Extreme cold exposure has emerged as a significant global public health challenge to cognitive function among populations such as military personnel, polar workers, and residents of high-latitude regions. However, the complex mechanisms underlying cold environment-induced cognitive impairment remain to be systematically elucidated. This systematic review synthesizes the effects of cold exposure (CE) on cognitive function and the potential biological mechanisms involved. CE impairs cognition through four interconnected pathways: neuroendocrine dysregulation, oxidative stress, neuroinflammation, and mitochondrial dysfunction. The dual dysregulation of the hypothalamic-pituitary-adrenal axis and the hypothalamic-pituitary-thyroid axis constitutes the core neuroendocrine mechanism, wherein excessive glucocorticoids mediate hippocampal structural damage through mitochondrial reactive oxygen species bursts, autophagic dysregulation, and synaptic plasticity impairment. Oxidative stress is characterized by ROS accumulation and a collapse of antioxidant defenses, with time-dependent decompensation of the Nrf2 pathway exacerbating lipid peroxidation and oxidative modification of synaptic proteins. Neuroinflammation features hippocampal microglial activation and a positive feedback loop involving the HMGB1-NLRP3 inflammasome, driving the cascade release of pro-inflammatory cytokines such as interleukin-1 and tumor necrosis factor-α. Mitochondrial dysfunction manifests as suppressed biogenesis, imbalanced dynamics (Drp1-mediated excessive fission), and decreased oxidative phosphorylation efficiency, leading to neuronal energy crisis and apoptosis. These four pathways amplify each other through positive feedback cycles, ultimately culminating in synaptic plasticity collapse and hippocampal-dependent memory deficits. Based on these mechanisms, this review proposes comprehensive protective strategies, including cold acclimatization training, pharmacological interventions, and targeted therapies. Current research faces challenges such as high heterogeneity in exposure parameters, lack of core body temperature monitoring, and insufficient mechanistic validation. Future efforts should establish standardized research paradigms, quantitatively delineate the relationship between CE intensity/duration and neural injury, and explore precision intervention targets based on the neuroendocrine-immune-metabolic interaction network, thereby providing theoretical foundations and practical approaches for brain health protection in extreme environments.

The pathophysiology of post-traumatic stress disorder (PTSD) shows notable associations with compromised hippocampal neurophysiology. Notwithstanding ongoing debates, PTBP1 knockdown (KD) demonstrates the capacity to drive glia-to-neuron reprogramming, potentially offering therapeutic benefits for some neurodegenerative pathologies. However, PTBP1 KD can upregulate the expression of Nogo-A by alternative splicing, triggering the inhibition of nerve regeneration. Currently, the role of PTBP1 in PTSD remains unknown. Here we sought to elucidate the neurorestorative effects of modulating the PTBP1/Nogo-A/NgR axis in a mouse model of PTSD established through the single prolonged stress paradigm, and the mechanisms were further investigated through a series of experiments including pathological and molecular detection. The results indicated that PTBP1 KD ameliorates PTSD-like behaviors in mice by balancing Bcl-2/Bax expression and suppressing Caspase-3 splicing activation to inhibit hippocampal neuronal apoptosis, enhancing synaptic plasticity through upregulating PSD95 and SYN1, increasing dendritic spine density and stabilizing axonal architecture via elevated NF200 expression. However, compared with single prolonged stress alone, PTBP1 KD potentiates the activation of Nogo-A/NgR pathway, adversely impacting both dendritic morphology and axonal elongation. Therefore, we proposed a combined KD of PTBP1 and NgR to counteract the adverse effects mediated by Nogo-A signal activation, effectively promoting dendritic growth and axonal extension in hippocampal neurons of PTSD mice. Our findings underscore the potential and limitations of PTBP1 as a therapeutic target and propose a novel method for PTSD treatment through combined target intervention of PTBP1 and NgR. This study provides a theoretical foundation for multitarget intervention strategies in the treatment of PTSD and related disorders.

