Neurodegenerative diseases (NDs) represent a major global health challenge in aging populations, with their incidence continuing to rise worldwide. Although substantial progress has been made in elucidating the clinical features and molecular underpinnings of these disorders, the precise mechanisms driving neurodegeneration remain incompletely understood. This review examines the increasing significance of the gut–brain–immune triad in the pathogenesis of NDs, with particular attention to Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis, and multiple sclerosis. It explores how disruptions in gut microbiota composition and function influence neuroinflammation, blood–brain barrier integrity, and immune modulation through microbial-derived metabolites, including short-chain fatty acids, lipopolysaccharides, and bacterial amyloids. In both Alzheimer’s and Parkinson’s diseases, a reduced abundance of short-chain fatty acid-producing bacterial taxa has been consistently associated with heightened pro-inflammatory signaling, thereby facilitating disease progression. Although detailed mechanistic understanding remains limited, experimental evidence—primarily from rodent models—indicates that microbial metabolites derived from a dysbiotic gut may initiate or aggravate central nervous system dysfunctions, such as neuroinflammation, synaptic dysregulation, neuronal degeneration, and disruptions in neurotransmitter signaling via vagal, humoral, and immune-mediated pathways. The review further highlights how gut microbiota alterations in amyotrophic lateral sclerosis and multiple sclerosis contribute to dysregulated T cell polarization, glial cell activation, and central nervous system inflammation, implicating microbial factors in disease pathophysiology. In addition to identifying critical knowledge gaps, the review emphasizes the need for sustained, multifactorial research efforts, including the development of physiologically relevant brain–gut organoid models and the implementation of standardized experimental protocols. A major limitation in the field remains the difficulty of establishing causality, as clinical manifestations often arise after extended preclinical phases—lasting years or decades—during which aging, dietary patterns, pharmacological exposures, environmental factors, and comorbidities collectively modulate the gut microbiome. Finally, the review discusses how microbial influences on host epigenetic regulation may offer innovative avenues for modulating neuroimmune dynamics, underscoring the therapeutic potential of targeted microbiome-based interventions in neurodegenerative diseases.

Radiotherapy remains one of the essential treatment modalities for brain gliomas, brain metastases, pediatric neuroblastomas, and primary central nervous system lymphomas. With continuous advancements in modern radiotherapy techniques, patients have achieved significantly improved local control rates and prolonged survival. However, the long-term complications associated with radiotherapy have become increasingly evident. Radiation-induced brain injury (RIBI) is a clinical syndrome characterized primarily by neurological dysfunction following focal or whole-brain radiotherapy. It negatively impacts patients’ quality of life and imposes a considerable burden on families and society. With the rapid development of medical imaging and artificial intelligence technologies, multimodal imaging techniques, including structural magnetic resonance imaging, diffusion-weighted imaging, functional magnetic resonance imaging, perfusion imaging, positron emission tomography-computed tomography metabolic imaging, and radiomics, have demonstrated significant potential for early detection, dynamic monitoring, and quantitative evaluation of RIBI. Meanwhile, treatment strategies for RIBI are shifting from traditional symptomatic and supportive care toward multidimensional interventions aimed at protecting the blood-brain barrier, modulating neuroinflammation, and implementing precise targeted therapies. Additionally, emerging studies have explored neuromodulation techniques and gut-brain axis regulation, offering new directions for the prevention and treatment of RIBI. Although conventional imaging methods remain valuable for diagnosing RIBI, they exhibit notable limitations in the early stages of the disease and in differentiating RIBI from tumor recurrence. This review focuses on the current state of technological development, key findings, and existing limitations, with the aim of providing a theoretical foundation and technical support for the early identification and precise intervention of RIBI.

Type 1 diabetes (T1D) develops when the immune system targets and destroys pancreatic β-cells responsible for insulin production, ultimately resulting in reduced insulin levels. Islet transplantation has garnered significant attention as a potential treatment, but it presents numerous challenges that hinder its effectiveness for T1D patients. A primary issue is the immune system’s tendency to reject transplanted islets, leading to a gradual decline in their functionality. Furthermore, many individuals remain reliant on additional insulin therapy. These challenges are exacerbated by the global shortage of organ donors, which limits the availability of pancreata for transplantation. This review outlines several innovative strategies to regenerate insulin-producing β-cells for the treatment of T1D, with a primary focus on pancreatic progenitor and stem cells. The strategy of converting non-β cells, particularly pancreatic α-cells, into functional β-cells continues to show promise. Moreover, α-cells, which are less vulnerable to autoimmune attacks, present a distinct opportunity for β-cell regeneration in individuals with T1D. While the use of progenitor or stem cells for β-cell regeneration appears encouraging, various hurdles, such as immune rejection, suboptimal differentiation, and other challenges, still impede the implementation of this strategy. Nonetheless, this approach may ultimately pave the way for long-lasting treatment and potential cures for T1D.

Amyotrophic lateral sclerosis (ALS) and other motor neuron diseases (MNDs) are major global causes of death. However, their global incidence, mortality, and disability-adjusted life years remain largely unknown, despite their importance for disease prevention and resource allocation. We therefore examined the global epidemiology of ALS/MNDs.

This study analyzed data from the Global Burden of Disease 2021 database for 204 regions (1990–2021), focusing on ALS/MNDs. Data from the world, China, and the G8 countries were analyzed separately. Age-standardized incidence rates were reported for the 1990s, 2000s, 2010s, and 2020s.

A rising global burden of ALS/MNDs, with significant variations across regions and levels of the social development index, was observed in the Global Burden of Disease database. A significant overlap of etiology between neurological diseases and ALS was also identified. Among the G8 countries and China, China and the USA exhibited the highest prevalence rates in the 1990s, 2000s, 2010s, and 2020s, with China showing 3.3 per 10,000 and the USA 4.0 per 10,000 in the 2020s.

Understanding the common etiologies of ALS/MNDs is key to their effective control. Recommended strategies include pollution control, chemical and radiation safety management, disease monitoring, public health education, multi-departmental collaboration, and scientific research.

With the widespread application of systemic treatments for hepatocellular carcinoma, liver injury caused by molecular targeted drugs and immune checkpoint inhibitors has become a common clinical problem. The Chinese Society of Hepatology, Chinese Medical Association, organized domestic experts to summarize and analyze adverse liver reactions, as well as advances in the diagnosis and treatment related to systemic therapy for liver cancer, both domestically and internationally. Based on this work, we formulated the “Consensus on the Management of Liver Injury Associated with Targeted Drugs and Immune Checkpoint Inhibitors for Hepatocellular Carcinoma”, aiming to provide practical recommendations and decision-making guidance for clinicians in hepatology and related specialties. This guidance focuses on the monitoring, diagnosis, prevention, and treatment of liver injury during targeted and immune checkpoint inhibitor therapy, ultimately helping more liver cancer patients benefit from targeted immunotherapy.