Breaking New Ground: Immune System Discovery Offers Potential Solution to Alzheimer’s

A groundbreaking study has shed new light on the relationship between the immune system and Alzheimer’s disease. Researchers at the University of Virginia School of Medicine have discovered that an immune molecule called STING plays a crucial role in driving the formation of amyloid plaques and tau tangles, hallmarks of Alzheimer’s.

The study found that blocking STING activity in lab mice protected them from mental decline, suggesting a promising new target for developing treatments. This breakthrough has far-reaching implications for understanding and treating not only Alzheimer’s but also other neurodegenerative diseases like Parkinson’s disease, amyotrophic lateral sclerosis (ALS), and dementia.

“The findings demonstrate that the DNA damage that naturally accumulates during aging triggers STING-mediated brain inflammation and neuronal damage in Alzheimer’s disease,” said researcher John Lukens, PhD. “These results help to explain why aging is associated with increased Alzheimer’s risk and uncover a novel pathway to target in the treatment of neurodegenerative diseases.”

The study, published in Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association, involved a team of researchers from UVA’s Department of Neuroscience and Center for Brain Immunology and Glia (BIG Center). They found that removing STING dampened microglial activation around amyloid plaques, protected nearby neurons from damage, and improved memory function in Alzheimer’s model mice.

The discovery of STING as a key player in the development of neurodegenerative diseases opens new doors for research into potential treatments. While much more work is needed to translate these findings into effective therapies, this breakthrough has sparked hope among researchers and patients alike.

“Our hope is that this work moves us close to finding safer and more effective ways to protect the aging brain,” said Lukens. “Shedding light on how STING contributes to that damage may help us target similar molecules and ultimately develop effective disease-modifying treatments.”

Research has discovered that men who carry a common genetic variant are twice as likely to develop dementia in their lifetime compared to women. This groundbreaking study, published in Neurology, used data from the ASPirin in Reducing Events in the Elderly (ASPREE) trial to investigate whether people with variants in the haemochromatosis (HFE) gene might be at increased risk of dementia.

One in three people carry one copy of the H63D variant, while one in 36 carry two copies. Having just one copy of this gene variant does not impact someone’s health or increase their risk of dementia. However, having two copies of the variant more than doubled the risk of dementia in men, but not women.

The researchers emphasize that the genetic variant itself cannot be changed, but the brain pathways affected by it could potentially be treated if we understood more about it. Further research is needed to investigate why this genetic variant increased the risk of dementia for males but not females.

The findings suggest that perhaps testing for the HFE gene could be offered to men more broadly, considering its routine testing in most Western countries, including Australia, when assessing people for haemochromatosis – a disorder that causes the body to absorb too much iron. The study found no direct link between iron levels in the blood and increased dementia risk in affected men.

This points to other mechanisms at play, possibly involving the increased risk of brain injury from inflammation and cell damage in the body. Understanding why men with the double H63D variant are at higher risk could pave the way for more personalized approaches to prevention and treatment.

The ASPREE trial was a groundbreaking study that created a treasure trove of healthy ageing data, which has underpinned a wealth of research studies. This collaboration between Curtin University, Monash University, The University of Melbourne, The Royal Children’s Hospital, Murdoch Children’s Research Institute, and Fiona Stanley Hospital demonstrates the importance of diverse Australian research groups working together to improve health outcomes for people around the world.

The implications of this study are significant, considering that more than 400,000 Australians are currently living with dementia, with around a third of those being men. This discovery could lead to improved outcomes for people at risk of developing dementia and ultimately contribute to a better understanding of these progressive diseases.

The medical community has made a groundbreaking discovery in understanding how our bodies handle insulin. Researchers at the University of Copenhagen have found that each individual has a unique ‘molecular fingerprint’ for insulin sensitivity, which could revolutionize diabetes treatment and diagnosis.

In a recent study published in the scientific journal Cell, the team from the Novo Nordisk Foundation Center for Basic Metabolic Research, CBMR, collaborated with Karolinska Institutet in Sweden and Steno Diabetes Center in Denmark. They used cutting-edge protein analysis, known as proteomics, to study how insulin affects muscle tissue.

The researchers mapped molecular changes in muscle biopsies from over 120 individuals, revealing that certain proteins change consistently as insulin resistance develops. These ‘molecular signatures’ can help identify people at risk earlier than current clinical methods allow – even before symptoms appear.

“We found huge variation in insulin sensitivity, even among people considered healthy and among those diagnosed with type 2 diabetes,” says Associate Professor Atul Deshmukh from CBMR. “There are even some individuals living with type 2 diabetes who respond better to insulin than healthy individuals. Our study highlights the need to move beyond separating people into two boxes and recognize individual variation.”

The breakthrough could lead to more accurate diagnosis and treatment of type 2 diabetes, potentially even before the disease develops. By learning more about the molecular signatures of insulin resistance, researchers are building the foundation for precision medicine tailored to each patient.

“When we combine this deep, clinical data with the molecular signatures of insulin resistance, we suddenly understand a lot more about people’s insulin resistance that we can use to design precision medicine,” says Jeppe Kjærgaard Northcote, first author of the study and researcher at CBMR.

This revolutionary discovery has the potential to transform diabetes treatment and diagnosis, making it possible for healthcare professionals to provide personalized care to individuals based on their unique ‘molecular fingerprints.’