Research reveals new insights into retinal thickness that may detect type 2 diabetes, dementia early
Parkville: : Researchers have conducted one of the largest eye studies in the world to reveal new insights into retinal thickness, highlighting its potential in the early detection of diseases like type 2 diabetes, dementia and multiple sclerosis.
The Walter and Eliza Hall Institute (WEHI) led study used cutting-edge artificial intelligence technology to analyse over 50,000 eyes and produced maps of the retina in unprecedented detail to better understand how retinal differences link to various diseases.
The retina is part of the central nervous system, which also comprises the brain and spinal cord. Many diseases are linked to degeneration or disruption of this critical system, including neurodegenerative conditions such as dementia and metabolic disorders like diabetes.
Sported by AI, the research has created the most detailed maps of the retina ever produced.
WEHI researchers have used these maps to link retinal thinning to a range of diseases as well as identifying new genetic factors that influence retinal thickness.
The findings could pave the way for routine eyecare imaging as a disease screening tool. Unlocking a window into the brain..
Lead researcher, WEHI's Dr Vicki Jackson, said the findings broaden the horizons for using retinal imaging as a doorway into the central nervous system, to help manage disease.
"We've shown that retinal imaging can act as a window to the brain, by detecting associations with neurological disorders like multiple sclerosis and many other conditions," said Dr Jackson, a statistician and gene expert.
"Our maps' fine-scale measurements reveal critical new details about connections between retinal thinning and a range of common conditions."
The study also identified new genetic factors that influence retinal thickness, which are likely to play a role in the growth and development of a person's retina.
"This research underscores the potential for retinal thickness to act as a diagnostic biomarker to aid in detecting and tracking the progression of numerous diseases. We can now pinpoint specific locations of the retina which show key changes in some diseases."
The international research team, led by WEHI, applied AI methods to big population data of retinal imaging and compared information about each person's genetics and health to reveal unprecedented links to disease.
The results created 50,000 maps with measurements at over 29,000 locations across the retina, identifying retinal thinning relating to 294 genes that play an important role in disease.
Sign up for the Daily Briefing
Get the latest news and updates straight to your inbox
Try Our AI Features
Explore what Daily8 AI can do for you:
Comments
No comments yet...
Related Articles
Gulf News
16-03-2025
- Gulf News
AI could predict true biological age from 5 drops of blood
New Delhi: Scientists at Osaka University in Japan have devised a new AI model to estimate a person's biological age — a measure of how well their body has aged, rather than just counting the years since birth. Using just five drops of blood, this new method analyses 22 key steroids and their interactions to provide a more precise health assessment. The team's breakthrough study, published in Science Advances, offers a potential step forward in personalised health management, allowing for earlier detection of age-related health risks and tailored interventions. 'Our bodies rely on hormones to maintain homeostasis, so we thought, why not use these as key indicators of aging?' said Dr Qiuyi Wang, co-first author of the study. To test this idea, the research team focused on steroid hormones, which play a crucial role in metabolism, immune function, and stress response. The team developed a deep neural network (DNN) model that incorporates steroid metabolism pathways, making it the first AI model to explicitly account for the interactions between different steroid molecules. One of the study's most striking findings involves cortisol, a steroid hormone commonly associated with stress. The researchers found that when cortisol levels doubled, biological age increased by approximately 1.5 times. This suggests that chronic stress could accelerate aging at a biochemical level, reinforcing the importance of stress management in maintaining long-term health. 'Stress is often discussed in general terms, but our findings provide concrete evidence that it has a measurable impact on biological aging,' said Professor Toshifumi Takao, a corresponding author and an expert in analytical chemistry and mass spectrometry. The researchers believe this AI-powered biological age model could pave the way for more personalised health monitoring. Future applications may include early disease detection, customised wellness programmes, and even lifestyle recommendations tailored to slow down aging. Sign up for the Daily Briefing Get the latest news and updates straight to your inbox
Gulf Today
15-03-2025
- Gulf Today
Scientists make life-changing discovery on treating Parkinson's disease
Scientists have made a potentially 'life-changing' discovery that could pave the way for new drugs to treat Parkinson's disease. Experts have known for several decades that the PINK1 protein is directly linked to Parkinson's disease – the fastest growing neurodegenerative condition in the world. Until now, no one has seen what human PINK1 looks like, how PINK1 attaches to the surface of damaged mitochondria inside of cells, or how it is activated. But scientists have now discovered how the mutation switches on and can start using this knowledge to find a way to switch it off and slow the progression of the condition down. Researchers at the Walter and Eliza Hall Institute, Parkinson's Disease Research Centre, in Australia, have solved the decades-long mystery. The findings published in the journal Science reveal for the first time ever the structure of PINK1 and how it binds to mitochondria – the powerhouse of a cell – and stops it functioning properly. Parkinson's disease can take years, sometimes decades to diagnose. Often