Volume 117
Published on July 2025Volume title: Proceedings of ICBioMed 2025 Symposium: Computational Modelling and Simulation for Biology and Medicine
Under normal physiological conditions, tau protein can maintain the function of microtubules, while under pathological conditions, it dissociates from microtubules and aggregates, thereby disrupting microtubule function and ultimately leading to neuronal damage and the development of neurodegenerative diseases. Under pathological conditions, tau protein undergoes modifications such as phosphorylation, acetylation, ubiquitination, and truncation. These changes lead to the formation of neurofibrillary tangles through various mechanisms and ultimately cause Alzheimer's disease. In response to these diverse pathogenic mechanisms, people have developed a variety of potential therapeutic approaches targeting the underlying causes, such as modulating autophagy, inhibiting tau protein aggregation, clearing tau protein and so on. These studies demonstrate that the progression of neurodegenerative diseases, headed by Alzheimer's disease (AD), can be inhibited. This article aims to discuss the limitations in the aforementioned mechanisms and their corresponding therapeutic approaches, and to explore whether there are methods and ideas to address these shortcomings. Regrettably, the current potential therapeutic approaches are still unable to completely cure Alzheimer's disease, and the conditions required for treatment are rather demanding. However, these therapeutic methods may potentially serve as means for the early diagnosis and prevention of Alzheimer's disease. This article may provide more ideas for new therapeutic approaches to AD and other neurodegenerative diseases.

At present, the scientific research field has conducted in-depth research on its pathogenesis, and a large number of studies have shown that Gamma-Aminobutyric Acid (GABA) ergic neuronal downregulation plays a key role in the pathogenesis of major depression. As a critical inhibitory neurotransmitter in the central nervous system, the abnormal downregulation of GABA neurons will break the balance of the neurotransmitter system. This disruption subsequently interferes with the normal transmission and regulation of neural signals, ultimately leading to multifaceted abnormalities in emotional, cognitive, and physiological functions—processes that collectively drive the onset and progression of major depression. This article reviews the existing experimental evidence of GABA's influence on the development of depression, and provides the basis for further research.
Marathon, walking, cycling and other sports have been popularized and developed around the world, and more and more people around the world have devoted themselves to these sports. Cardiorespiratory endurance is the core element to describe human health, and it is also the key to supporting people to complete these high-intensity aerobic exercises, which are very important for the human body. In the pursuit of better sports performance and performance in sports, people often use a number of ways to train. However, different exercise methods have different goals and effects, and one training method is not suitable for all people. Inappropriate training methods may cause sports injuries and backfire. At present, the three mainstream training methods in the world are high-altitude training, continuous training and interval training. Choosing the appropriate training methods for oneself can make the training more efficient and help achieve the training goals smoothly. This article adopts the literature review method for research. By analyzing and summarizing domestic and foreign literature, it is found that different training methods have different effects on improving human cardiopulmonary endurance. This provides a relevant reference basis for various groups of people to choose scientific training methods to improve cardiopulmonary endurance and enhance sports performance in the future.
Nerve injuries are a prevalent category of neurological disorders with diverse etiologies. Despite timely medical intervention, full functional recovery remains elusive due to the inherently limited regenerative capacity of neural cells. Traditional treatments often fall short in promoting true nerve regeneration. Stem cells, characterized by their multipotent differentiation potential, offer a novel approach by providing the possibility of replacing damaged neural cells. This paper reviews the current challenges in nerve injury treatment and discusses the advantages and limitations of stem cell therapy, with a focus on the optic and spinal nerves. Particular attention is given to different types of stem cells, their mechanisms of action, and potential clinical applications.
The endosymbiotic origin of mitochondria is widely regarded as a defining moment in eukaryotic evolution, though its details and broader implications remain subjects of debate. This dissertation investigates the mitochondrial genesis and its pivotal function in transforming cellular energy dynamics and complexity, utilizing phylogenetic, bioenergetic, and theoretical paradigms. It tackles ongoing controversies, including the phylogenetic placement of mitochondria within Alphaproteobacteria and the relationship between enhanced energy availability and eukaryotic complexity. The analysis confirms mitochondria arose from an alphaproteobacterial endosymbiont, with a chimeric proteome blending contributions from both the symbiont and a pre-existing host premitochondrion. This endosymbiotic occurrence transcended the bioenergetic limitations inherent to prokaryotes, thereby catalyzing genomic proliferation and the emergence of advanced eukaryotic characteristics. Empirical data indicate that the host organism was probably an archaeon, potentially a hydrogen-dependent methanogen, with this pivotal event transpiring approximately 1.5 billion years ago. By resolving these debates, the thesis discussed how endosymbiosis triggered a cellular energy revolution, distinguishing eukaryotes from prokaryotes. This work highlights endosymbiosis as the key to unlocking eukaryotic genomic and functional complexity, laying a foundation for future studies into the evolutionary dynamics of life.

