Alzheimer's disease (AD) is characterized by cognitive decline and the accumulation of amyloid-beta plaques and hyperphosphorylated tau protein. The role of tau lactylation at the K677 site in AD progression is not well understood. This study explores how tau K677 lactylation affects ferritinophagy, ferroptosis, and their functions in an AD mouse model. Results show that mutating the K677 site to R reduces tau lactylation and inhibits ferroptosis by regulating iron metabolism factors like NCOA4 and FTH1.Tau-mutant mice showed improved memory and learning skills compared to wild-type mice. The mutation also reduced neuronal damage and was associated with decreased tau lactylation at the K677 site, regardless of phosphorylated tau levels. Gene set enrichment analysis showed that lactylation at this site was linked to the MAPK pathway, which was important for ferritinophagy in AD mice. In summary, our research indicates that the K677 mutation in tau protein may protect against AD by influencing ferritinophagy and ferroptosis through MAPK signaling pathways. Understanding these modifications in tau could lead to new treatments for AD.

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.

As aging progresses, the structures and functions of immune organs such as the thymus and spleen deteriorate, leading to impaired immune function and immune senescence. This study investigated the potential of umbilical cord mesenchymal stem cells (UC-MSCs) to mitigate d-galactose-induced immune senescence by enhancing the structural and functional integrity of aging immune organs and regulating the gut microbiota. The findings show that UC-MSCs treatment significantly delayed thymus and spleen atrophy and reduced the number of senescence-associated β-galactosidase (SA-β-gal) positive cells. At the molecular level, UC-MSCs treatment downregulated the expression of aging-related genes, including p16, p53, p21, and RB. It also boosted antioxidant enzyme activity, increasing the levels of catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px), while decreasing serum malondialdehyde (MDA) levels by activating the Nrf2/HO-1 pathway. Additionally, UC-MSCs treatment restored the balance of the gut microbiota. These results demonstrate that UC-MSCs significantly improve the structural and functional integrity of immune organs and enhance the composition of the gut microbiome, offering a potential strategy for delaying immune senescence.

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.