Age Tech World explores the latest research and science developments in the world of ageing and longevity.
AI tool developed to predict markers of Alzheimer’s disease
Researchers have built an AI tool that can accurately predict key signs of Alzheimer’s disease.
The markers the AI is able to predict include the presence of sticky proteins called amyloid beta and tau, using common and less expensive tests like brain scans, memory checks and health records.
The team gathered information from seven different cohorts, totaling 12,185 participants, including their age, health history, memory test scores, genetic information and brain scans.
They then trained an AI model on this data to learn patterns that match the presence of sticky proteins seen in expensive scans and even designed the model to work if some of the information was missing, and tested it on a separate group of people not used in training and found that the AI correctly predicted who had high amyloid or tau levels.
“While popular new blood tests can somewhat detect signs of Alzheimer’s, they can’t reveal exactly where in the brain the issues are occurring – unlike our AI tool, which provides important location-specific detail,” said corresponding author Vijaya Kolachalama, associate professor of medicine and computer science at Boston University.
Kolachalama believes this tool could make checking for Alzheimer’s disease easier and less costly for everyone.
“The tool can help doctors quickly pick people for treatment with new drugs or to participate in research studies, thus saving time and money while reaching more patients who might not have access to costly and complicated tests,” he said.
“For the public, this means faster diagnoses, fewer unnecessary exams and hope for treatments that slow the disease, improving daily life for those affected and their loved ones.”
According to the researchers, this study suggests AI could also change how we stage the disease, spotting it early before symptoms get bad, which might lead to personalised plans, like custom diets or exercises to slow it down.
Additionally, the team say that, one day, this tool could impact other disorders with similar protein issues, like frontotemporal dementia, a type of brain shrinkage causing personality changes and chronic traumatic encephalopathy, brain damage from head injuries, common in athletes.
Groundbreaking exercise programme for older adults at risk of mobility loss
The University of Birmingham is joining the national roll out of the REACT (REtirement in ACTion) exercise programme that will be made available to older people at higher risk of mobility-related disability.
The programme has three-year funding of over £1m, and older people in regions around England will soon be able to benefit from the group-based exercise programme that has been proven to support people to improve and maintain their mobility and ability to live independently.
The funding has been provided by the Vivensa Foundation, and the REACT programme will now be scaled up in two regions of England including North Central London and Bristol, North Somerset and South Gloucestershire.
A team of researchers from the Universities of Birmingham and Bath will work in partnership with local Integrated Care Boards, voluntary sector organisations including Age UK Bristol and groups of older people.
Backed by a major clinical trial funded by the National Institute for Health Research (NIHR), REACT has already been shown to significantly improve older adults’ physical function for at least two years and reduce health and social care costs.
Professor Afroditi Stathi, lead researcher from the University of Birmingham, said: “As people get older their physical functioning and mobility decrease, in fact, studies show that one in three older people will develop severe mobility limitations.
“This affects their health, ability to live independently, their quality of life and even how long they live.
“The REACT study provided strong evidence that this decline can be slowed and even reversed. We have a duty to accelerate the implementation of research, with such strong findings, into routine practice.
“The REACT programme has already been very successful in reaching economically disadvantaged and ethnically diverse communities in a small-scale community roll-out in Bristol.
“This new study will help us bridge the gap between research and real-world delivery, ensuring more older people across the UK can benefit from evidence-based support. Our goal is to create a national blueprint for commissioning and scaling REACT.”
Nuclear speckle rejuvenation “next frontier” for treating neurodegeneration
New research reveals that targeting cellular structures called nuclear speckles could be a completely new approach for treating proteinopathies – diseases driven by abnormal accumulation of misfolded proteins such as Alzheimer’s, Parkinson’s and prion diseases.
“Our research is painting a picture where dysregulation of nuclear speckles is important for neuron degeneration in the context of many diseases,” said senior author Bokai Zhu, assistant professor in University of Pittsburgh’s Department of Medicine and the Aging Institute.
