Archive for category: News

Vascular dementia–cognitive impairment caused by disease in the brain’s small blood vessels-is a widespread problem, but it has not been as thoroughly studied as Alzheimer’s disease, in which abnormal plaques and protein tangles are deposited in neural tissue.

One researcher at The University of New Mexico hopes to change that.

In a newly published paper featured by the editors of the American Journal of Pathology, Elaine Bearer, MD, PhD, the Harvey Family Endowed and Distinguished Professor in the UNM School of Medicine’s Department of Pathology, sets out a new model for characterizing and categorizing different forms of vascular dementia.

She hopes this approach will help researchers to better understand the various forms of the disease and find effective treatments.

Conditions like hypertension, atherosclerosis and diabetes have been linked to vascular dementia, but other contributing causes, including the recent discovery of significant quantities of nano– and microplastics in human brains, remain poorly understood, Bearer said.

“We have been flying blind,” she said. “The various vascular pathologies have not been comprehensively defined, so we haven’t known what we’re treating. And we didn’t know that nano– and microplastics were in the picture, because we couldn’t see them.”

Bearer identified 10 different disease processes that contribute to vascular-based brain injury, typically by causing oxygen or nutrient deficiency, leakage of blood serum and inflammation or decreased waste elimination. These cause tiny strokes that harm neurons. She lists new and existing experimental techniques, including special stains and novel microscopy, to detect them.

For the paper, Bearer used a specialized microscope to meticulously study tissue from a repository of brains donated by the families of New Mexicans who had died with dementia, employing stains that highlighted the damaged blood vessels. Surprisingly, many patients diagnosed with Alzheimer’s disease also had disease in the small blood vessels of the brain.

“We suspect that in New Mexico maybe a half of our Alzheimer’s people also have vascular disease,” she said.

Bearer contends a methodical approach to identifying different forms of vascular dementia will help neurologists and neuropathologists more accurately score the severity of the disease in both living and deceased patients and advance the search for potential treatments — and even cures. To make that happen, the National Institutes of Health (NIH) has raised the possibility of forming a consensus group of leading neuropathologists to work out a new classification and scoring system, she said.

Meanwhile, a fresh area of concern is the unknown health consequences of nano– and microplastics in the brain, Bearer said.

“Nanoplastics in the brain represent a new player on the field of brain pathology,” she said. “All our current thinking about Alzheimer’s disease and other dementias needs to be revised in light of this discovery.”

“What I’m finding is that there’s a lot more plastics in demented people than in normal subjects,” she said. “It seems to correlate with the degree and type of dementia.”

The quantity of plastics also was associated with higher levels of inflammation, she said.

Bearer’s work builds on years of collaboration with Gary Rosenberg, MD, professor of Neurology and director of the UNM Alzheimer’s Disease Research Center (ADRC), which won a five-year $21.7 million NIH grant in 2024 that supported Bearer’s research. Rosenberg, a longtime chair of the UNM Department of Neurology and also director of the UNM Center for Memory & Aging, has published extensively on the association of vascular disease with dementia symptoms.

“When we started thinking about putting this ADRC together, I thought one of the things I should look at is the vasculature, because nobody’s done it systematically and comprehensively, and we have a world’s expert here at UNM,” Bearer said.

“Describing the pathological changes in this comprehensive way is really new. What I’m hoping will come out of this paper is working with other neuropathology ADRC cores across the country to develop consensus guidelines for classifying vascular changes and the impact of nano– and microplastics on the brain.”

Reference:

Bearer, Elaine L., Exploring Vascular Contributions to Cognitive Impairment: Small-Vessel Disease of White Matter and Microplastics/Nanoplastics, American Journal Of Pathology, DOI: 10.1016/j.ajpath.2025.07.007.

New research from South Australia highlights the urgent need to establish a safe upper limit for folic acid intake during pregnancy and to improve guidelines on folic acid supplementation during pregnancy.

A study by Flinders University and Adelaide University researchers published in the journal Nutrients links the rise in gestational diabetes in part to excess maternal folate levels, due to the dual impact of folic acid (FA, or synthetic folate) in food fortification and higher-than-recommended supplementation doses during pregnancy.

National surveillance shows the incidence of gestational diabetes mellitus (GDM) in Australia has more than tripled, rising from 5.6% in 2010 to 19.3% in 2022.

The research – led by Dr Tanja Jankovic-Karasoulos, now at The University of Adelaide, and Professor Claire Roberts, at Flinders University – highlights both the need to establish a safe upper limit for FA intake during pregnancy, and to re-evaluate supplementation guidelines in the context of widespread food fortification and increased dose and duration of real-world supplementation practice.

“Our study shows that excess maternal folate significantly increases GDM risk in our post-fortification pregnancy cohort,” says Dr Jankovic-Karasoulos, from the Robinson Research Institute at University of Adelaide.

“We suspect that increased FA intake over the past 10-15 years is contributing to the steady rise in GDM prevalence in Australia.”

