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Traumatic central nervous system injury can cause imbalance in intestinal microenvironmental homeostasis by disrupting intestinal barrier function, while the disturbed intestinal microenvironment can react on the central nervous system and aggravate the secondary injury of it. A large number of studies suggest that the intestinal barrier plays an important role in the pathophysiological process of traumatic central nervous system injury and can be an important target for the action of central nervous system injury. This paper reviews the structural and functional changes of intestinal microbial, chemical, mechanical and immune barriers after traumatic central nervous system injury and their bidirectional interaction with the central nervous system, summarizes the possible mechanisms leading to the disruption of intestinal barrier, including malnutrition, ischemia-reperfusion injury, inflammatory response and the release of neurotransmitters and hormones, to provide theoretical basis and new ideas for the development of research on the intestinal microenvironment after traumatic central nervous injury.

Parkinson's disease(PD) is a common degenerative disease of the central nervous system in middle-aged and elderly people. The disease has a long course, complex etiology and difficult treatment, which brings a huge burden to patients and their families. At present, there are some limitations in the clinical treatment of PD, and the classical prescription Dihuang Yinzi has made some breakthroughs in the prevention and treatment of PD. This article reviews the clinical application and experimental pharmacological research of Dihuang Yinzi in the treatment of PD, in order to provide a theoretical basis for better application of Dihuang Yinzi in the prevention and treatment of PD. [ABSTRACT FROM AUTHOR]

Copyright of Journal of Sichuan University (Medical Science Edition) is the property of Editorial Board of Journal of Sichuan University (Medical Sciences) and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

To date, approximately 500 monogenic inherited kidney diseases have been reported, with more than 50 genes associated with the pathogenesis of monogenic isolated or syndromic nephrotic syndrome. Most of these genes are expressed in podocytes of the glomerulus. Neurological symptoms are common extrarenal manifestations of syndromic nephrotic syndrome, and various studies have found connections between podocytes and neurons in terms of morphology and function. This review summarizes the genetic and clinical characteristics of monogenic inherited diseases with concomitant glomerular and central nervous system lesions, aiming to enhance clinicians' understanding of such diseases, recognize the importance of genetic diagnostic techniques for comorbidity screening, and reduce the rates of missed diagnosis and misdiagnosis. [ABSTRACT FROM AUTHOR]

The meninges, a four ⁃ layer membrane ⁃ like enclosure around the central nervous system (CNS), house a significant population of immune cells and is an important barrier and pathway for entering the CNS；however, the specific immune processes remain elusive. Recent identification of meningeal lymphatic vessels has shed light on the involvement of meninges in metabolite clearance, immune surveillance and response. Here, we provide a comprehensive review of advancements in meningeal immunity research and its implications for associated disorders. Additionally, potential avenues for future investigations in the realm of meningeal immunity are suggested. [ABSTRACT FROM AUTHOR]

BACKGROUND: Spinal cord injury is a serious disease of the central nervous system, characterized by weak regeneration of neurons and complex pathological processes. Mitochondrial autophagy is a highly selective autophagy that can degrade damaged mitochondria and plays an important role in energy supply, cell metabolism and neuronal survival. OBJECTIVE: To explore the mechanism of mitochondrial autophagy and the effects of drugs on mitochondrial autophagy, and provide a new target for the treatment of spinal cord injury. METHODS: In CNKI, Wanfang and PubMed databases, “spinal cord injury, mitophagy, autophagy, mitochondria” were used as search terms. We searched for articles on the role and mechanism of mitophagy and spinal cord injury. RESULTS AND CONCLUSION: (1) The regulation of mitochondrial autophagy level plays a key role in the treatment of spinal cord injury, and its regulatory mechanism is complex, mainly including PINK1/Parkin, Nix/BNIP3L, FUNDC1, and Atg proteins. In addition, GIT1 regulatory pathway and down-regulated miRNA-124 induction pathway were also found. (2) In terms of treatment, rapamycin, acetyl-L-carnitine, salidroside, betulinic acid, and maltol can inhibit apoptosis and improve spinal cord injury by appropriately activating mitochondrial autophagy. In contrast, rosiglitazone ameliorates spinal cord injury by inhibiting mitochondrial autophagy. This suggests that activation or inhibition of mitochondrial autophagy may improve spinal cord injury, which is related to the different mechanisms of drug action. The specific mechanism of action of the drugs remains to be further studied. [ABSTRACT FROM AUTHOR]