associated with tremors, there are close to 40 symptoms including cognitive impairment, speech issues, body temperature regulation and vision problems. The neurological condition affects around 153,000 Britons. There is currently no cure for Parkinson's, although medicine, physiotherapy and surgery can help manage symptoms. Death of brain cells One of the hallmarks of Parkinson's is the death of brain cells. Around 50 million cells die and are replaced in the human body every minute. But, unlike other cells in the body, when brain cells die, the rate at which they are replaced is extremely low. When mitochondria are damaged, they stop making energy and release toxins into the cell. In a healthy person, the damaged cells are disposed of in a process called mitophagy. In a person with Parkinson's and a PINK1 mutation, the mitophagy process no longer functions correctly and toxins accumulate in the cell, eventually killing it. Brain cells need a lot of energy and are especially sensitive to this damage. In particular, PINK1 has been linked to young-onset Parkinson's Disease, which affects people under the age of 50. Despite the known link, researchers have previously been unable to visualise the protein or how it works. 'This is a significant milestone for research into Parkinson's. It is incredible to finally see PINK1 and understand how it binds to mitochondria,' said Professor David Komander, corresponding author on the study. 'Our structure reveals many new ways to change PINK1, essentially switching it on, which will be life-changing for people with Parkinson's,' he added. 4 steps Lead author on the study, Dr Sylvie Callegari, said PINK1 works in four distinct steps, with the first two steps not having been seen before. First, PINK1 senses mitochondrial damage. Then, it attaches to damaged mitochondria. Once attached, it links to a protein called Parkin so that the damaged mitochondria can be recycled. 'This is the first time we've seen human PINK1 docked to the surface of damaged mitochondria, and it has uncovered a remarkable array of proteins that act as the docking site. We also saw, for the first time, how mutations present in people with Parkinson's disease affect human PINK1,' said Dr Callegari. The idea of using PINK1 as a target for potential drug therapies has long been touted but not yet achieved because the structure of PINK1 and how it attaches to damaged mitochondria were unknown. The research team hope to use the knowledge to find a drug to slow or stop Parkinson's in people with a PINK1 mutation. Researchers in the UK also believe the discovery could lead to better drug design. Consultant neurologist Dr Richard Ellis said: 'It is a crucial step towards understanding the impact of PINK1 in Parkinson's disease. These observations may hopefully create new opportunities for developing novel strategies for slowing the progression of Parkinson's disease.' Dr Zhi Yao, research scientist, Life Arc, said: 'A robust understanding of these aspects could present a significant opportunity for accelerating drug discovery for Parkinson's disease and potentially other neurodegenerative conditions too.' Becky Jones, research communications manager at Parkinson's UK, said: 'Changes in the PINK1 have long been linked to Parkinson's, and a specific mutation in the gene that contains the instructions for making the protein are known to cause a rare inherited form of the condition. 'It's encouraging to see this research, which will help us understand how changes in PINK1 might be causing damage to dopamine-producing brain cells in people with Parkinson's. 'This knowledge unlocks future avenues for better drug design and discovery of a treatment that could slow or even stop Parkinson's progression. This is vital, as despite it being the fastest growing neurological condition in the world, we don't yet have any drug treatments that can do this.'
Gulf News
10-03-2025
- Gulf News
Sleep debt, night shifts can raise infection risk: Study
New Delhi: Sleep debt and night shifts increase the risk of several common infections, according to a study on Monday. According to researchers from Norway, sleep debt, defined as the gap between sleep need and actual sleep duration, increased infection risk in a dose-dependent manner. The study, published in the journal Chronobiology International, examined the effects of sleep patterns and shift work on the immune system among 1,335 nurses from Norway. The findings showed that shift work - particularly night shifts - was associated with a higher risk of several infections, including the common cold. The risk of pneumonia/bronchitis was 129 per cent higher for nurses with moderate sleep debt and 288 per cent for severe sleep debt. Both sinusitis and gastrointestinal infections also showed higher risks with increasing levels of sleep debt. "These findings highlight the need for tailored interventions to reduce infection risks among healthcare workers," said Siri Waage, from the Norwegian Competence Center for Sleep Disorders, Haukeland University Hospital, Bergen. "Sleep debt and irregular shift patterns, including night work, not only compromise nurses' immune health but could also impact their ability to provide high-quality patient care," Waage added. In the study, the participants -- mostly female nurses (90.4 per cent), with an average age of 41.9 years -- reported their sleep duration, sleep needs, shift work patterns, and how often they had experienced specific infections over the past three months. Nurses with moderate sleep debt (one to 120 minutes less sleep than needed) had a 33 per cent higher risk of the common cold, while those with severe sleep debt (more than two hours) had more than double compared to those with no sleep debt. The analysis also revealed that night work was linked with an increased risk of the common cold, but was not associated with any of the other infections examined. The study emphasises the importance of adequate sleep and shift management in reducing susceptibility to infection. Sign up for the Daily Briefing Get the latest news and updates straight to your inbox