Exposure to severe psychological trauma is a recognized etiological precursor to post-traumatic stress disorder (PTSD), a potentially debilitating psychiatric condition. Increasing evidence indicates a strong connection between mental disorders and the metabolic system, in which the gut microbiota, as a key component, exerts significant influence on psychiatric health. The gut is often referred to as the “second brain”, the gut engages in bidirectional communication with the central nervous system to maintain physiological homeostasis. Trauma affecting the nervous system and cognitive functions such as learning and memory can disrupt the gut microbial community and even trigger inflammatory responses. Conversely, changes in the gut microbiota can adversely affect neurocognitive function. This review systematically summarizes the bidirectional relationship between PTSD and gut microbiota, the pathways through which microbial dysbiosis influences PTSD symptoms, and the underlying mechanisms involving immune regulation, microbial metabolites, and vagus nerve signaling. It also discusses microbiota-based intervention strategies for PTSD, aiming to provide a theoretical foundation for microbial-targeted therapeutic approaches.

Post-traumatic stress disorder (PTSD) is a long-term delayed mental disorder caused by sudden, threatening or catastrophic life events. Chlorogenic acid (CGA) is a polyphenolic acid rich in Eucommia ulmoides and other plants with potential neuroprotective effects, effectively enhances learning and memory, and exerts a beneficial impact on improving mood and attention. However, the effects and mechanisms of CGA on PTSD-like behaviors remain uncertain. This study is to explore the effects and mechanisms of CGA on PTSD by using network pharmacology analysis, molecular docking and experimental validation, and try to provide new strategies for the treatment of PTSD. The results indicated that 9 core targets with a strong binding affinity with CGA were screened out, and they were mainly enriched in apoptosis, inflammation, and oxidative stress. The followed vivo experiments indicated that CGA could alleviate single prolonged stress (SPS)-induced PTSD-like behaviors, and improve hippocampal pathological damage, apoptosis and synaptic plasticity through antioxidant and anti-inflammatory effects by regulating Nrf2 and NF-κB pathways. Thus, CGA may inhibit hippocampal neuronal apoptosis, reduce neuroinflammatory and oxdiative stress response, and enhance hippocampal synaptic plasticity through regulating the crosstalk between Nrf2 and NF-κB signaling pathway, thereby improving SPS-induced PTSD-like behaviors.

Post-traumatic stress disorder (PTSD) is a persistent mental illness caused by severe traumatic events, and its pathogenesis is still unclear. Recent studies indicate that p75 neurotrophic factor receptor (p75NTR) plays a crucial role in neurological diseases, but the role of p75NTR in PTSD is currently unknown. To investigate the effects and mechanisms of p75NTR in PTSD, in this study, a functional p75NTR-deficient mouse was used to establish a PTSD model by single prolonged stress (SPS) paradigm, then the behavioral effects and underlying mechanisms were further investigated. The results demonstrated that p75NTR deletion alleviated anxiety-like behavior and spatial learning and memory impairment in SPS-induced PTSD mice. Further study indicated that deletion of p75NTR downregulated the expression of apoptosis (Bax) and autophagy (Beclin-1) related proteins in the hippocampus of PTSD mice, protected against hippocampal neuronal damage, upregulated the expression of synaptic-related proteins (PSD95 and Synapsin I), increased dendritic complexity and dendritic spine density, and improved synaptic plasticity through the PI3K/Akt/mTOR pathway. In conclusion, deletion of p75NTR rescues behavioral and cognitive dysfunction through PI3K/Akt/mTOR pathway mediated regulation of hippocampal autophagy, apoptosis and synaptic plasticity in SPS-induced PTSD mice, which provides a potential therapeutic target for the treatment of PTSD.

Synaptic plasticity is the basis for the proper functioning of the central nervous system. Synapses are the contact points between neurons and are crucial for information transmission, the structure and function of synapses change adaptively based on the different activities of neurons, thus affecting processes such as learning, memory, and neural development and repair. Synaptic activity requires a large amount of energy provided by mitochondria. Mitochondrial transport proteins regulate the positioning and movement of mitochondria to maintain normal energy metabolism. Recent studies have shown a close relationship between mitochondrial transport proteins and synaptic plasticity, providing a new direction for the study of adaptive changes in the central nervous system and new targets for the treatment of neurodegenerative diseases.