Astrocytes constitute the most abundant cell type in the central nervous system. Under physiological conditions, astrocytes have a variety of functions, and play an important role in maintaining the homeostasis of the central nervous system. However, in response to insults such as injury, inflammation and hypoxia, astrocytes undergo rapid changes in gene expression, morphology and function, and these responses collectively called as astrocyte reactivity. Activated astrocytes have been divided into neurotoxic phenotype (type A1) and neuroprotective phenotype (type A2). Recent studies have shown that A1 astrocytes are widely involved in the occurrence and development of various central nervous system diseases. Therefore, targeted regulation of activated astrocytes by combining multiple techniques is expected to be a potential treatment for central nervous system diseases. Here, we review recent advances of A1 astrocytes, including the molecular mechanism of phenotypic transformation and its role in neurodegenerative and neuroinflammatory diseases. [ABSTRACT FROM AUTHOR]

Central nervous system(CNS)is a complex system closely related to anesthesiology. The molecular biological mechanisms of many CNS diseases were not exactly clear. Long noncoding RNA(lncRNA) H19 is abundant in human brain and plays an important role in the regulation of various CNS diseases. Besides, lncRNA H19 is also involved in the mechanism of several anesthetics. In this review, we emphasized the role and addressed the specific mechanisms of lncRNA H19 in CNS diseases and anesthetics, hoping to provide a new theoretical basis for future researches. [ABSTRACT FROM AUTHOR]

Neurophysiological technique uses the bioelectrical principle to record the spontaneous or external stimulation-induced electrical activities of the central or peripheral nervous system. Due to the essential difference in the pathophysiological mechanism of functional and organic movement disorders, neurophysiology is of great significance for the diagnosis and differential diagnosis of the central and peripheral nervous systems. In order to improve the understanding of the pathogenesis of functional movement disorder (FMD) and provide the basis for the accurate diagnosis, this paper reviews the common clinical neurophysiological techniques and their application in FMD. [ABSTRACT FROM AUTHOR]

Spinal cord injury (SCI) is a serious disease of the central nervous system (CNS), which often leads to motor dysfunction and is associated with a variety of serious complications, seriously affecting the quality of life of patients. N6-methyladenosine (m6A) is a methylation modification that occurs at the N6 site of adenos- ine, also known as the m6A methylation modification, which is of great interest because of its great potential for diagnosis and treatment of neurological diseases. m6A modifications are catalyzed by methyltransferases, removed by demethylases, recognized by methyl-recognition proteins, and its associated regulatory proteins can affect the development of SCI and its secondary damage through various pathways. Up to now, the mechanism of m6A modi- fication in SCI has not been fully elucidated. In this paper, we review the basic functions of m6A modification and its role and mechanism in SCI. [ABSTRACT FROM AUTHOR]

BACKGROUND: In recent years, with the rapid development of biomedicine, the study of brain aging and exosomes has attracted more and more attention, but there is no bibliometrics analysis in this field. OBJECTIVE: To objectively analyze domestic and foreign literature on brain aging and exosomes in the past 15 years, to summarize the research status, hot spots, and development trends in this field. METHODS: Using the core database of Web of Science as a search platform, we downloaded the literature on brain aging and exosomes published from the establishment of the database to December 28, 2022, and analyzed the data from the aspects of country or region, institution, author, keywords, and co-cited literature using CiteSpace 6.1.R6 visualization software. RESULTS AND CONCLUSION: A total of 1 045 research articles were included, and the number of publications on brain aging and exosomes research both domestically and internationally was showing an increasing trend year by year. The United States ranked first with 429 papers, and China ranked second with 277 papers. Louisiana State University ranked first with 16 articles. Professor Lukiw Walter J from Louisiana State University in the United States was the author with the highest number of publications, and Professor Bartel DP from the Massachusetts Institute of Technology was the author with the most citations. The most prolific Journal was the International Journal of Molecular Sciences. Alzheimer’s disease, microRNA, gene expression, extracellular vesicles, exosomes, oxidative stress, and biomarkers are the most relevant terms. According to the research on hot topics, biomarkers have become a new research hotspot. The above results indicate that the research on brain aging and exosomes has gradually increased in the past 15 years. The research direction has gradually shifted from the initial exploration of the expression of miRNAs in central nervous system diseases related to brain aging to the search for biomarkers that can identify and diagnose neurodegenerative diseases. The study of exocrine miRNAs to protect central nervous system from damage has emerged as promising therapeutic strategy. [ABSTRACT FROM AUTHOR]

