Gut microbiota disruption has been implicated in Alzheimer's disease (AD) pathogenesis. Although Astragalus polysaccharides (APS) exert neuroprotective effects and modulate gut microbial composition, the precise mechanisms underlying these actions remain unknown. This research sought to clarify how APS modulates the gut microbiota during AD progression. Triple‐transgenic (3xTg) AD mice received daily oral APS for 4 weeks. Cognitive performance was evaluated with the Morris water maze (MWM). Immunofluorescence (IF), immunohistochemistry (IHC), and western blotting measured β‐amyloid (Aβ) deposition and microglial and astrocyte markers. IHC also evaluated intestinal tight‐junction proteins (zonula occludens‐1 and occludin). Inflammatory markers in the brain, blood, and intestine were quantified using enzyme‐linked immunosorbent assay (ELISA). Gut microbiota was analyzed through 16S rRNA sequencing. Treatment with APS significantly improved learning and memory performance in 3xTg mice. APS administration reduced cerebral Aβ deposition, decreased phosphorylated tau, presenilin‐1, and β‐secretase 1 levels, and elevated ADAM10 expression. APS significantly altered gut microbiota, notably increasing Akkermansia and decreasing Alistipes . At the intestinal level, APS enhanced expression of tight‐junction proteins ZO‐1 and occludin and reversed AD‐associated structural alterations in the intestinal lining. Furthermore, APS reduced inflammatory cytokine levels in intestinal tissue, peripheral blood, and brain tissue, as reflected by modulated IL‐4, IL‐10, TGF‐β, TNF‐α, IL‐1β, and IL‐6 expressions. The attenuation of neuroinflammation may be attributed to the inhibitory effect of APS on microglial and astrocyte activation. APS reduces neuroinflammation in AD by modulating gut microbiota, contributing to cognitive and pathological improvements, thus indicating its therapeutic potential for AD.

Cerebral ischemic stroke (CIS) is a severe cerebrovascular disease that poses numerous challenges in diagnosis and treatment, primarily attributed to blood-brain barrier (BBB) constraints and inherent drug targeting limitations. Biomimetic membrane nanotechnology, as an emerging therapeutic approach, offers a novel therapeutic strategy by emulating biological membrane structures and functions. This review comprehensively examines biomimetic nanomedicines (BMNPs) in CIS management, encompassing preparation methodologies, material characterization, and specific diagnostic/therapeutic applications. We discussed in detail various types of biomimetic nano-materials such as conventional extracellular membranes, bacterial outer membranes, and virus-like particles, and explore their capacity in enhancing BBB penetration, improving target specificity, and evading immune clearance. Current challenges regarding biosafety profiles, manufacturing quality control, targeted modification precision, and controlled drug release kinetics are delineated in this review. Looking to the future, advancing synergies between nanotechnology and biomedicine hold significant promise for optimizing CIS theranostics and expanding clinical treatment modalities.

Correction on: Long Y, Zou Z, Wu Y, Feng H, Chen T, Yang Z, Jian X, Yin Y and Li X (2025) The original version of this article has been updated.

Introduction: Alzheimer’s disease (AD) is an age-related and progressive neurodegenerative disorder characterized by cognitive impairment and irreversible neuronal degeneration, affecting approximately 55 million individuals worldwide. Despite extensive research efforts, the underlying pathogenic mechanisms of AD remain incompletely understood, and effective therapeutic strategies for preventing or delaying disease progression are still lacking. Increasing evidence suggests that the microbiota-gut-brain axis plays an important role in neurodegenerative diseases, including AD. However, the dynamic alterations of gut microbiota during AD progression across different transgenic mouse models remain poorly characterized. Methods: In the present study, we investigated age-dependent changes in gut microbiota composition in three commonly used AD mouse models, including APP/PS1, 3xTg, and 5xFAD mice, using 16S rRNA gene sequencing. Fecal samples were collected longitudinally at 2, 4, 6, and 8 months of age to evaluate microbial diversity, community structure, and differential bacterial taxa during aging and disease progression. Results: Our results demonstrated distinct and model-dependent alterations in gut microbiota composition across different stages of AD progression. Significant changes in microbial diversity and bacterial community structure were observed among the three AD mouse models and wild-type controls. In particular, dynamic alterations in Verrucomicrobiota, Proteobacteria, and Actinobacteriota were consistently identified during aging in AD mice. In addition, β-diversity, Linear discriminant analysis effect size (LEfSe), and correlation network analyses further revealed differential microbial signatures associated with different AD mouse models and age stages. Discussion: Overall, our findings provide additional evidence that gut microbiota composition undergoes dynamic alterations during aging in multiple AD mouse models and may be associated with AD-related progression. This study may contribute to a better understanding of microbiota-associated changes during AD development and provide a basis for future mechanistic studies targeting the microbiota-gutbrain axis in AD.