Army aviation is a modern high-tech branch in the army establishment sequence, and has the advantages of flexible mobility and rapid strikes. However, the army aviators face harsh environments, such as low pressure, lack of oxygen, noise, and vibration during long-term flight missions, and often develop various military stresses, bearing greater physical and mental pressure than ordinary people, which is often more likely to lead to psychological stress disorders, thus seriously affecting the combat effectiveness of the army aviation. In this paper, we mainly introduce a series of psychological stress disorders, such as emotional instability, air discomfort, nervousness, anxiety and depression caused by the special circumstances of army aviation while flying, and put forward corresponding countermeasures on this basis, such as optimizing the psychological selection and training standards of army aviation pilots, strengthening psychological tolerance training, paying special attention to the detection and evaluation of mental health in ordinary times, and regularly conducting psychological consultation, intervention and counseling. These measures are of great significance to promote the mental health of army aviators and prevent the occurrence of psychological stress disorder in future wars. Identifying the influencing factors and countermeasures of psychological stress disorder are essential to improve the operational capacity and combat effectiveness of army aviation force.

Whole-body vibration (WBV) is a physical stimulation method that transmits mechanical oscillations to the entire body through a vibration platform or device. Biokinetic and epidemiologic studies have shown that prolonged exposure to high-intensity WBV increases health risks, primarily to the lumbar spine and the nervous system connected to it. There is currently insufficient evidence to demonstrate a quantitative relationship between vibration exposure and risk of health effects. The positive effects of WBV on increasing muscle strength and improving balance and flexibility are well known, but its effects on cognitive function are more complex, with mixed findings, largely related to vibration conditions, including frequency, amplitude, and duration. Studies have shown that short-term low-frequency WBV may have a positive impact on cognitive function, demonstrates potential rehabilitation benefits in enhancing learning and memory, possibly by promoting neuromuscular coordination and enhancing neural plasticity. However, long term exposure to vibration may lead to chronic stress in nerve tissue, affecting nerve conduction efficiency and potentially interfering with neuroprotective mechanisms, thereby having a negative impact on cognitive ability, even causes symptoms such as cognitive decline, mental fatigue, decreased attention, and drowsiness. This literature review aimed to explore the effects of WBV on cognitive function and further to analyze the possible mechanisms. Based on the analysis of literatures, we came to the conclusion that the impact of WBV on cognitive function depends mainly on the frequency and duration of vibration, short-term low-frequency WBV may have a positive impact on cognitive function, while long term exposure to WBV may lead to cognitive decline, and the mechanisms may be involved in neuroinflammation, oxidative stress, synaptic plasticity, and neurotransmitter changes. This review may provide some theoretical foundations and guidance for the prevention and treatment of WBV induced cognitive impairment.

AIMS:Major depressive disorder (MDD) is an enduring and severe mood disorder. Previous studies have indicated that p75NTR is involved in neuronal survival and death. However, the specific mechanism of p75NTR in depression remains unknown. The present study aimed to explore the role and mechanism of p75NTR in depression, and try to provide a new target for the treatment of MDD. MAIN METHODS:The p75NTR knockout and overexpression mice were used to establish a mouse model of depression induced by chronic restraint stress (CRS), and the behavioral effects and potential mechanisms associated with p75NTR knockout/overexpression on CRS-induced depressive mice were investigated by animal behavior, histopathology, immunofluorescence and western blot, respectively. KEY FINDINGS:The results demonstrate that p75NTR knockout/overexpression can ameliorate the depressive-like behaviors observed in CRS-induced depressive mice. Furthermore, p75NTR knockout/overexpression safeguards the tissue morphology of the hippocampus, inhibits the mTOR signaling pathway to restore autophagy, and modulates apoptosis-related proteins (Bcl-2 and Bax) to reestablish normal levels of autophagy and apoptosis in hippocampal neurons of depressed mice. Importantly, p75NTR knockout/overexpression can improve synaptic plasticity through protecting the dendritic structure and dendritic spines of hippocampal neurons, and upregulating the expression of hippocampal synaptic-related proteins (PSD95 and SYN1). SIGNIFICANCE:These findings suggest that p75NTR knockout/overexpression can alleviate CRS-induced depression-like behaviors by reinstating autophagy and suppressing apoptosis in hippocampal neurons, and enhancing hippocampal synaptic plasticity via mTOR pathway. These insights may provide potential targets for clinical treatment of depression.