BACKGROUND: The quality of cultured neurons is the key to the study of central nervous system diseases, but there has been no unified standard for the methods used. OBJECTIVE: To explore the effects of best selection site and cytarabine treatment conditions on the viability, purity and maturity of primary cultured neurons. METHODS: The cells were obtained at 2.0-3.0 mm on the surface of the cerebral cortex of Sprague-Dawley rats within 24 hours of the newborn, and treated with cytarabine at a concentration of 5 μmol/L or 10 μmol/L at 24, 48, and 72 hours after culture. In addition, the whole cerebral cortex was removed for primary culture and treated with cytarabine at a concentration of 5 μmol/L for 48 hours at 48 hours after culture. At 7 days after culture, the morphology of neuron was observed using inverted microscope and the effect of cytarabine on neuronal viability was detected by CCK-8 assay. The purity and maturity of neurons were assessed by immunofluorescence and western blot assay. RESULTS AND CONCLUSION: (1) Inverted microscope: The density of neurons in the 10 μmol/L cytarabine group at 24, 48, and 72 hours was lower than that in the 5 μmol/L cytarabine group at the same time point, and the neuronal processes in the six groups could be connected to each other to form a dense network structure. The neuron cell body was plump and full of refractive properties. The cell density of the whole cortex group was lower than that of the normal control group, and non-neuronal cells could be clearly observed. (2) CCK-8 assay: The cell viability of each cytarabine group was lower than that of the normal control group (P < 0.001), and the neuronal viability of the 10 μmol/L cytarabine 24-, 48-, and 72-hour groups was lower than that of 5 μmol/L cytarabine group at the same time point (P < 0.05). The neuronal viability in the 5 μmol/L cytarabine 24-hour group was lower than that in the 5 μmol/L cytarabine 48- and 72- hour group (P < 0.01). (3) Immunofluorescence staining: The purity of neurons in each cytarabine group was greater than that in the normal control group and all cortical groups (P < 0.001), and there was no difference in the purity of neurons in each cytarabine group. (4) Western blot assay detection of neuronspecific enolase protein expression: The neuron maturity of each cytarabine group was higher than that of the normal control group (P < 0.05), and the 5 μmol/L cytarabine 48-hour group had the highest maturity. (5) The results showed that the cortex at 2.0-3.0 mm on the surface of the rat cerebral cortex within 24 hours of the newborn treated with 5 μmol/L cytarabine at 48 hours after culture can obtain better neuronal viability, maturity and purity. [ABSTRACT FROM AUTHOR]

Copyright of Journal of Modern Laboratory Medicine is the property of Journal of Modern Laboratory Medicine Editorial Department and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Alzheimer's disease (AD) is a degenerative disease of the central nervous system. The pathogenesis of AD is complex and diverse, and its occurrence and development is the result of the interaction of multiple factors. A number of studies have shown that mTOR signaling pathway is closely related to AD. In recent years, people in exploring relevant methods for the treatment of AD and the process of drugs, more and more studies have found that traditional Chinese medicine compound traditional Chinese medicine monomer, and can be applied to mTOR signaling pathway to improve symptoms in patients with AD. This paper will review the mechanism of action and treatment of TCM in Alzheimer's disease based on mTOR signaling pathway in recent years, so as to provide reference and expand thinking for the prevention and treatment of AD. [ABSTRACT FROM AUTHOR]

Renin⁃angiotensin system (RAS) plays an important role in maintaining cardiovascular homeostasis, water and electrolyte balance in the body, and angiotensin converting enzyme Ⅱ (ACE2) and its axis of action angiotensin⁃(1⁃7) [Ang⁃(1⁃7)] and Mas receptor (MasR) composed of Ang⁃(1⁃7) and MasR axis can play an important role in this process, it can widely participate in the pathophysiological process of central nervous system diseases. Based on the structure and function of RAS, this study plans to sort out the latest relevant research results on the role of ACE2⁃Ang⁃(1⁃7)⁃MasR axis in ischemic stroke, cognitive dysfunction, anxiety state and neurodegenerative disease, improve the understanding of researchers and clinicians, and provide ideas for the development of new targets for central nervous system disease drugs in the future.

Copyright of Chinese Journal of Contemporary Pediatrics is the property of Xiangya Medical Periodical Press and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Chinese Journal of Preventive Veterinary Medicine / Zhongguo Yufang Shouyi Xuebao is the property of Chinese Journal of Preventive Veterinary Medicine Editorial Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Cell metabolomics is an important branch of metabolomics, which could dynamically monitor cell response and metabolic changes after drugs acting on cells, and look for potential biomarkers. Cell metabolomics has been widely used in illustration of disease mechanism, evaluation of drug efficacy and development of new drug through elucidating the pathophysiological mechanism of the disease and the effect of drug treatment intervention. The researches process of cellular metabolomics and its application in central nervous system diseases were reviewed in order to provide theoretical basis for in-depth study of the pathogenesis and prevention and treatment of central nervous system diseases. [ABSTRACT FROM AUTHOR]

