Monthly Archives: March 2026

Researchers uncover a promising new drug target for Alzheimer’s disease

Scientists at Indiana University School of Medicine have uncovered a promising new therapeutic target for Alzheimer’s disease, offering a potential fresh direction for treatment development. Their research shows that removing a specific enzyme from neurons in the brain can dramatically reduce amyloid plaques, one of the defining pathological features of the disease. Beyond lowering plaque levels, this approach may also strengthen the brain’s resilience to ongoing neurodegeneration, raising hope for more durable clinical benefits.

In recent years, progress in Alzheimer’s treatment has begun to accelerate. The U.S. Food and Drug Administration has approved two disease-modifying therapies, lecanemab and donanemab, which work by clearing amyloid plaques from the brain. These drugs have shown that it is possible to slow disease progression and stabilise patients at their current level of function. However, their effects are limited, and there remains an urgent need for alternative strategies that target the disease through different biological mechanisms.

The Indiana University team, led by Hande Karahan and Jungsu Kim, focused on an enzyme known as IDOL. Their findings suggest that suppressing IDOL specifically in neurons offers a new way to reduce amyloid accumulation while also improving communication between brain cells and regulating lipid metabolism. According to the researchers, this dual effect could be particularly valuable, as Alzheimer’s disrupts not only protein clearance but also fundamental cellular signalling and metabolic balance in the brain.

Kim emphasised that the appeal of IDOL lies in its suitability as a drug target. Enzymes have clearly defined active sites, which makes it possible to design highly specific molecules that block their activity. This precision increases the likelihood of developing treatments that are both effective and associated with fewer side effects. The identification of IDOL, therefore, opens the door to an entirely new class of therapeutic compounds aimed at Alzheimer’s disease.

To explore how IDOL functions in different brain cell types, the researchers created two animal models of Alzheimer’s disease. In one, the IDOL gene was deleted from neurons, while in the other, it was removed from microglia, the brain’s immune cells. The team initially expected microglia to play the dominant role in clearing amyloid, as immune cells are known to be heavily involved in plaque removal and are the primary producers of IDOL in the brain.

Unexpectedly, the most striking effects were seen when IDOL was removed from neurons. This intervention not only reduced amyloid plaques but also lowered levels of apolipoprotein E, a protein strongly linked to Alzheimer’s risk and disease progression. In addition, receptors involved in lipid metabolism and healthy neuronal communication increased in abundance, suggesting broader protective effects. Previous research has shown that activating related pathways can help preserve cognitive function even in patients with high plaque burdens.

From a clinical perspective, these findings are especially significant. Most patients are diagnosed only after substantial amyloid accumulation has already occurred. An approach that both lowers amyloid levels and enhances the brain’s resilience to existing pathology could therefore maximise therapeutic impact. Looking ahead, Kim and his colleagues plan to develop and test compounds that inhibit IDOL, carefully assessing their safety and effects in preclinical models. They will also investigate whether targeting this enzyme can preserve synaptic connections and reduce tau pathology, two critical factors in the progression of Alzheimer’s disease.

More information: Hande Karahan et al, Deletion of neuronal Idol ameliorates Alzheimer’s disease–related pathologies via APOE receptors, Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association. DOI: 10.1002/alz.70949

Journal information: Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association Provided by Indiana University

Fall-prevention efforts in emergency departments could benefit older adults once they return home

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Falls are among the most frequent reasons older adults seek care in emergency departments, and many of these patients are sent home on the very same day. The point of discharge can be particularly risky, as the underlying causes of a fall are not always fully explored or managed during a brief hospital visit. Emerging evidence now indicates that emergency departments can use this critical window to introduce practical measures that help older adults remain safer once they return home.

These insights come from the GAPcare II trial, titled Emergency Department Visit Outcomes of a Multicentre Randomised Trial of a Fall Prevention Intervention, published in Academic Emergency Medicine. The study examined whether a structured fall-prevention programme could realistically be delivered during emergency department visits for adults aged 65 and over who had experienced an accidental fall within the previous seven days. All participants were expected to be discharged and did not have injuries that severely limited mobility. In total, 852 patients took part in the intervention, which combined assessments by physical therapists with medication reviews conducted by pharmacists.

The research demonstrated that these assessments could be completed during the emergency visit and resulted in tailored recommendations for individual patients. Interventions included advice on mobility support, changes to medication regimens, and referrals for further care after discharge. Participants received consultations at the bedside from both pharmacists and physical therapists, allowing recommendations to be integrated directly into the emergency care process rather than deferred to a later setting.