Post-traumatic stress disorder (PTSD) is a complex mental disorder, closely associated with stress and traumatic events. Salidroside (Sal) has been reported to possess neuroprotective effects. However, the behavioral effects and mechanisms of Sal on PTSD remain unknown. In this study, we utilized a rat model of PTSD induced by single prolonged stress (SPS) and administered Sal intraperitoneally (25, 50, 75 mg/kg/d) for 14 days. We then examined the behavioral effects and underlying mechanisms of Sal on SPS-induced PTSD rats. Our findings demonstrated that Sal alleviated anxiety-like behavior and spatial learning and memory impairment in SPS-induced PTSD rats. Furthermore, Sal treatment preserved the histomorphology of the hippocampal region. It was observed that Sal protected against hippocampal neuronal apoptosis in PTSD rats by reducing the number of TUNEL-positive cells and modulating apoptosis-related proteins (Bcl-2 and Bax). Additionally, Sal inhibited the activation of the NF-κB/iNOS/COX-2 signaling pathway in the hippocampus of PTSD rats, thereby suppressing the release of inflammatory factors (TNF-α and IL-1β) and the activation of microglia. Notably, Sal increased the expression of synapse-associated proteins PSD95 and Synapsin I in the hippocampus, while also enhancing dendritic density in the region. In conclusion, our results demonstrated that Sal could attenuate SPS-induced PTSD-like behaviors by inhibiting hippocampal neuronal apoptosis, enhancing hippocampal synaptic plasticity, and reducing neuroinflammatory responses. These findings may provide a foundation for the potential clinical application of Sal in the treatment of PTSD.

With the outbreak of the Ukrainian crisis, extremely cold environment warfare has once again become the focus of international attention. People exposed to extremely cold environments may suffer from cold damage, further aggravate trauma, trigger high disability and mortality rates, and even cause serious sequelae. To declare the effects and mechanisms of the extremely cold environment on the body after trauma, this paper reviews, firstly, physiological reaction of human body in an extremely cold environment. Then, the post-traumatic body response in an extremely cold environment was introduced, and finally, the sequelae of trauma in extremely cold environment was further summarized in the paper. The results indicated that extremely cold environment can cause a series of damage to the body, especially the body after trauma. The extremely cold factor is a double-edged sword, showing a favorable and unfavorable side in different aspects. Moreover, in addition to the trauma suffered by the body, the subsequent sequelae such as cognitive dysfunction, anxiety, depression and even post-traumatic stress disorder may also be induced. The paper summarizes the human body's physiological response in an extremely cold environment, and declares the effects and mechanisms of the extremely cold environment on the body after trauma, which may provide a theoretical basis for effectively improving the level of combat trauma treatment in extremely cold regions.

The mammalian central nervous system consists of a large number of cells, which contain not only different types of neurons, but also a large number of glial cells, such as astrocytes, oligodendrocytes, and microglia. These cells are capable of performing highly refined electrophysiological activities and providing the brain with functions such as nutritional support, information transmission and pathogen defense. The diversity of cell types and individual differences between cells have brought inspiration to the study of the mechanism of central nervous system diseases. In order to explore the role of different cells, a new technology, single-cell sequencing technology has emerged to perform specific analysis of high-throughput cell populations, and has been continuously developed. Single-cell sequencing technology can accurately analyze single-cell expression in mixed-cell populations and collect cells from different spatial locations, time stages and types. By using single-cell sequencing technology to compare gene expression profiles of normal and diseased cells, it is possible to discover cell subsets associated with specific diseases and their associated genes. Therefore, scientists can understand the development process, related functions and disease state of the nervous system from an unprecedented depth. In conclusion, single-cell sequencing technology provides a powerful technology for the discovery of novel therapeutic targets for central nervous system diseases.

