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Brain Injury

Brain Training Game Offers New Hope for Drug-Free Pain Management

A trial of an interactive game that trains people to alter their brain waves has shown promise as a treatment for nerve pain — offering hope for a new generation of drug-free treatments.

Published

2 months ago

June 4, 2025

Veronic D.

A groundbreaking trial of an interactive game that trains people to alter their brain waves has shown promise as a treatment for nerve pain – offering hope for a new generation of drug-free treatments.

The PainWaive technology, developed by UNSW Sydney researchers, teaches users how to regulate abnormal brain activity linked to chronic nerve pain, providing a potential in-home, non-invasive alternative to opioids.

A recent trial led by Professor Sylvia Gustin and Dr Negin Hesam-Shariati from UNSW Sydney’s NeuroRecovery Research Hub has delivered promising results, published in the Journal of Pain. The study compared hundreds of measures across participants’ pain and related issues like pain interference before, during, and after four weeks of interactive game play.

Their brain activity was tracked via EEG (electroencephalogram) headsets, with the app responding in real time to shifts in brainwave patterns. Three out of the four participants showed significant reductions in pain, particularly nearing the end of the treatment. Overall, the pain relief achieved by the three was comparable to or greater than that offered by opioids.

“Restrictions in the study’s size, design, and duration limit our ability to generalise the findings or rule out placebo effects,” Dr Hesam-Shariati says. “But the results we’ve seen are exciting and give us confidence to move to the next stage and our larger trial.”

The PainWaive project builds on UNSW Professor Sylvia Gustin’s seminal research into changes in the brain’s thalamus – a central relay hub in the brain – associated with nerve (neuropathic) pain. “The brainwaves of people with neuropathic pain show a distinct pattern: more slow theta waves, fewer alpha waves, and more fast, high beta waves,” Prof. Gustin says.

“We believe these changes interfere with how the thalamus talks to other parts of the brain, especially the sensory motor cortex, which registers pain.” I wondered, can we develop a treatment that directly targets and normalises these abnormal waves?” The challenge was taken up by an interdisciplinary team at UNSW Science and Neuroscience Research Australia (NeuRA), led by Prof. Gustin and Dr Hesam-Shariati, and resulted in PainWaive.

The four participants in its first trial received a kit with a headset and a tablet preloaded with the game app, which includes directions for its use. They were also given tips for different mental strategies, like relaxing or focusing on happy memories, to help bring their brain activity into a more “normal” state. The user data was uploaded to the research team for remote monitoring.

“After just a couple of Zoom sessions, participants were able to run the treatment entirely on their own,” says Dr Hesam-Shariati. “Participants felt empowered to manage their pain in their own environment. That’s a huge part of what makes this special.”

Initially, Dr Hesam-Shariati says, the team planned to use existing commercial EEG systems but were either too expensive or didn’t meet the quality needed to deliver the project. Instead, they developed their own. “Everything except the open-source EEG board was built in-house,” says Dr Hesam-Shariati.

“And soon, even that will be replaced by a custom-designed board.” Thanks to 3D printing, Prof. Gustin says, the team has cut the cost of each headset to around $300 – a fraction of the $1,000 to $20,000 price tags of existing systems.

The headset uses a saline-based wet electrode system to improve signal quality and targets the sensorimotor cortex. “We’ve worked closely with patients to ensure the headset is lightweight, comfortable, and user-friendly,” says Prof. Gustin.

The researchers are now calling for participants to register their interest in two upcoming trials of the neuromodulation technology: the Spinal Pain Trial, investigating its potential to reduce chronic spinal pain, and the StoPain Trial, exploring its use in treating chronic neuropathic pain in people with a spinal cord injury.

Source:University of New South Wales

Original Link:https://www.sciencedaily.com/releases/2025/06/250602155330.htm

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Alzheimer's

Rewinding Stroke Damage and Beyond: The Promise of GAI-17

Stroke kills millions, but Osaka researchers have unveiled GAI-17, a drug that halts toxic GAPDH clumping, slashes brain damage and paralysis in mice—even when given six hours post-stroke—and shows no major side effects, hinting at a single therapy that could also tackle Alzheimer’s and other tough neurological disorders.

Published

4 days ago

July 16, 2025

Veronic D.

The devastating effects of stroke can be irreversible, leading to loss of neurons and even death. However, researchers have made a groundbreaking discovery that may change this grim reality. A team led by Osaka Metropolitan University Associate Professor Hidemitsu Nakajima has developed a revolutionary drug called GAI-17, which inhibits the protein GAPDH involved in cell death.

GAPDH, or glyceraldehyde-3-phosphate dehydrogenase, is a multifunctional protein linked to various debilitating brain and nervous system diseases. The team’s innovative approach was to create an inhibitor that targets this protein, preventing its toxic effects on neurons. When administered to model mice with acute strokes, GAI-17 showed astonishing results: significantly reduced brain cell death and paralysis compared to untreated animals.

The significance of GAI-17 extends far beyond stroke treatment. Experiments revealed no adverse effects on the heart or cerebrovascular system, making it a promising candidate for addressing other intractable neurological diseases, including Alzheimer’s disease. Moreover, the drug demonstrated remarkable efficacy even when administered six hours after a stroke – a critical window that could revolutionize stroke care.