Adequate folate is essential for DNA formation and proper cell growth and development. Current guidelines recommend supplementation with 400–500 µg of FA daily, starting at least one month prior to conception and continuing through the first trimester to reduce the risk of neural tube defects such as spina bifida.

“Our study suggests that higher-than-recommended FA intake may have unintended consequences for pregnancy,” says Dr Jankovic-Karasoulos, who last year was awarded an NHMRC Ideas Grant, Flinders Foundation Health Seed Grant and Diabetes Australia Project Grant to further investigate the effects of high FA intake during pregnancy on placental function, maternal insulin resistance and glucose handling.

“The placenta is central to regulating maternal glucose tolerance in pregnancy, so we need to understand how high FA intake affects placental function and, in turn, insulin resistance and gestational diabetes risk.”

NHMRC Investigator Research Fellow Professor Claire Roberts, from the Pregnancy Health and Beyond Laboratory at Flinders University, says understanding the potential harms of excess FA intake is of major public health importance.

“The use of FA is widely recommended worldwide, but we need to keep investigating unexpected implications, plus how to identify women at risk of gestational diabetes early in pregnancy to protect the baby from adverse effects of high maternal blood glucose for the best start in life,” says Professor Roberts, from the Flinders Health and Medical Research Institute.

Researchers emphasise the importance of adequate folate in pregnancy but highlight the need to establish a safe upper limit of FA intake. They would also like to see improved guidelines on FA supplementation during pregnancy which would protect the fetus right at the beginning of gestation against neural tube defects but also protect the mother and fetus from adverse effects of high blood glucose.

Reference:

Jankovic-Karasoulos T, Smith MD, Leemaqz S, Mittinty M, Williamson J, McCullough D, Arthurs AL, Dekker GA, Roberts CT. Maternal Folate Excess, Placental Hormones, and Gestational Diabetes Mellitus: Findings from Prospective Cohorts Before and After Mandatory Folic Acid Food Fortification. Nutrients. 2025; 17(17):2863. https://doi.org/10.3390/nu17172863

Ivabradine did not reduce the occurrence of myocardial injury after noncardiac surgery (MINS), according to late-breaking research presented in a Hot Line session today at ESC Congress 2025.

MINS is a common and serious complication, which has been found to account for approximately 13% of all deaths within 30 days of surgery. Explaining the rationale of the PREVENT-MINS trial, Principal Investigator, Professor Wojciech Szczeklik from Jagiellonian University Medical College, Krakow, Poland, said: “It has been proposed that increased heart rate at the time of surgery leads to higher myocardial oxygen consumption, a supply-demand mismatch and myocardial injury. Giving beta-blockers around the time of surgery lowers heart rate and decreases the risk of myocardial infarction, but these benefits may be offset by increased risk of hypotension, death and stroke. Ivabradine is a currently available medicine used in angina and heart failure that more selectively slows heart rate than beta-blockers. The PREVENT-MINS trial assessed whether ivabradine could prevent MINS in patients after noncardiac surgery with, or at risk of, atherosclerotic disease.”

The double-blind, placebo-controlled, randomised PREVENT-MINS trial was conducted at 26 hospitals in Poland. Eligible patients were aged ≥45 years and had either established atherosclerotic disease (i.e. coronary artery disease, peripheral artery disease or prior stroke) or substantial risk factors for atherosclerotic disease (e.g. diabetes, hypertension and age ≥70 years). Patients were randomised 1:1 to receive ivabradine (5 mg orally twice daily for up to 7 days, starting one hour before surgery) or placebo. The primary outcome was MINS within 30 days from randomisation. The trial had intended to enrol around 2,500 patients; however, the independent Data Monitoring Committee recommended early termination in March 2025 for futility, based on the prespecified interim analysis.

All 2,101 participants who underwent randomisation were included in the intention-to-treat population. The median age was 70.0 years and 49.4% were women.

MINS occurred in 17.0% of patients in the ivabradine group and 15.1% in the placebo group (relative risk [RR] 1.12; 95% confidence interval [CI] 0.92 to 1.37; p=0.25). In prespecified subgroup analyses, ivabradine was associated with an increased risk of MINS among patients with a history of coronary artery disease (RR 1.49; 95% CI 1.03 to 2.16) but not among patients without a history of coronary artery disease (RR 0.98; 95% CI 0.78 to 1.24).

The intraoperative mean heart rate was lower in the ivabradine group by 3.2 beats per minute than in the placebo group, with no difference in intraoperative mean arterial pressure. Clinically important bradycardia was more common in the ivabradine group (RR 1.18; 95% CI 1.00 to 1.40).

Professor Szczeklik concluded: “Ivabradine did not reduce the risk of MINS in patients undergoing noncardiac surgery. Heart-rate lowering was modest and the possible higher MINS incidence in patients with known coronary artery disease is contrary to our original hypothesis. Further research is needed to establish a method to safely control the heart’s stress associated with noncardiac surgery.”

Reference:

Wojciech Szczeklik, Jakub Fronczek, Ivabradine in Patients Undergoing Noncardiac Surgery: a Randomized Controlled Trial, Circulation, https://doi.org/10.1161/CIRCULATIONAHA.125.076704