Alzheimer’s disease (AD) is a neurodegenerative disorder that severely impacts cognitive function, posing significant physical and psychological burdens on patients and substantial economic challenges to families and society, particularly in aging populations where its prevalence is rising. Current diagnostic and therapeutic strategies, including pharmacological treatments and non-pharmacological interventions, exhibit considerable limitations in early diagnosis, etiological treatment, and disease management. This study aims to investigate the application of artificial intelligence (AI) in the early diagnosis and progression monitoring of AD through a bibliometric analysis of relevant literature. A systematic search in the Web of Science Core Collection identified 530 publications related to AI and AD, consisting of 361 original research articles and 169 review articles, with a notable increase in annual publication rates, particularly between 2019 and 2024. The United States and China emerged as leading contributors, emphasizing the importance of international collaboration. Institutional analysis revealed that Harvard University and Indiana University System are at the forefront, highlighting the role of academic institutions in fostering interdisciplinary research. Furthermore, the Journal of Alzheimer’s Disease was identified as the most influential publication outlet. Key highly cited papers provided essential theoretical foundations for ongoing research. This study underscores the growing relevance of AI in AD research and suggests promising avenues for future investigations, particularly in enhancing diagnostic accuracy and therapeutic strategies through advanced data analytics and machine learning techniques.

Mesenchymal stem cells (MSCs) have shown great potential for the treatment of liver injuries, and the therapeutic efficacy greatly depends on their homing to the site of injury. In the present study, we detected significant upregulation of hepatocyte growth factor (HGF) in the serum and liver in mice with acute or chronic liver injury. In vitro study revealed that upregulation of miR-9-5p or miR-221-3p promoted the migration of human MSCs (hMSCs) toward HGF. Moreover, overexpression of miR-9-5p or miR-221-3p promoted hMSC homing to the injured liver and resulted in significantly higher engraftment upon peripheral infusion. hMSCs reduced hepatic necrosis and inflammatory infiltration but showed little effect on extracellular matrix (ECM) deposition. By contrast, hMSCs overexpressing miR-9-5p or miR-221-3p resulted in not only less centrilobular necrosis and venous congestion but also a significant reduction of ECM deposition, leading to obvious improvement of hepatocyte morphology and alleviation of fibrosis around central vein and portal triads. Further studies showed that hMSCs inhibited the activation of hepatic stellate cells (HSCs) but could not decrease the expression of TIMP-1 upon acute injury and the expression of MCP-1 and TIMP-1 upon chronic injury, while hMSCs overexpressing miR-9-5p or miR-221-3p led to further inactivation of HSCs and downregulation of all three fibrogenic and proinflammatory factors TGF-β, MCP-1, and TIMP-1 upon both acute and chronic injuries. Overexpression of miR-9-5p or miR-221-3p significantly downregulated the expression of α-SMA and Col-1α1 in activated human hepatic stellate cell line LX-2, suggesting that miR-9-5p and miR-221-3p may partially contribute to the alleviation of liver injury by preventing HSC activation and collagen expression, shedding light on improving the therapeutic efficacy of hMSCs via microRNA modification.

Background: Alzheimer’s disease (AD) is a neurodegenerative disorder marked by cognitive decline and memory loss. Recent research underscores the crucial role of astrocytes in AD. This study reviews research trends and contributions on astrocytes in AD from 2000 to 2024, shedding light on the evolving research landscape.Methods: We conducted a bibliometric analysis using data from the Web of Science Core Collection, covering publications from January 1, 2000, to July 6, 2024, on “Alzheimer’s disease” and “astrocytes.” We identified 5,252 relevant English articles and reviews. For data visualization and analysis, we used VOSviewer, CiteSpace, and the R package “bibliometrix,” examining collaboration networks, co-citation networks, keyword co-occurrence, and thematic evolution.Results: Between 2000 and 2024, 5,252 publications were identified, including 4,125 original research articles and 1,127 review articles. Publications increased significantly after 2016. The United States had the most contributions (1,468), followed by China (836). Major institutions were the University of California system (517) and Harvard University (402). The Journal of Alzheimer’s Disease published the most articles (215). Verkhratsky A was the top author with 51 papers and 1,585 co-citations.Conclusion: Our extensive bibliometric analysis indicates a significant increase in research on astrocytes in AD over the past 20 years. This study emphasizes the growing acknowledgment of astrocytes’ crucial role in AD pathogenesis and points to future research on their mechanisms and therapeutic potential.

