Medical Bulletin 03/November/2025 - Video
Overview
Scientists have developed an innovative nanotechnology treatment that reverses Alzheimer's disease in mice by restoring the brain’s blood-brain barrier (BBB), a critical vascular checkpoint maintaining brain health. Published in the journal Signal Transduction and Targeted Therapy, the study was led by the Institute for Bioengineering of Catalonia (IBEC) and West China Hospital Sichuan University (WCHSU), in partnership with UK collaborators. Unlike conventional nanomedicines used as drug carriers, these bioactive nanoparticles act directly as “supramolecular drugs,” repairing BBB function and promoting the clearance of toxic waste proteins from the brain.
Alzheimer’s disease is closely linked to vascular dysfunction, particularly in the brain’s dense capillary network supplying neurons. The BBB protects the brain by regulating substance exchange with the bloodstream, but its dysfunction in Alzheimer's leads to harmful amyloid-β (Aβ) protein accumulation, disrupting neuronal function and contributing to cognitive decline. The treatment targets a delicate molecular system involving LRP1, a receptor that transports Aβ across the BBB for removal.
Using mouse models genetically predisposed to accumulate high Aβ and develop Alzheimer-like cognitive deficits, researchers administered three doses of engineered nanoparticles. These particles mimic LRP1 ligands, binding Aβ and facilitating its transport across the BBB. Nanoparticle size and ligand count were precisely engineered to optimize receptor interaction and clearance mechanisms. Behavioral and memory assessments were conducted over several months to evaluate neurological recovery.
Remarkably, one hour after treatment, Aβ levels in the brain dropped by 50–60%. Over subsequent months, treated mice showed substantial cognitive improvements, with behavior resembling healthy counterparts. The nanoparticles restored normal BBB clearance function, reactivating the brain’s natural waste removal and vascular balance. No toxicity was observed, supporting safety and tolerability.
Lead researcher Professor Lorena Ruiz Perez emphasized that this strategy opens a new pathway for clinical therapies, shifting focus from neurons to vascular health to combat Alzheimer’s and potentially other neurodegenerative diseases. This breakthrough could significantly improve patient outcomes by addressing vascular contributions to dementia.
REFERENCE: Junyang Chen, Pan Xiang, Aroa Duro-Castano, Huawei Cai, Bin Guo, Xiqin Liu, Yifan Yu, Su Lui, Kui Luo, Bowen Ke, Lorena Ruiz-Pérez, Qiyong Gong, Xiaohe Tian, Giuseppe Battaglia. Rapid amyloid-β clearance and cognitive recovery through multivalent modulation of blood–brain barrier transport. Signal Transduction and Targeted Therapy, 2025; 10 (1) DOI: 10.1038/s41392-025-02426-1
Gum disease could silently cause serious brain damage, Study warns
Adults with gum disease are more likely to have signs of brain white matter damage, called white matter hyperintensities, according to a study published on October 22, 2025, in Neurology® Open Access. These bright spots on brain scans represent areas of tissue injury linked to impaired memory, coordination, and increased stroke risk. While the study does not prove causation, it highlights a potential connection between oral health and brain aging.
White matter consists of nerve fibers that facilitate communication between different brain areas. Damage to this tissue can lead to cognitive decline and movement difficulties. Researchers suspect that chronic inflammation from gum disease may adversely affect blood vessels in the brain, contributing to these changes.
The study examined 1,143 adults with an average age of 77. Participants underwent thorough dental exams to assess gum disease presence and brain MRI scans to detect cerebral small vessel disease markers, focusing on white matter hyperintensities, cerebral microbleeds, and lacunar infarcts. Among them, 800 had gum disease, and 343 did not. White matter hyperintensity volumes were categorized into four groups based on extent. Researchers adjusted analyses for age, sex, race, blood pressure, diabetes, and smoking to isolate the association between gum health and brain changes.