“The concept of rejuvenating nuclear speckles to treat these diseases is completely novel, but I believe it’s the next frontier of neurodegenerative research.”
Nuclear speckles are structures within cell nuclei that regulate proper protein production, folding and degradation, a balance known as proteostasis. Zhu’s previous research found that nuclear speckle shape affects function: more spherical speckles were linked with worse proteostasis than irregularly shaped ones.
Hypothesising that drugs that make nuclear speckles less round could treat proteinopathies, Zhu’s team screened hundreds of FDA-approved drugs. When they measured the effects on nuclear speckle sphericity, one stood out: pyrvinium pamoate, originally approved for treating pinworm infections.
They found that pyrvinium pamoate improved proteostasis within cells in a dish, found first author William Dion, a former graduate student in Zhu’s lab.
“We were thrilled that our hypothesis was correct,” said Zhu. “This led us to ask: Does this drug work in disease models, and how does it work?”
Promising Disease Model Results
Zhu collaborated with Xu Chen at UC San Diego, who studies tauopathies – diseases driven by tau protein buildup in the brain, causing memory, cognitive and locomotive deficits.
In mouse neurons expressing human tau, pyrvinium pamoate reduced the pathological protein by about 70 per cent.
Human neurons carrying a frontotemporal dementia-associated tau mutation had abnormally shaped nuclear speckles and elevated tau levels.The researchers showed that low doses of the drug restored nuclear speckle shape and dramatically reduced tau levels without causing cellular stress or toxicity.
In fly models of tauopathy, locomotive symptoms can be measured by assessing climbing ability. Adding pyrvinium pamoate greatly improved climbing prowess in both larvae and adult flies – important evidence of the drug’s effectiveness in living creatures.
In experiments, the researchers used mouse retinas cultured in a dish to show that the drug held promise for treating retinitis pigmentosa, a disease caused by a faulty gene that leads to misfolding of the retinal protein rhodopsin, which clogs up the rod cells of the eye and causes progressive vision loss.
To understand how the drug works, the team carried out experiments with optical tweezers, which use lasers to precisely manipulate microscopic structures.
Nuclear speckles were typically difficult to stretch because of high surface tension, but adding the drug dramatically lowered surface tension, making speckles easy to stretch and rupture.
According to Zhu, when nuclear speckles have lower surface tension, they become less round and spread out to make better contact with chromosomes, leading to greater production of genes regulating proteostasis.
Zhu hopes to move this research into clinical trials soon to test whether pyrvinium pamoate could effectively treat proteinopathies in humans.
New gene linked to aggressive, treatment-resistant prostate cancer
In a new study, researchers have investigated a group of genes known as the R-spondin family in advanced prostate cancer. The RSPO gene family regulates Wnt signaling, a pathway involved in cancer progression.
Prostate cancer is the most common cancer among men in the United States and becomes especially dangerous when it spreads beyond the prostate. Most patients are treated with hormone therapies that target the androgen receptor; however, many tumours eventually become resistant.
The research team analysed thousands of tumour samples and found that RSPO2 alterations were more common than changes in other R-spondin genes or even some well-known cancer-related genes like CTNNB1 and APC.
RSPO2 amplification occurred in over 20 per cent of metastatic prostate cancer. Patients with these alterations showed signs of more aggressive disease, including higher mutation rates and greater tumour complexity.
Using laboratory models, the team discovered that RSPO2 increases cancer cell growth and triggers a biological process called epithelial-mesenchymal transition (EMT). EMT is known to promote tumour spread and resistance to standard treatments.
Unlike other genes in the same pathway, RSPO2 also appeared to reduce the activity of androgen receptor genes, suggesting it drives a type of prostate cancer that no longer relies on hormones for growth.
Importantly, RSPO2 showed structural differences from other R-spondin proteins, which may allow researchers to design drugs that specifically block its activity. Current therapies targeting the Wnt pathway are limited, and there are no approved drugs that inhibit RSPO2.
However, this study highlights RSPO2 as a promising therapeutic target, especially for patients who do not respond to existing hormone-based treatments.