Background: To investigate the therapeutic mechanisms of miR‐9‐5p‐overexpressing human umbilical cord mesenchymal stromal cells (hUC‐MSCs) in neonatal rat models of hypoxic‐ischemic brain damage (HIBD). Methods: Fresh neonatal umbilical cords were collected to isolate and culture human umbilical cord mesenchymal stromal cells (hUC‐MSCs). Recombinant adenovirus was used to amplify miR‐9‐5p and transduce hUC‐MSCs, generating miR‐9‐5p‐overexpressing cells. Functional assessments included: ELISA to evaluate secretory function (e.g., neurotrophic and anti‐inflammatory factors), real‐time cell analysis to measure proliferation capacity, Transwell and Dunn chamber assays to assess chemotactic migration ability. Healthy 7‐day‐old Sprague‐Dawley (SD) rats of both sexes were randomly allocated into four groups ( n = 12/group, with 4 rats per group assigned to TTC staining, Western blot, or Morris water maze assay, respectively): Sham‐operated control group (mock surgery), Hypoxic‐ischemic brain damage (HIBD) model group, miR‐9‐5p‐hUC‐MSCs treatment group, and Adenovirus‐transduced hUC‐MSCs (Ad‐hUC‐MSCs) treatment group. The HIBD model was induced in groups 2–4. At 24 h post‐modeling, 1×10 ⁶ miR‐9‐5p‐hUC‐MSCs or Ad‐hUC‐MSCs were transplanted into the left lateral ventricle (injured side) of the pups. Neurological function was evaluated 48 h later using righting reflex tests for short‐term neurobehavioral assessment. Subsequently, 4 rats per group were sacrificed for 2,3,5‐triphenyltetrazolium chloride (TTC) staining to quantify cerebral infarction volume. Hippocampal tissues from another 4 rats per group were analyzed by Western blot for Beclin‐2 and Caspase‐3 protein expression. The remaining 4 rats per group underwent 28‐day Morris water maze testing for long‐term neurobehavioral evaluation. Results: Spindle‐shaped and polygonal adherent cells emerged within 3–5 days following umbilical cord tissue block inoculation, with flow cytometric analysis confirming their identity as mesenchymal stromal cells (MSCs). Compared to the Ad‐hUC‐MSCs treatment group, miR‐9‐5p enhanced the secretion of neuroreparative and anti‐inflammatory factors (e.g., NGF, BDNF, IL‐6) in hUC‐MSCs while suppressing pro‐inflammatory cytokines (e.g., IL‐1, IL‐2) (p < 0.05). Furthermore, miR‐9‐5p significantly promoted hUC‐MSCs proliferation and augmented the chemotactic migratory capacity of miR‐9‐5p‐hUC‐MSCs. At 48 h post‐transplantation in the miR‐9‐5p‐hUC‐MSCs group, the sham‐operated controls showed no detectable cerebral infarction, whereas the model group exhibited distinct pale infarct foci occupying 33.15% ± 4.38% of total brain volume (vs. controls, p < 0.05), indicating severe cerebral injury. Both miR‐9‐5p‐hUC‐MSCs and Ad‐hUC‐MSCs treatments markedly reduced infarct volumes to 14.85% ± 2.79% and 19.11% ± 4.57%, respectively, with the miR‐9‐5p‐hUC‐MSCs group demonstrating a statistically superior therapeutic effect compared to Ad‐hUC‐MSCs (p < 0.05). Transplantation of either Ad‐hUC‐MSCs or miR‐9‐5p‐hUC‐MSCs significantly improved short‐ and long‐term neurobehavioral outcomes in hypoxic‐ischemic brain damage (HIBD) rats. At 48 h post‐HIBD induction, upregulated expression of Beclin‐2 and Caspase‐3 proteins was observed in brain tissue. Notably, these elevated protein levels were attenuated following treatment with miR‐9‐5p‐hUC‐MSCs or Ad‐hUC‐MSCs. Conclusion: MiR‐9‐5p enhances the secretion of immunomodulatory factors and improves the migratory and proliferative capacities of hUC‐MSCs. Overexpression of miR‐9‐5p promotes in vivo homing of hUC‐MSCs, which mitigate cerebral injury and exert neuroprotective and reparative effects through dual mechanisms: modulating immune responses and providing neurotrophic support. Furthermore, hUC‐MSCs significantly reduce cerebral infarct volume in hypoxic‐ischemic brain damage (HIBD) rats and downregulate levels of apoptotic proteins (Beclin‐2 and Caspase‐3) in brain tissue, demonstrating potent cerebroprotective effects.

Retinitis pigmentosa (RP) is among the most irreversible inherited blindness diseases. Previous evidences have demonstrated that ferroptosis plays a significant role in various neurodegenerative diseases. Thus, elucidating the relationship between ferroptosis and retinitis pigmentosa may yield valuable insights for identifying therapeutic targets for inherited retinal degeneration. In the current study, a public dataset of GSE56473 from the Gene Expression Omnibus (GEO) database was analysed to identify the differentially expressed ferroptosis related genes (DE-FRGs) within the degenerative retinas between Rd10 mice and control individuals. Gene Ontology (GO), Kyoto Encyclopedia of Genomes (KEGG) and protein-protein interaction (PPI) network analyses were performed on these DE-FRGs. Hub ferroptosis-related genes (HFRGs) were subsequently identified using multiple bioinformatic algorithms. Changes in the expression profiles of the identified HFRGs were validated through the GSE178928 dataset. Immunofluorescence staining, quantitative PCR (qPCR) and a single cell sequencing dateset analysis were performed to evaluated the expression patterns of several HFRGs in the Rd10 mice. Furthermore, potential target drugs were predicted utilizing the DGIdb database. In total, 37 ferroptosis-related genes were identified among the 2096 differentially expressed genes, which were enriched in several biological processes including the response to oxidative stress, positive regulation of neuron death, ferroptosis and the PPAR signaling. Through protein–protein interaction network and multiple bioinformatics analyses, eight HFRGs (Egr1, Cd44, Egfr, Tlr4, Timp1, Cybb, Lcn2, and Ppara) were ultimately identified, with most being upregulated in the retinas of Rd10 mice. Among these HFRGs, Egr1 expression was significantly increased in rod and cone photoreceptors, whereas Cd44 expression was markedly upregulated in Müller cells. Several potential therapeutic compounds, such as Genipin, were also predicted. Our study provides novel biomarkers and therapeutic targets for the inherited retinal degeneration.