BACKGROUND: Spinal cord injury is a kind of common central nervous system disease, causing dysfunction below the injury plane, which affects patient’s living quality and endangering human’s life seriously. The use of motor imagery therapy in the treatment of spinal cord injury is a new rehabilitation field in recent years, and it is a kind of rehabilitation treatment technology with a great development potential. OBJECTIVE: To review the basic principles of motor imagery, the possible mechanism of motor imagery applied to spinal cord injury and the research progress. METHODS: “Spinal cord injury, motor imagery” were used as search terms to retrieve articles on PubMed, Web of Science, CNKI, and Wanfang databases from inception to September 2021. The author excluded the articles that were not correlated with the research purpose, were repetitive, and had low credibility, and summarized the 94 articles that finally met the standard. RESULTS AND CONCLUSION: (1) Motor imagery first was put forward in the 1950s, and then it is identified that motor imagery is a special kind of movement function status, and is repeatedly simulation and rehearse some movement of patients with a mental state. It exists in memory, activates the motor memory center, and without any obvious motor output, and follows the principle of central motion control. (2) The theoretical model of motor imagery therapy is generally recognized as psycho-neuromuscular theory, which holds that motor imagery is similar to the neuromuscular activity induced by motor execution. (3) The mechanism of motor imagery therapy for spinal cord injury is unclear. For patients with spinal cord injury, because brain structure is not damaged, the patient’s ability of motor imagery should be properly preserved. The current studies show that the mechanism may be that spinal cord injury patients and healthy people could activate similar brain regions. In patients with spinal cord injury, similar brain regions are activated by motor imagery and motor execution. Patients can induce the development of central nerve plasticity and functional reorganization through continuous motor imagery training, which can promote the recovery of function. (4) Clinically, current studies have shown that motor imagery training can relieve neuropathic pain, improve motor and bladder function in patients with spinal cord injury. Motor imagery therapy as an adjuvant therapy should be adopted in conventional rehabilitation programs for patients with spinal cord injury. However, there is high heterogeneity in clinical efficacy, and further research is necessary. (5) Brain computer interface can convert the signals generated during the patient’s motor imagery into driving signals to control external devices to achieve the re-movement of paralyzed limbs. The development of motor imagery with brain computer interface is considered to be a revolutionary change in rehabilitation after spinal cord injury and has a very good development prospect. [ABSTRACT FROM AUTHOR]

Central nervous system immune diseases include multiple sclerosis (MS), neuromyelitis optica spectrum disorders (NMOSDs), myelin oligodendrocyte glycoprotein⁃IgG associated disorders (MOGAD) and anti⁃N⁃methyl⁃D⁃aspartate receptor (NMDAR) encephalitis. The pathogenesis of these diseases is complex, and a variety of central nervous system and peripheral cells are involved. Single⁃cell omics has achieved high⁃resolution detection of the expression profile at the level of single⁃cell through a series of sequencing techniques to analyze cell heterogeneity and functional phenotype. This review will summarize the single cell sequencing (SCS) and its applications in the above⁃mentioned diseases.

BACKGROUND: Alzheimer’s disease is a degenerative disease of the central nervous system with the loss of brain cells and neurons, mainly manifested as cognitive dysfunction and memory decline. Abnormal synaptic plasticity is an important cause of cognitive decline in patients with Alzheimer’s disease. Numerous studies have shown that aerobic exercise can significantly improve patient’s cognitive decline due to Alzheimer’s disease; however, there is a lack of systematic and comprehensive understanding of the mechanism by which aerobic exercise improves synaptic plasticity as well as the effect of aerobic exercise on synaptic plasticity. OBJECTIVE: To comprehensively review the domestic and foreign literature on the synaptic plasticity induced by aerobic exercise stimulation and its alleviation of cognitive decline in Alzheimer’s disease patients, and to reveal the mechanism by which aerobic exercise improves cognitive function of Alzheimer’s disease patients, so as to provide theoretical basis and practical reference for the prevention and delay of Alzheimer’s disease progression by aerobic exercise. METHODS: The first author retrieved relevant literature in ELSEVIER, Web of Science, PubMed, CNKI, and WanFang using the keywords of “aerobic exercise, synaptic plasticity, cognitive function, exercise training, physical activity, cognitive neuroscience, Alzheimer’s disease” in English and Chinese, respectively. As per the inclusion criteria, 82 documents were finally selected and discussed. RESULTS AND CONCLUSION: Aerobic exercise can activate brain synaptic plasticity at molecular level to improve cognitive function in patients with Alzheimer’s disease. (1) Aerobic exercise can inhibit amyloid β deposition and aberrant phosphorylation of Tau protein, promote brain neurotrophic factor expression, regulate mitochondrial biogenesis, and reduce mitochondrial dysfunction through molecular signaling pathways, thereby improving brain microenvironment and stimulating the positive changes in synaptic plasticity. (2) Aerobic exercise intervention has a positive effect on to the cognitive function of patients with Alzheimer’s disease. Low-intensity aerobic exercise can improve the expression of synaptic plasticity-related proteins and reduce synaptic loss. High-frequency aerobic exercise can promote an increase in synaptic density. Mid-and-long-term can continuously up-regulate the level of synaptic-related proteins in the brain and maintain the changes in synaptic plasticity. (3) Aerobic exercise is a complex variable, and interventions for Alzheimer’s disease need to be individualized as per patient’s conditions, and appropriate exercise prescriptions should be taken according to the severity of the disease. [ABSTRACT FROM AUTHOR]