Traumatic brain injury (TBI) is a major reason for temporary or permanent dyskinesia and cognitive impairment of the organism. Generally, TBI induces subsequent neuroinflammation to assist cell debris removal and tissue repair and regeneration after injury. However, overactivation or long-term activation of immune cells will exacerbate nerve damage or death, cause cognitive dysfunction, and ultimately lead to neurodegenerative diseases. Therefore, secondary damage caused by persistent inflammation is a key component of TBI pathological process. As the main metabolite of anaerobic glycolysis, lactate is increased after TBI and participates in brain inflammation as an important immune regulatory molecule rather than a metabolic waste. Importantly, histone lysine lactylation as a novel type of histone post-translational modifications (HPTM) derived from lactate allows lactate to participate in the regulation of complex immunopathophysiological processes of the central nervous system after TBI. Further study on the process of histone lactylation and its immune regulation mechanism during TBI may provide new insights for early intervention and improvement of TBI prognosis. Thus, the authors reviewed the role of histone lactylation in the immune regulation of TBI, so as to further elucidate the mechanism of TBI and the explore new warning and prevention measures from the perspective of HPTM.

Mitochondria are a crucial energy source for maintaining neuronal growth and synaptic function. Neurons possess unique morphological characteristics, which make the proper regulation of mitochondrial transport essential for meeting their energy demands. Syntaphilin (SNPH) is capable of specifically targeting the outer membrane of axonal mitochondria, anchoring them to microtubules, and thereby preventing their transport. SNPH also interacts with other mitochondrial proteins to regulate mitochondrial transport. The regulation of mitochondrial transport and anchoring mediated by SNPH is indispensable for axonal growth during neuronal development, maintenance of ATP levels during neuronal synaptic activity, and regeneration of mature neurons following damage. Precise blocking of SNPH may be an effective therapeutic strategy for neurodegenerative diseases and related mental disorders.

Alternative pre-mRNA splicing, which produces various mRNA isoforms with distinct structures and functions from a single gene, is regulated by specific RNA-binding proteins and is an essential method for regulating gene expression in mammals. Recent studies have shown that abnormal change during neuronal development triggered by splicing mis-regulation is an important feature of various neurological diseases. Polypyrimidine tract binding protein 1 (PTBP1) is a kind of RNA-binding proteins with extensive biological functions. As a well-known splicing regulator, it affects the neuronal development process through its involvement in axon formation, synaptogenesis, and neuronal apoptosis, according to the most recent studies. Here, we summarized the mechanism of alternative splicing, structure and function of PTBP1, and the latest research progress on the role of alternative splicing events regulated by PTBP1 in axon formation, synaptogenesis and neuronal apoptosis, to reveal the mechanism of PTBP1-regulated changes in neuronal development process.

BACKGROUND:In recent years, Salvia miltiorrhiza and its active substances have remarkably progressed in treating central neurological disorders. Tanshinone IIA (TSA) is an active ingredient derived from the rhizome of Salvia miltiorrhiza that has been found to alleviate the symptoms of several psychiatric illnesses. Post-traumatic stress disorder (PTSD) is a mental disorder that results after experiencing a serious physical or psychological injury. The currently used drugs are not satisfactory for the treatment of PTSD. However, it has been reported that TSA can improve PTSD-like symptoms like learning and memory, cognitive disorder, and depression through multi-target regulation.PURPOSE:This paper discusses the ameliorative effects of TSA on PTSD-like symptoms and the possible mechanisms of action in terms of inhibition of neuronal apoptosis, anti-neuroinflammation, and anti-oxidative stress. Based on the pathological changes and clinical observations of PTSD, we hope to provide some reference for the clinical transformation of Chinese medicine in treating PTSD.METHODS:A large number of literatures on tanshinone in the treatment of neurological diseases and PTSD were retrieved from online electronic PubMed and Web of Science databases.CONCLUSION:TSA is a widely studied natural active ingredient against mental illness. This review will contribute to the future development of TSA as a new clinical candidate drug for improving PTSD-like symptoms.

