Microglia are the resident immune cells of the CNS, maintaining brain homeostasis partially through phagocytosis. In Alzheimer’s disease (AD), microglial phagocytosis is significantly impaired, contributing to the accumulation of pathological aggregates. Microglial phenotypes are dynamic and can shift depending on the disease stage and local environment. While some subpopulations retain or enhance phagocytic activity, especially under inflammatory conditions, others lose their capacity to clear toxic debris effectively. This variability underscores the need for a more nuanced understanding of microglial regulation and function. This paper explores the dual role of microglial phagocytosis in AD and discusses the emerging insights into microglial heterogeneity and how phenotypic shifts affect phagocytic capacity throughout disease progression. A comprehensive understanding of microglial phagocytosis and its dysregulation in AD is essential for designing targeted treatments. Modulating microglial activity to enhance their protective roles without triggering harmful inflammation represents a promising direction for therapeutic intervention in AD.

Brain tumor (BT) is one of many malignancies that have substantially enhanced global human morbidity and mortality rates. Early detection and characterization of glioma are essential for effective preventive strategies. Currently, the use of Transformers, a deep learning model for BT diagnosis and treatment, is attracting significant attention. The transformer self‐attention mechanism automatically learns the associations between input data for efficient processing and analysis. Research indicates that Transformers could play an essential role in the BT segmentation of magnetic resonance imaging (MRI) images, the MRI and histopathology‐based grading of brain cancer, BT molecular expression prediction, the classification of primary brain metastasis sites, voxel‐level dose and BT radiotherapy outcome prediction, synergistic prediction, and the pathway deconvolution of drug combinations. In this review, the feasibility, accuracy, and applicability of various algorithms are systematically analyzed and their prospects are discussed. Overall, this review aimed to discuss and provide an overview of the increasing applications of Transformers in real‐time BT detection and therapy, indicating their broad prospects and potential. In the future, Transformers are expected to be increasingly used for the diagnosis and subsequent treatment of BT because of the continuous development and improvement of Transformer‐based deep learning technology. However, more work is required to investigate their properties for anomaly detection, medical image classification, network design development, and application to other medical data.

Cancer of the central nervous system (CNS) can crosstalk systemically and locally in the tumor microenvironment and has become a topic of attention for tumor initiation and advancement. Recently studied neuronal and cancer interaction fundamentally altered the knowledge about glioma and metastases, indicating how cancers invade complex neuronal networks. This review systematically discussed the interactions between neurons and cancers and elucidates new therapeutic avenues. We have overviewed the current understanding of direct or indirect communications of neuronal cells with cancer and the mechanisms associated with cancer invasion. Besides, tumor‐associated neuronal dysfunction and the influence of cancer therapies on the CNS are highlighted. Furthermore, interactions between peripheral nervous system and various cancers have also been discussed separately. Intriguingly and importantly, it cannot be ignored that exosomes could mediate the “wireless communications” between nervous system and cancer. Finally, promising future strategies targeting neuronal–brain tumor interactions were reviewed. A great deal of work remains to be done to elucidate the neuroscience of cancer, and future more research should be directed toward clarifying the precise mechanisms of cancer neuroscience, which hold enormous promise to improve outcomes for a wide range of malignancies.

The role of traumatic brain injury in the development of glioma is highly controversial since first presented. This is not unexpected because traumatic brain injuries are overwhelmingly more common than glioma. However, the causes of post-traumatic glioma have been long discussed and still warrant further research. In this review, we have presented an overview of previous cohort studies and case–control studies. We have summarized the roles of microglial cells, macrophages, astrocytes, and stem cells in post-traumatic glioma formation and development, and reviewed various carcinogenic factors involved during traumatic brain injury, especially those reported in experimental studies indicating a relationship with glioma progression. Besides, traumatic brain injury and glioma share several common pathways, including inflammation and oxidative stress; however, the exact mechanism underlying this co-occurrence is yet to be discovered. In this review, we have summarized current epidemiological studies, clinical reports, pathophysiological research, as well as investigations evaluating the probable causes of co-occurrence and treatment possibilities. More efforts should be directed toward elucidating the relationship between traumatic brain injury and glioma, which could likely lead to promising pharmacological interventions towards designing therapeutic strategies.