making under conditions that more closely replicate the demands of both daily life and athletic competition — engaging neuroplasticity, dopamine release, and neuromuscular coordination simultaneously.

Academic and Clinical Validation
The University of Illinois Chicago Department of Kinesiology and Nutrition selected Jukestir as the central intervention equipment for The Green Light Study, a randomized research trial examining how dynamic, unpredictable movement tasks enhance functional movement performance, adaptability, and engagement. Results are expected in peer-reviewed publications by late 2026.

Jukestir is also an official partner of Rock Steady Boxing, the nation’s leading non-contact boxing-based exercise program for people with Parkinson’s disease. The partnership extends Jukestir’s reach into the Parkinson’s rehabilitation community, where reaction training, balance training, and fall prevention are critical priorities for maintaining quality of life.

“Jukestir is more affordable than the competition, with more application for movement and random reactive activities,” said Dr. Jordan West, Professor of Physical Therapy.

Jukestir was originally designed for combat sports, a training tool built to develop the reactive timing and unpredictable movement recognition that fighters need under pressure. Professional athletes adopted it first, including UFC fighters and a Wimbledon champion. But as the device moved through the sports performance world, clinicians began recognizing what it could do for their patients. Physical therapists started using it for balance training and vestibular rehabilitation. Neurological rehab programs brought it in for Parkinson’s disease and stroke recovery. Today it is used in more than 100 hospitals and rehabilitation facilities, a trajectory its inventor, a high school sports psychology teacher in Utah, never originally planned. “I built it for fighters,” Brad said. “Then a physical therapist called me and said, ‘Do you know what you actually made?’ That changed everything.”

Jukestir is available at jukestir.com and on Amazon.

BRAD Evans
Health and Fitness Technologies, LLC
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"Like Having Family Nearby": An LLM-Powered Family-Resembling Avatar for offering Psychological Support and Training Guidance during Stroke Rehabilitatio

You still haven't figured out that EXACT 100% recovery protocols that obviate the need for psychological support? You're wasting research dollars better spent on recovery protocols!

You create EXACT 100% recovery protocols, and your survivor will be motivated to do the millions of reps needed because they are looking forward to 100% recovery.

 "Like Having Family Nearby": An LLM-Powered Family-Resembling Avatar for offering Psychological Support and Training Guidance during Stroke Rehabilitation

Peixuan Xiong Computational Media and Arts Thrust The Hong Kong University of Science and Technology (Guangzhou) Guangzhou, China pxiong843@connect.hkust-gz.edu.cn 

Zhenyu Wang Intelligent Transportation Thrust The Hong Kong University of Science and Technology (Guangzhou) Guangzhou, China zwang209@connect.hkust-gz.edu.cn Kaishun 

Wu Hong Kong University of Science and Technology (Guangzhou) Guangzhou, China wuks@hkust-gz.edu.cn Yuling Wang∗ 

Bingchen Guo The Hong Kong University of Science and Technology (Guangzhou) Guangzhou, China ucabbg1@ucl.ac.uk Xian Li School of Design Southern University of Science and Technology Shenzhen, Guangdong, China 12011010@mail.sustech.edu.cn 

Xian Li

School of Design

Southern University of Science and

Technology

Shenzhen, Guangdong, China

12011010@mail.sustech.edu.cn

Xian Li

The Sixth Affiliated Hospital, Sun

Yat-sen University

Guangzhou, China

sophielixian@163.com

Chao Liu The Hong Kong University of Science and Technology (Guangzhou) Guangzhou, China cliu009@connect.hkust-gz.edu.cn 

Nianci Zhao The Chinese University of Hongkong, Shenzhen Shenzhen, Guangdong, China niancizhao@link.cuhk.edu.cn 

Chen Gong The Sixth Affiliated Hospital, Sun Yat-sen University Sun Yat-sen University Guangzhou, Guangdong, China gongch33@mail.sysu.edu.cn The Hong Kong University of Science The Sixth Affiliated Hospital, Sun Yat-sen University Guangzhou, China 

Yuling Wang∗

Bingchen Guo

The Hong Kong University of Science

and Technology (Guangzhou)

Guangzhou, China

ucabbg1@ucl.ac.uk

wangyul@mail.sysu.edu.cn and Technology (Guangzhou) Guangzhou, China The Hong Kong University of Science and Technology Hong Kong, China 

Mingming Fan∗

Department of Rehabilitation

Medicine

and Technology (Guangzhou)

Guangzhou, China

The Hong Kong University of Science

and Technology

Hong Kong, China

mingmingfan@ust.hk

Figure 1: Personalized companion–coach system: (A) Avatar enrollment. Assembling a family-member avatar by reconstructing head avatars from a single photo and voice cloning from voice recording. (B)Runtime. The patient converses with the avatar. The avatar uses Gemini for dialogue and uses Qwen3-VL for action understanding. The avatar can simultaneously serve as a conversational companion and provide rehabilitation training guidance. 

Abstract 

Stroke rehabilitation is prolonged and emotionally demanding, yet family members cannot provide continuous companionship or coaching. We explore a family-resembling avatar that offers psy chological support and training guidance when relatives cannot be present. We conducted an empirical user study with six stroke patients and their family members (N=12). Our qualitative find ings suggest such companions may reduce loneliness and increase perceived warmth, while action-relevant guidance can comple mentcaregivers’ limited rehabilitation knowledge. Participants also raised concerns about emotional dependence, privacy, and the need for stronger clinical alignment to avoid inappropriate guidance. We discuss implications for designing family-resembling companion coach avatars with clear boundaries, privacy-preserving personal ization, and supervised deployment in rehabilitation workflows.