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Nanoparticles target disease proteins in dementia

Scientists have developed a nanoparticle strategy to broaden which disease-causing proteins medicines can target, giving options for dementia and brain cancer.
A perspective outlines an approach designed to remove harmful proteins that drive disease. By broadening the proteins that can be treated, the technology could help tackle conditions such as dementia and brain cancer.
The work was led by chair professor in nanomedicine Bingyang Shi at the University of Technology Sydney, in collaboration with professor Kam Leong of Columbia University and professor Meng Zheng of Henan University.
Professor Shi said: “Proteins are essential for nearly every function in the body, but when they become mutated, misfolded, overproduced or build up in the wrong place, they can disrupt normal cell processes and trigger disease.
He added: “Many conditions, including cancer, dementia, and autoimmune disorders, are driven by abnormal proteins, and some have shapes or behaviours that make them particularly resistant to drug treatments.”
To tackle these challenges, the researchers created a type of engineered nanoparticle called nanoparticle-mediated targeting chimeras (NPTACs).
The particles are designed to recognise specific disease-associated proteins and promote their breakdown in the body.
Professor Shi said: “We have developed an efficient and flexible method to guide disease-causing proteins, whether inside or outside the cell, into the body’s natural recycling system, where they can be broken down and removed.”
Interest in targeted protein degradation has surged in recent years.
Companies such as Arvinas have attracted more than US$1bn in investment and formed partnerships with pharmaceutical firms including Pfizer, Bayer and Roche.
However, existing protein degradation technologies face limitations.
Challenges such as poor tissue penetration, unintended interactions with other proteins and complex chemical design have slowed their use, particularly for brain disorders and solid tumours.
Professor Shi said: “Our nanoparticle-based strategy overcomes these bottlenecks.”
The researchers say the NPTAC platform can enable degradation of both proteins inside and outside cells, offers tissue and disease-specific targeting including across the blood-brain barrier (the protective barrier around the brain), and has plug-and-play modularity to adapt to diverse protein targets.
They say it is scalable and clinically translatable, leveraging FDA-approved nanomaterials and industry-proven synthesis strategies, and can combine with diagnostic or therapeutic capabilities.
Protected by multiple international patents, NPTACs have shown preclinical results against targets such as EGFR (a protein often driving tumour growth) and PD-L1 (a protein that helps cancer cells evade the immune system).
Professor Shi said: “This progress paves the way for applications in oncology, neurology, and immunology. It changes how we think about nanoparticles, not only as delivery tools but also as active therapeutic agents.
He added: “With the targeted protein degradation market expected to surpass $10 billion USD by 2030, NPTACs provide a powerful platform for the next generation of smart, precision therapies.
“We are now seeking strategic industry partners to accelerate clinical development, licence applications across therapeutic fields, and prepare for regulatory approval.”
News
French biotech raises €12m for osteoarthritis trial

A French biotech has raised €12m to test whether GLP-1 drugs can modify osteoarthritis progression.
The funding will advance 4Moving Biotech’s lead programme, 4P004, toward a phase 2a proof-of-concept readout in knee osteoarthritis, a joint disease that causes pain and stiffness.
Despite affecting more than 600 million people worldwide, no therapy approved in Europe or the US has yet been shown to slow or modify disease progression in osteoarthritis.
4Moving Biotech is testing whether GLP-1 receptor agonists, drugs best known for diabetes and obesity, can succeed where others have fallen short.
“With this closing in place, we are well equipped to reach the next value-creation milestone by delivering robust phase 2a data and reaching a proof-of-concept inflection point,” said Luc Boblet, chief executive of 4Moving Biotech.
Rather than systemic administration, the company is testing whether GLP-1 biology can be made relevant to osteoarthritis by acting directly in the joint, targeting local inflammation and tissue responses that systemic approaches have repeatedly failed to address.
“By acting directly in the joint, 4P004 tackles pain, inflammation and tissue damage through GLP-1-mediated pathways,” said professor Francis Berenbaum, the company’s chief medical officer.
The study is designed to assess “dual efficacy: symptom relief and synovial health improvement via contrast-enhanced MRI,” which images the joint lining, with topline results expected in the second half of 2026.
The round was secured from private investors and family offices investing directly into 4Moving Biotech, a subsidiary of 4P-Pharma, and combines equity with loans, a structure the company says is aligned with long-term value creation.
It follows a €7.6m France 2030 i-Démo grant awarded last year and coincides with the transatlantic expansion of the INFLAM-MOTION phase 2a study to the US.
Founded in 2020 as a spin-off from 4P-Pharma, 4Moving Biotech has now raised around €30m in total, combining private capital with non-dilutive public funding.
The broader landscape for disease-modifying osteoarthritis drugs offers little room for overconfidence.
A 2025 review of phase two and three osteoarthritis trials found that while “many DMOADs have progressed to clinical trials, very few have made a significant impact and none have been approved for clinical use.
Reviewing eleven candidates tested between 2010 and 2024, including small molecules, biologics and cell or gene-based therapies, authors conclude that failure has been driven less by any single mechanism than by the difficulty of demonstrating truly disease-modifying benefit.
Several programmes reported statistically significant effects on either pain or joint structure, but rarely both.
The review notes that “the clinical relevance of a marginal increase in one without the other remains unclear,” warning that structural effects without symptom relief may be clinically meaningless, while pain relief without structural protection could even accelerate disease progression.
Over the past decade, major programmes at Pfizer, Eli Lilly, AbbVie, GlaxoSmithKline and Sanofi have been discontinued or deprioritised after failing to deliver regulator-acceptable evidence of disease modification.
In 2020, Unity Biotechnology reported phase two data showing that its senolytic candidate UBX0101, developed as a disease-modifying therapy for knee osteoarthritis, failed to deliver clinically meaningful improvements in pain or joint structure.
Unity subsequently discontinued its osteoarthritis programme, exited the field entirely and ceased operations in 2025.
The phase 2a readout will be the point at which the GLP-1 approach in osteoarthritis either earns its next chapter or joins a long list of programmes that fell short.
News
Test predicts dementia risk years earlier