Skeletal muscle injury has been a significant problem that people face, as there are limited solutions to reform it. As there are already various amounts of reviews and researches focusing on in vitro developments, this reviews mainly focuses on how resistance exercise enhances skeletal muscle recovery in humans by making large amounts of insulin growth factor I (IGF-I). The role of IGF-I and how it enhances skeletal muscular recovery will be clarified in this review. This paper only focuses on humans in post-exercise conditions, and how increased muscle mass is beneficial for muscular recovery. As it has been a controversial question of whether resting is more beneficial after injury or whether other components could enhance and hasten muscular recovery, this review points out the differences in composition of IGF-I in resistance exercise and resting stages. The result shows that resistance exercise is a source that stimulates IGF-I concentration in humans’ bodies, which encourages the synthesis of muscle fibers, resistance exercise can be proven as a non-pathological tool that is beneficial for muscular recovery.

Idiopathic scoliosis (IS) is a prevalent three-dimensional spinal deformity in children and adolescents, characterized by a complex pathogenesis that remains unclear. Current research has predominantly focused on single susceptibility factors contributing to IS development, including genetic, environmental, hormonal, and metabolic influences, while overlooking potential interactions among these multiple factors.This paper categorizes these susceptibility factors into congenital genetic factors and acquired environmental factors, and explores their roles and interactions in the onset and progression of IS. Regarding congenital factors, the focus is on the impact of hormone levels, age at menarche, and obesity on IS development. As for acquired factors, the analysis centers on the influence of body mass index (BMI) and body composition, physical activity, bone mineral density, and paraspinal muscles. Furthermore, the paper analyzes the interactions between congenital and acquired factors, and then summarizes these relationships to construct a gene-environment interaction network. Understanding these interactions provides a reference for formulating precise and effective prevention and treatment strategies for IS in children and adolescents, facilitating early detection, prevention, and intervention.
The CRISPR-Cas system has emerged as a revolutionary gene-editing technology, yet its clinical translation is constrained by off-target effects, suboptimal delivery efficiency, and limited adaptability across therapeutic contexts. This article presents a "multi-dimensional engineering" framework, systematically integrating the collaborative strategies of tool innovation, delivery optimization, and precise regulation to break through existing technical bottlenecks. In tool innovation, various regulatory tools have significantly improved editing accuracy and safety, reducing off-target activities. In the field of delivery systems, new universal delivery platforms have achieved the efficient and safe delivery of CRISPR components and enhanced tissue targeting. At the clinical translation level, CRISPR technology has been successfully applied in POC detection of infectious diseases, cancer immunotherapy, and the construction of genetic disease stem cell models. This article further explores the self-targeting repair mechanism of archaeal CRISPR systems to provide insights into precise regulation and proposes future directions to achieve a leap from the laboratory to the clinic.
Melanoma, a highly aggressive malignancy originating from melanocytes, poses significant therapeutic challenges due to its rapid progression and metastatic potential. While conventional treatments such as surgery, chemotherapy, and immunotherapy have improved outcomes, their limitations in efficacy and safety necessitate complementary approaches. Traditional Chinese Medicine (TCM), with its holistic philosophy and multi-targeted interventions, has demonstrated potential in enhancing therapeutic outcomes and mitigating adverse effects. This review synthesizes current evidence on TCM's role in melanoma management, focusing on its theoretical foundations, molecular mechanisms, and clinical applications. Key strategies including herbal formulations, acupuncture, and dietary interventions are analyzed, highlighting their synergistic effects when combined with conventional therapies. Challenges such as standardization of TCM protocols and mechanistic elucidation are discussed, with future directions emphasizing translational research and integrative treatment models. Clinical studies demonstrate that TCM combined with chemotherapy improves objective response rates by 16% (from 22% to 38%) while reducing myelosuppression incidence by 30%.