The devastating effects of spinal cord injuries have left millions without hope for recovery. However, groundbreaking research at Waipapa Taumata Rau, University of Auckland, has sparked new possibilities. Scientists have successfully used an implantable electronic device to restore movement in rats with spinal cord injuries, offering a glimmer of hope for humans and their pets.

Spinal cord injuries disrupt the communication between the brain and body, resulting in a loss of function. Unlike cuts on the skin, which typically heal on their own, the spinal cord does not regenerate effectively, making these injuries currently incurable. However, researchers have harnessed the same electrical guidance system that naturally occurs before birth to encourage nerve tissue growth along the spinal cord.

Lead researcher Dr. Bruce Harland explains, “We developed an ultra-thin implant designed to sit directly on the spinal cord, precisely positioned over the injury site in rats.” The device delivers a carefully controlled electrical current across the injury site, aiming to stimulate healing and restore lost functions.

In a 12-week study, rats that received daily electric field treatment showed improved movement and responded more quickly to gentle touch compared to those who did not. This indicates that the treatment supported recovery of both movement and sensation, with no signs of inflammation or damage to the spinal cord.

The new study, published in Nature Communications, is a result of a partnership between the University of Auckland and Chalmers University of Technology in Sweden. Long-term, the goal is to transform this technology into a medical device that could benefit people living with life-changing spinal-cord injuries.

“This study offers an exciting proof of concept showing that electric field treatment can support recovery after spinal cord injury,” says doctoral student Lukas Matter from Chalmers University. The next step is to explore how different doses and treatment regimens affect recovery, to discover the most effective recipe for spinal-cord repair.

The scientific community has made another groundbreaking discovery that reveals how our beloved morning coffee might be doing more than just waking us up. A recent study conducted by researchers at Queen Mary University of London’s Cenfre for Molecular Cell Biology sheds light on the potential anti-ageing properties of caffeine, the world’s most popular neuroactive compound.

The research, published in the journal Microbial Cell, delves into the intricate mechanisms within our cells and how they respond to stress and nutrient availability. The scientists used a single-celled organism called fission yeast as a model to understand how caffeine affects ageing at a cellular level.

One of the key findings was that caffeine doesn’t act directly on the growth regulator called TOR (Target of Rapamycin), which is responsible for controlling energy and stress responses in living things for over 500 million years. Instead, it works by activating another crucial system called AMPK, a cellular fuel gauge that is evolutionarily conserved in yeast and humans.

“When your cells are low on energy, AMPK kicks in to help them cope,” explains Dr Charalampos (Babis) Rallis, Reader in Genetics, Genomics, and Fundamental Cell Biology at Queen Mary University of London, the study’s senior author. “And our results show that caffeine helps flip that switch.”

The implications of this discovery are significant, as AMPK is also the target of metformin, a common diabetes drug being studied for its potential to extend human lifespan together with rapamycin. The researchers demonstrated using their yeast model that caffeine’s effect on AMPK influences how cells grow, repair their DNA, and respond to stress – all of which are tied to ageing and disease.

These findings open up exciting possibilities for future research into how we might trigger these effects more directly – with diet, lifestyle, or new medicines. So, the next time you reach for your coffee, remember that it might be doing more than just boosting your focus – it could also be giving your cells a helping hand in slowing down your ageing process.

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.