Pharmacists frequently suggested practical medication-related changes that could reduce fall risk. These included adjusting the timing of medications for 26 per cent of patients, discontinuing medications associated with increased fall risk in 19 per cent of cases, and modifying dosages for a further 18 per cent. Physical therapists focused on functional support and follow-up needs, recommending assistive devices for two-thirds of patients, outpatient therapy services for over a third, and admission to a skilled nursing facility for a quarter of those assessed.

Commenting on the findings, Sarah D. Berry, MD, MPH, emphasised that a fall is rarely an isolated event. Instead, it often signals unresolved health issues or environmental hazards that require attention. She noted that the study illustrates how emergency departments can move beyond simply addressing the immediate injury, helping to identify modifiable risk factors and equipping patients and caregivers with a clearer plan to reduce the likelihood of future falls once they return home.

Although the trial was primarily designed to assess how feasible the programme was to implement, rather than to measure long-term outcomes such as repeat falls or hospitalisations, the results underscore the potential of emergency departments as an important point of intervention. By integrating fall-prevention strategies into routine emergency care, hospitals can play a meaningful role in supporting safer recovery and independence for older adults after discharge.

More information: Elizabeth M. Goldberg et al, Emergency Department Visit Outcomes of a Multicenter Randomized Trial of a Fall Prevention Intervention, Academic Emergency Medicine. DOI: 10.1111/acem.70228

Journal information: Academic Emergency Medicine Provided by Hebrew SeniorLife Hinda and Arthur Marcus Institute for Aging Research

Advancing Bone Healing in Older Adults Through Non-Invasive Therapy

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Bone repair is a complex but carefully organised biological process that depends on stem and progenitor cells to rebuild damaged tissue. In younger people, these cells respond quickly after a fracture, maturing into osteoblasts, the specialised cells responsible for forming new bone. This rapid response allows broken bones to knit together efficiently and regain strength. With increasing age, however, this process becomes much slower and less reliable. Doctors have long recognised that fractures in older adults take longer to heal and are more likely to lead to complications, yet the underlying biological reasons have remained poorly understood.

This slowdown in healing is becoming an increasingly serious problem as populations age worldwide. Fractures among older adults often result in extended hospital stays, reduced mobility, and lasting loss of independence. Until recently, most treatments have focused on stabilising bones surgically rather than improving the body’s own ability to regenerate tissue. As a result, scientists have been searching for the molecular signals that actively interfere with bone repair during ageing, in the hope that targeting these signals could restore the body’s natural healing capacity.

Recent research has identified a key player in this age-related decline: apolipoprotein E, or ApoE. ApoE is a protein best known for its role in lipid transport and is produced mainly by the liver. The study found that levels of ApoE in the bloodstream rise with age and that this increase has a direct negative effect on bone healing. Rather than helping repair, ApoE acts as a systemic inhibitor, interfering with the signals that normally drive stem and progenitor cells to become bone-forming osteoblasts.

To understand how this happens, researchers compared fracture healing in young and aged animal models using a combination of molecular, cellular, and tissue-level analyses. They observed that higher ApoE levels in older subjects suppressed a key signalling pathway known as β-catenin signalling within bone marrow stromal cells. This pathway is essential for pushing immature cells towards an osteoblast fate. When β-catenin signalling is blocked, these progenitor cells stall before fully maturing, leaving the repair process incomplete and fragile.

The study also revealed how ApoE exerts this effect. ApoE binds to a receptor on bone marrow stromal cells called Lrp4, which disrupts downstream β-catenin activity and effectively places a molecular “brake” on bone formation. When researchers used antibodies to block ApoE, this brake was released. β-catenin signalling resumed, osteoblast formation increased, and fracture healing improved significantly. Notably, aged animals treated in this way formed stronger, more complete bone calluses, closely resembling the quality of healing normally seen in much younger individuals.

Perhaps most striking was how reversible the process appeared to be. Even in advanced age, bone-forming cells retained their ability to regenerate once the inhibitory influence of ApoE was removed. This suggests that ageing does not permanently damage the bone’s regenerative machinery but instead suppresses it through circulating signals. The findings also highlight the unexpected role of the liver in controlling skeletal repair, showing that organs far from the injury site can strongly influence healing outcomes.