An EEG test can identify dementia risk five to seven years before progression to mild cognitive impairment or Alzheimer’s dementia, new research suggests.
Using EEG data, which measures the brain’s electrical activity, from older adults with only subjective memory concerns, the longitudinal study found this non-invasive test can flag functional changes long before standard tools detect disease.
Researchers collected baseline resting EEG recordings from 88 older adults who had subjective cognitive impairment (self-reported decline without a clinical diagnosis of mild cognitive impairment, early memory problems or dementia).
The study was conducted by BrainScope, a commercial-stage neurotechnology company in Maryland, US, which applies artificial intelligence and computational neuroscience to brain electrical signals.
Participants then received annual clinical assessments and staging of cognitive decline. Over time, some progressed to mild cognitive impairment or dementia, while others remained cognitively normal.
Using BrainScope’s proprietary EEG-based biomarker platform, researchers identified distinct brain-activity patterns at the initial visit that accurately predicted future decline.
BrainScope’s EEG biomarker achieved an area under the curve (AUC) of 0.90, a measure of diagnostic accuracy, and performance was validated across independent international cohorts.
The findings suggest that with BrainScope’s signal processing and AI-enabled analytics, EEG could serve as a rapid, affordable and non-invasive assessment to identify Alzheimer’s-related brain dysfunction years before meaningful memory loss.
Early identification matters because by the time traditional imaging detects Alzheimer’s pathology, significant and often irreversible neurological damage may already have occurred.
Identifying risk earlier also fits a fast-evolving therapeutic landscape in which many disease-modifying therapies and prevention trials require people to be found years before conventional diagnosis.
Earlier awareness can help individuals and families pursue evidence-based lifestyle changes, proactive care planning and research participation, shifting care from reactive management to earlier intervention.
“The rapid evolution of Alzheimer’s therapeutics demands equally innovative biomarkers.” Howard Fillit, co-founder and chief science officer of the Alzheimer’s Drug Discovery Foundation, said.
“As the field moves towards more complex, combination therapy strategies and precision prevention, tools like BrainScope’s will play a critical role in early risk identification and enabling a tailored approach to treatment.” Fillit said.
Key funding for the biomarker’s development was provided by the Alzheimer’s Drug Discovery Foundation, whose early support BrainScope credits as instrumental in achieving this milestone.
The foundation has a longstanding record of advancing Alzheimer’s diagnostics, including early support for technologies such as the first amyloid PET scan and the first blood-based biomarker test for the disease.
“At BrainScope, our mission has always been to translate the brain’s electrical signals into clinically meaningful insights and build the platform that becomes the brain’s vital sign,” Matt Adams, chief executive of BrainScope, said.
“This publication in Scientific Reports validates years of research using EEG to detect functional brain changes in normal elderly with subjective cognitive complaints,” Leslie Prichep, chief scientific officer of BrainScope and first author of the study, said.
“The importance of identifying risk of future cognitive decline, long before structural damage occurs, can have significant impact on brain health in the elderly early enough to meaningfully change outcomes.”
BrainScope is expanding its AI-enabled EEG platform into new clinical indications, including neurodegenerative diseases and stroke.
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