Abscisic acid (ABA), a conserved hormone existing in plants and animals, not only regulates blood glucose and inflammation but also has good therapeutic effects on obesity, diabetes, atherosclerosis and inflammatory diseases in animals. Studies have shown that exogenous ABA can pass the blood-brain barrier and inhibit neuroinflammation, promote neurogenesis, enhance synaptic plasticity, improve learning, memory and cognitive ability in the central nervous system. At the same time, ABA plays a crucial role in significant improvement of Alzheimer's disease, depression, and anxiety. Here we review the previous research progress of ABA on the physiological effects and clinical application in the related diseases. By summarizing the biological functions of ABA, we aim to reveal the possible mechanisms of ameliorative function of ABA on learning and memory, to provide a theoretical basis that ABA as a novel and safe drug improves learning memory and cognitive impairment in central system diseases such as aging, neurodegenerative diseases and traumatic brain injury.

Central nervous system injury diseases can cause the loss of many neurons, and it is difficult to regenerate. The field of regenerative medicine believes that supplementing the missing neurons may be an ideal method for nerve injury repair. Recent studies have found that down-regulation of polypyrimidine tract binding protein 1 (PTBP1) expression can make glial cells transdifferentiate into different types of neurons, which is expected to be an alternative therapy to restore neuronal function. This article summarized the research progress on the structure and biological function of the PTBP family, the mutual regulation of PTBP1 and PTBP2, their role in neurogenesis, and the latest research progress in targeting PTBP1 to mediate the transdifferentiation of glial cells into neurons, which may provide some new strategies and new ideas for the future treatment of central nervous system injury and neurodegenerative diseases. This article is categorized under: RNA Processing > Splicing Regulation/Alternative Splicing.

为了解创伤后应激障碍(posttraumatic stress disorder,PTSD)在大学生中的流行病学特征及影响因素,以重庆市某大学学生为研究对象,采取随机抽样法,利用自拟问卷和创伤后应激障碍症状自评量表平民版(PTSD check-list-civilian version,PCL-C)对大学生PTSD的流行病学进行调查,并利用卡方检验及多因素非条件Logistic回归分析相关影响因素.研究结果表明:在调查的387名大学生中,PTSD阳性症状者64名,占16.54％;不同性别的大学生PCL-C得分女性高于男性,两者差异显著(P<0.05),而不同年龄段间的PCL-C得分无显著差异(P>0.05);暴露于创伤性事件的时间越长PCL-C得分越高,越易患PTSD(P<0.05),而是否经历创伤及在创伤事件中的角色不影响PTSD的患病率(P>0.05);父母去世者可能更易患PTSD(P<0.05).因此,本调查范围的大学生中PTSD的发生率为16.54％,且性别、创伤事件暴露时间及父母是否健在可能为PTSD的主要影响因素.可见,重庆大学生PTSD状况不容乐观,应引起相关高校及教育管理部门高度重视,针对PTSD的影响因素采取相应的干预措施.

当今世界由海上争端引发的局部冲突时有发生,导致以非接触和精准打击为特点的军事行动不断增加.高爆武器可导致舰船人员发生爆炸损伤,爆炸伤员在抛掷落水、跳水逃生、浅海登陆等情况下,可发生海水淹溺,使伤情更为复杂.随着海上搜救技术、伤员自救互救以及战术战伤救治力量的前伸,爆炸受伤后落水伤员获救机会增加,但海水作为一种独特的致伤因素,给伤情及其救治带来特殊影响,本文就爆炸伤合并海水淹溺的伤情特点及救治原则进行综述,为特殊环境下战伤防治研究提供参考.