Together, these results reshape how ageing-related bone repair is understood. By identifying a circulating protein that actively suppresses regeneration, the research opens the door to new, non-invasive therapies aimed at neutralising systemic inhibitors rather than directly manipulating bone tissue. Such approaches could significantly improve fracture healing in older adults, reduce complications, and help preserve mobility and quality of life in an ageing society.

More information: Mingjian Huang et al, Neutralizing hepatic apolipoprotein E enhances aged bone fracture healing, Bone Research. DOI: 10.1038/s41413-025-00489-y

Journal information: Bone Research Provided by Editorial Office of West China School of Stomatology, Sichuan University

South Asian adults in the U.S. show heart disease risk factors at younger ages

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South Asian adults living in the United States were more likely to have risk factors for atherosclerotic cardiovascular disease (ASCVD) by the age of 45 compared with white, Black, Chinese and Hispanic adults of the same age, according to new research published in the Journal of the American Heart Association. ASCVD risk factors, when left untreated or poorly managed, can contribute to the earlier development of heart disease, underscoring the importance of timely detection and prevention.

To explore the reasons behind this increased risk, researchers examined health data from approximately 2,700 adults aged 45 to 55 who participated in two large, national studies conducted in the United States. These long-term studies followed diverse populations from different regions of the country: the Mediators of Atherosclerosis in South Asians Living in America (MASALA) Study and the Multi-Ethnic Study of Atherosclerosis (MESA). By comparing data across these cohorts, investigators were able to assess how cardiovascular risk factors emerged and progressed across ethnic groups.

The MASALA Study, led by research teams at Northwestern University in Chicago and the University of California, San Francisco, focused specifically on South Asian adults with ancestral roots in Bangladesh, India, Nepal, Pakistan or Sri Lanka. Initial health assessments were conducted between 2010 and 2013, with follow-up examinations taking place from 2016 to 2018. These data were compared with publicly available information from MESA, which enrolled white, Black, Hispanic and Chinese adults beginning in 2000–2002 and continued follow-up visits approximately every two years through 2016–2018.

Researchers evaluated a range of medical conditions known to increase the risk of heart disease, including high blood pressure, prediabetes and type 2 diabetes, as well as abnormal cholesterol and triglyceride levels. Lifestyle factors were also analysed, such as dietary quality, physical activity, tobacco use, alcohol consumption and differences between men and women. Several of these measures align with components of the American Heart Association’s Life’s Essential 8, with diet, exercise and alcohol intake assessed through self-reported information gathered during clinic visits. Alcohol use was defined as consuming at least one alcoholic drink per week.

The findings showed that elevated rates of prediabetes, diabetes and high blood pressure largely drove higher cardiovascular risk among South Asian adults. At age 45, South Asian men had a markedly higher prevalence of prediabetes than men from other ethnic groups, as well as higher rates of high blood pressure and dyslipidaemia. South Asian women also showed nearly double the prevalence of prediabetes compared with women in other population groups. By age 55, both South Asian men and women were at least twice as likely to develop type 2 diabetes as white adults of the same age.

Despite these elevated medical risk factors, South Asian adults demonstrated several favourable lifestyle patterns. They reported the highest diet quality overall, lower levels of alcohol consumption and physical activity levels comparable to those of other groups. These findings suggest that traditional risk factors alone do not fully explain the earlier onset of cardiovascular risk in this population.

The study highlights the need for earlier and more tailored screening and prevention strategies for South Asian adults in the U.S. Identifying cardiovascular risk factors at younger ages may allow for earlier intervention, improved management and a reduced likelihood of developing heart disease later in life. However, the researchers also noted limitations, including reliance on self-reported behaviours and the possibility that results may not be fully generalisable beyond the study populations, which tended to include participants with higher educational and socioeconomic status.

More information: Havisha Pedamallu et al, Prevalence and Trends in Cardiovascular Risk Factors Among Middle‐Aged South Asian Adults Compared With Other Racial and Ethnic Groups in the United States: A Longitudinal Analysis of 2 Cohort Studies, Journal of the American Heart Association. DOI: 10.1161/JAHA.124.041221

Journal information: Journal of the American Heart Association Provided by American Heart Association

The Hidden Cost of Age Anxiety: Faster Ageing in Women

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Anxiety about getting older, especially fears centred on declining health, may extend beyond the mind and register at a biological level, potentially speeding up the ageing process in women. New research suggests that these worries can be reflected in measurable cellular changes associated with accelerated ageing. Rather than being a purely emotional or psychological response, concern about ageing may have tangible effects on the body, reinforcing the idea that how people experience ageing internally can influence how they age physically.