“We believe our GAPDH aggregation inhibitor has the potential to be a single treatment for many debilitating neurological conditions,” Professor Nakajima expressed. “We will continue to explore its effectiveness in various disease models and strive towards creating a healthier, longer-lived society.”

Brain Injury

Scientists Edge Closer to Reversing Parkinson’s Symptoms — A Breakthrough for Humans?

Scientists at the University of Sydney have uncovered a malfunctioning version of the SOD1 protein that clumps inside brain cells and fuels Parkinson’s disease. In mouse models, restoring the protein’s function with a targeted copper supplement dramatically rescued movement, hinting at a future therapy that could slow or halt the disease in people.

Published

2 weeks ago

July 6, 2025

Veronic D.

Here is the rewritten article:

Scientists have taken a groundbreaking step towards reversing Parkinson’s symptoms in mice, paving the way for potential treatments for humans. A team of researchers at the University of Sydney has identified a new brain protein involved in the development of Parkinson’s disease and found a way to modify it.

Parkinson’s disease is a degenerative neurological disorder that affects over 150,000 people in Australia alone, making it the second most common condition after dementia. The research team, led by Professor Kay Double from the Brain and Mind Centre, has spent more than a decade studying the biological mechanisms behind the condition.

In their latest study, published in Acta Neuropathologica Communications, the researchers found that targeting the faulty SOD1 protein with a drug treatment improved motor function in mice bred to have Parkinson-like symptoms. The mice treated with the special copper supplement showed significant improvements in their motor skills, which is a promising sign for potential human treatments.

Professor Double said: “We were astonished by the success of the intervention. We had hoped that treating this malfunctioning protein might improve the Parkinson-like symptoms in the mice, but even we were surprised by the dramatic improvement.”

The study involved two groups of mice: one group received the special copper supplement, while the other received a placebo. The results showed that the mice receiving the placebo experienced a decline in their motor symptoms, whereas those receiving the copper supplement did not develop movement problems.

Professor Double said: “The results were beyond our expectations and suggest that this treatment approach could slow the progression of Parkinson’s disease in humans.”

Parkinson’s disease is caused by the death of dopamine-producing cells in the brain, leading to a range of symptoms including tremors, muscle stiffness, slow movement, and impaired balance. Currently, there is no known cure, and only limited treatments are available.

The researchers hope that their discovery will lead to improved treatments for Parkinson’s disease. Professor Double said: “As our understanding of Parkinson’s disease grows, we are finding that there are many factors contributing to its development and progression in humans – and faulty forms of the SOD1 protein is likely one of them.”

Their next step is to identify the best approach to targeting the faulty SOD1 protein in a clinical trial, which could be the start of a new therapy to slow the development of Parkinson’s disease.

Alzheimer's

Groundbreaking Study Suggests Link Between Semaglutide and Lower Dementia Risk in Type 2 Diabetes Patients

A blockbuster diabetes and weight-loss drug might be doing more than controlling blood sugar—it could also be protecting the brain. Researchers at Case Western Reserve University found that people with type 2 diabetes who took semaglutide (the active ingredient in Ozempic and Wegovy) had a significantly lower risk of developing dementia. The benefit was especially strong in women and older adults.

Published

4 weeks ago

June 26, 2025

Veronic D.

A recent study by researchers at the Case Western Reserve School of Medicine has made an astonishing discovery that may revolutionize the way we approach dementia prevention. The research team found that semaglutide, a popular medication used to treat diabetes and aid in weight loss, could significantly lower the risk of dementia in people with type 2 diabetes (T2D).

Dementia is a devastating condition that affects millions worldwide, causing memory loss and cognitive decline. It occurs when brain cells are damaged, disrupting their connections and ultimately leading to this debilitating state. Encouragingly, studies indicate that approximately 45% of dementia cases could be prevented by addressing modifiable risk factors.

The study, published in the Journal of Alzheimer’s Disease, analyzed three years’ worth of electronic records from nearly 1.7 million T2D patients nationally. The researchers used a statistical approach that mimicked a randomized clinical trial to determine the effectiveness of semaglutide in preventing dementia.

Their findings suggest that patients prescribed semaglutide had a significantly lower risk of developing Alzheimer’s disease-related dementia compared to those taking other anti-diabetic medications, including GLP-1R-targeting medications. These results were even more pronounced in women and older adults.

Semaglutide, a glucagon-like peptide receptor (GLP-1R) molecule that decreases hunger and regulates blood sugar levels in T2D patients, has shown remarkable benefits beyond its primary use as a diabetes treatment. It also reduces the risk of cardiovascular diseases, further solidifying its potential in preventing dementia.

The study’s lead researcher, biomedical informatics professor Rong Xu, stated, “There is no cure or effective treatment for dementia, so this new study provides real-world evidence for its potential impact on preventing or slowing dementia development among at-high risk populations.”

While the findings are promising, it’s essential to note that further research through randomized clinical trials will be necessary to confirm the causal relationship between semaglutide and dementia prevention. Nevertheless, this groundbreaking study offers a glimmer of hope in the quest to combat dementia and improve the lives of millions worldwide.