Individuals with gum disease had higher average white matter hyperintensity volumes (2.83% of brain volume) compared to those without gum disease (2.52%). Notably, 28% of those with gum disease belonged to the highest damage category versus 19% without gum disease. After adjustments, gum disease was linked to a 56% greater likelihood of significant white matter damage. No significant associations were found between gum disease and other brain injury types like microbleeds or lacunar infarcts.
Lead author Dr. Souvik Sen emphasized that while further research is needed, maintaining oral health could support brain health by potentially reducing inflammation-driven vascular damage. This study underscores the importance of dental care as part of strategies to preserve cognitive function and reduce stroke risk.
REFERENCE: Jaclyn Meyer, Chylee Martin, Stefanie Wood, Forrest Lowe, Leonardo Bonilha, Hamdi S. Adam, Ryan Demmer, Bruce A. Wasserman, Wayne D. Rosamond, James D. Beck, Souvik Sen. Periodontal Disease Independently Associated With White Matter Hyperintensity Volume. Neurology Open Access, 2025; 1 (4) DOI: 10.1212/WN9.0000000000000037
Study finds early-day fasting does not significantly boost metabolism
Scientists have investigated whether Time-Restricted Eating (TRE), a dietary pattern limiting food intake to a 10-hour or shorter window daily, enhances metabolic health and insulin sensitivity in women with overweight or obesity. A recent randomized crossover trial published in Science Translational Medicine compared early Time-Restricted Eating (8 am–4 pm) and late Time-Restricted Eating (1 pm–9 pm) under carefully controlled caloric intake to isolate the effects of meal timing from calorie reduction.
Time-Restricted Eating has gained interest for potential benefits in weight management and cardiometabolic health, possibly by aligning eating with circadian rhythms. While animal studies and some human trials have indicated improvements in glucose regulation, lipid levels, and blood pressure, many have lacked rigorous control of calorie intake and physical activity, leading to inconsistent findings. This study uniquely focused on women, an often-underrepresented group, to assess metabolic and circadian responses to Time-Restricted Eating.
Thirty-one women with a mean BMI of 30.5 kg/m² participated in a 10-week crossover design, undergoing two 2-week intervention phases (eTRE and lTRE) separated by washout. Participants maintained their usual diets and activities, consuming food only within the assigned 8-hour window. Insulin sensitivity was measured via oral glucose tolerance tests (OGTT), alongside assessments of body composition, continuous glucose monitoring, blood pressure, lipids, inflammatory markers, appetite hormones, sleep timing, and gene expression related to circadian rhythms. Caloric intake and physical activity were closely monitored and controlled.
Neither early Time-Restricted Eating nor late Time-Restricted Eating significantly improved insulin sensitivity or other key cardiometabolic markers when calorie intake was constant. Both interventions produced modest weight loss (greater in eTRE) and shifts in circadian phase, with late Time-Restricted Eating delaying internal timing by approximately 40 minutes. Hormonal changes affecting appetite were noted, including increased Peptide YY in late Time-Restricted Eating mornings and decreased leptin in both groups. Circadian gene expression was altered, confirming food timing as a modulator of biological rhythms.
These results suggest that metabolic benefits observed in prior Time-Restricted Eating studies likely stem from calorie restriction rather than timing alone. Meal timing influences circadian regulation but may not independently improve insulin sensitivity absent caloric changes. Further long-term trials with diverse populations are needed to clarify Time-Restricted Eating’s role in metabolic health.
REFERENCE: Peters, B., Schwarz, J., Schuppelius, B., Ottawa, A., Koppold, D.A., Weber, D., Steckhan, N., Mai, K., Grune, T., Pfeiffer, A.F.H., Michalsen, A., Kramer, A., Pivovarova-Ramich, O. (2025). Intended isocaloric time-restricted eating shifts circadian clocks but does not improve cardiometabolic health in women with overweight. Science Translational Medicine, 17(822). DOI: 10.1126/scitranslmed.adv6787.
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