The researchers behind the study argue that subjective perceptions and fears can translate into objective biological outcomes. One of the study’s authors explains that anxiety related to ageing should not be dismissed as an abstract mental state, as it may leave lasting physiological traces with meaningful consequences for long-term health. This perspective challenges the traditional separation between mental and physical health by highlighting how emotional experiences may actively shape biological processes linked to ageing.

Stress about ageing is common, with many people worrying about physical decline, chronic illness, and the potential loss of independence. Previous research has already demonstrated that psychological distress can influence biological ageing through epigenetic mechanisms, which affect how genes are expressed without altering the underlying DNA sequence. Anxiety and depression have long been associated with poorer physical health outcomes. Yet, little attention has been paid to whether worrying about ageing itself influences the speed at which ageing occurs.

Women, in particular, may be especially vulnerable to anxiety about ageing due to social and cultural pressures that place a high value on youth and physical appearance, alongside concerns about fertility. Midlife can be a period of intensified stress, as many women balance multiple roles, including work, family responsibilities, and caregiving for older relatives. Witnessing the illness or decline of parents and other family members may prompt fears about facing similar challenges in the future, reinforcing health-related anxieties about growing older.

To explore these links more closely, the researchers examined data from over seven hundred women participating in a large, long-running study of midlife health. Participants reported how frequently they worried about becoming less attractive, experiencing worsening health, or being too old to have children. Blood samples were also collected and analysed using two established epigenetic clocks: one designed to measure the pace of biological ageing and another that estimates cumulative biological damage over time. The results showed that higher overall anxiety about ageing was associated with a faster pace of biological ageing according to one of these measures.

Notably, worries about declining health showed the strongest connection to accelerated ageing at the cellular level, while concerns about appearance and fertility were not significantly linked. The researchers suggest this is because health-related anxieties persist and intensify over time, whereas fears about beauty or reproduction may diminish as priorities shift with age. Although the study cannot prove cause and effect, it underscores the close relationship between mental and physical health and points to ageing anxiety as a potentially modifiable factor. Further research may help clarify how reducing this type of anxiety could support healthier ageing and encourage a broader societal conversation about how ageing is understood, experienced, and supported.

More information: Mariana Rodrigues et al, Aging anxiety and epigenetic aging in a national sample of adult women in the United States, Psychoneuroendocrinology. DOI: 10.1016/j.psyneuen.2025.107704

Journal information: Psychoneuroendocrinology Provided by New York University

Cognitive Processing Speed Exercises Show Lasting Protection Against Dementia

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Older adults aged 65 and above who took part in a short course of cognitive speed training were significantly less likely to develop dementia many years later. The training focused on improving speed of processing, helping participants rapidly locate visual information on a computer screen and cope with progressively more complex tasks under time pressure. Those who completed five to six weeks of training and later attended follow-up or “booster” sessions one to three years afterwards showed a reduced likelihood of being diagnosed with dementia, including Alzheimer’s disease, even up to 20 years later. These outcomes were reported in newly published findings in a leading dementia research journal.

The National Institutes of Health funded the study and represents the first randomised clinical trial to examine dementia outcomes over 20 years. It was conducted as part of a large project designed to explore the long-term effects of different types of cognitive training in older adults. Between 1998 and 1999, researchers enrolled 2,802 participants and randomly assigned them to one of three training programmes—memory, reasoning, or speed of processing—or to a control group that received no training. Participants in the training groups completed up to ten sessions lasting just over an hour, delivered across five to six weeks.

To further test long-term impact, half of those in the training groups were randomly selected to receive additional booster sessions at approximately one and three years after the initial programme. These sessions reinforced the original training and allowed researchers to assess whether ongoing engagement made a difference. Over two decades later, the results showed a clear advantage for those who had received speed-of-processing training with boosters. In this group, 40% were diagnosed with dementia, compared with 49% in the control group, representing a meaningful 25% reduction in incidence.

Researchers based their analysis on Medicare records from 2,021 participants, covering the period from 1999 to 2019. The follow-up group closely resembled the original study population: around three-quarters were women, most were white, and the average age at enrolment was 74. During the long follow-up period, roughly three-quarters of participants died, with an average age at death of 84. Despite these changes over time, the findings remained robust and consistent.

Dementia involves a decline in thinking abilities severe enough to interfere with independent daily living, and it affects a large proportion of older adults. Alzheimer’s disease accounts for the majority of cases, while vascular and other forms make up the remainder. Researchers noted that even modest delays in dementia onset could have substantial public health benefits, reducing both personal suffering and the enormous economic costs associated with long-term care.

The authors suggest that speed training may be particularly effective because it is adaptive, adjusting task difficulty to each person’s performance in real time, and because it relies on implicit learning rather than conscious memorisation strategies. Previous work from the same research programme showed benefits for everyday functioning up to ten years later, with each booster session providing added protection. While further studies are needed to understand the biological mechanisms involved, the findings support the idea that targeted, non-drug cognitive training could play a meaningful role in healthy ageing and dementia prevention.

More information: Norma B. Coe et al, Impact of cognitive training on claims-based diagnosed dementia over 20 years: evidence from the ACTIVE study, Alzheimer’s & Dementia: Translational Research and Clinical Interventions. DOI: 10.1002/trc2.70197

Journal information: Alzheimer’s & Dementia: Translational Research and Clinical Interventions Provided by Johns Hopkins Medicine

Optical Technology Spots Molecular Cancer Markers at an Early Stage

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Researchers have created a new light-based sensor that can detect vanishingly small amounts of cancer-related molecules in the blood. This highly sensitive technology is designed to pick up early warning signs of disease long before symptoms appear, potentially allowing doctors to identify cancer and other conditions using a straightforward blood test rather than invasive procedures or complex imaging.

Many diseases, including cancer, leave behind molecular traces known as biomarkers. These can include proteins, fragments of DNA, or other biological molecules that signal the presence or progression of illness. The difficulty is that, at very early stages of disease, these biomarkers are present in extremely low concentrations, often too low for conventional tests to detect reliably. Overcoming this limitation is one of the biggest challenges in early diagnosis, when treatment is most effective.

The new sensor addresses this problem by combining several advanced technologies into a single system. It uses carefully designed DNA nanostructures, tiny semiconductor particles called quantum dots, and a CRISPR-based detection mechanism. Together, these components work with a light-based method known as second harmonic generation, or SHG. This optical technique is especially powerful because it produces very little background noise, making it easier to spot weak signals from just a few biomarker molecules.

At the heart of the sensor is a thin layer of a two-dimensional material called molybdenum disulfide. When light shines on its surface, SHG causes light at a new wavelength to be produced. To amplify this signal, the researchers attach quantum dots to the surface using DNA tetrahedrons—small, pyramid-shaped structures made entirely from DNA. These DNA structures act like nanoscale scaffolding, positioning the quantum dots at precise distances from the surface so they enhance the light signal as much as possible.

CRISPR technology provides the sensor’s ability to recognise specific biomarkers. When the system encounters a target molecule, a CRISPR-associated protein cuts the DNA strands holding the quantum dots in place. This causes the quantum dots to detach, leading to a noticeable drop in the SHG signal. Because this change is easy to measure and does not require amplifying the biomarker itself, the sensor can detect extremely low concentrations quickly and efficiently. The design treats DNA not just as genetic material, but as a programmable construction tool that allows precise control at the nanometre scale.

To test the system, the researchers focused on miR-21, a microRNA commonly linked to lung cancer. They first demonstrated that the sensor could detect this biomarker in a simple laboratory solution. More importantly, they then showed it could identify the same molecule in human blood serum from lung cancer patients, closely mimicking real clinical conditions. The sensor proved highly specific, responding only to the intended target and ignoring similar molecules that could otherwise cause false results.

Looking ahead, the team aims to make the technology smaller and more practical for everyday use. By miniaturising the optical components, they hope to develop a portable device that could be used in hospitals, clinics, or even remote and low-resource settings. In the long term, this approach could enable routine blood screening for cancer before tumours are visible on scans, support personalised treatment by tracking biomarker levels frequently, and reduce both healthcare costs and the burden on patients.

More information: Bowen Du et al, Sub-attomolar-level biosensing of cancer biomarkers using SHG modulation in DNA-programmable quantum dots/MoS2disordered metasurfaces, Optica. DOI: 10.1364/OPTICA.577416