Multiple sclerosis is an immune disease characterized by inflammatory demyelinating disease of the central nervous system. The disease is a lifelong disease. The main goal of treatment in remission stage is to control the progress of the disease. Disease-modifying treatment is the standard treatment in remission stage of multiple sclerosis, which can reduce the clinical attack and disability progress of patients with recurrence remission to varying degrees. In recent years, more progress has been made in the disease correction treatment of multiple sclerosis. A variety of monoclonal antibodies and oral preparations have been listed at home and abroad, providing a variety of options for the disease correction treatment of multiple sclerosis and improving the treatment effects. This paper reviews the drugs for disease-modifying treatment listed at home and abroad, so as to provide reference for clinical medication. [ABSTRACT FROM AUTHOR]

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Objective To study the dangerous variations of vertebral artery (VA) at craniovertebral junction (V3 segment). Methods The imaging data of 834 patients who underwent DSA in Jining No. 1 People's Hospital from January 2019 to October 2020 were collected, the incidences of dangerous anatomical variation and dangerous functional variation of persistent first intersegmental artery, VA fenestration, posterior inferior cerebellar artery (PICA) with lower origin, dominant VA and terminating PICA were analyzed. Results The variation of V3 segment of VA was divided into dangerous anatomical variation and dangerous functional variation. Dangerous anatomic variation included persistent first intersegmental vertebral artery, VA fenestration and PICA with lower origin. The incidence of the three types of unilateral dangerous anatomical variation was 1.92% (17/834), 1.80% (16/834) and 1.68 (15/834). The incidence of bilateral dangerous anatomical variation was 0.12% (1/834), while one side of the VA was fenestrated and the other side was the persistent first intersegmental artery. Dangerous functional variation included dominant VA and terminating PICA. The incidence of these two functional variation was 13.19% (110/834) and 3.72% (31/834). The left dominant VA was more common (79.09%, 87/110), while the right was 23 cases (20.91%, 23/110). Thirty-one cases (3.72%, 31/834) of terminating PICA, while 26 cases (83.87%, 26/31) in the right and 5 cases (16.13%, 5/31) in the left. Conclusions The incidence of dangerous variation in V3 segment of VA is high. Imaging dangerous anatomical variation and dangerous functional variation should be routinely performed before craniovertebral junction surgery to evaluate the possible VA examinations variation patients, so as to reduce the risk of VA injury during surgery. [ABSTRACT FROM AUTHOR]

Central nervous system(CNS) disorders can significantly impact patients' daily lives, impairing their ability to work and imposing a substantial financial burden on their families. In recent years, the incidence of CNS diseases has shown a significant increase with the continuous improvement of the quality of life and the aging problem. Therefore, the search for new preventive and curative drugs has been a research hotspot for this group of diseases. Osthole(OST), isolated from Umbelliferae such as Cnidium monnieri, Angelica sinensis, and Heracleum hemsleyanum, possesses a variety of pharmacological effects such as neuroprotective, antioxidant, anti-inflammatory, and antithrombotic effects. There is increasing evidence that OST has demonstrated significant preventive and curative effects in various CNS disease models. This paper systematically reviewed the research progress of OST in preventing and treating CNS diseases by reviewing domestic and international literature to provide more in-depth theoretical support for the future clinical application of OST in the prevention and treatment of CNS diseases.

BACKGROUND: Central nervous system diseases are often closely related to neuronal apoptosis. Astrocytes are closely related to neurons. It remains poorly understood whether extracellular vesicles, which are derived from astrocytes, especially activated astrocytes, may inhibit glutamate-induced neuronal apoptosis, thereby exerting neuroprotective effect. OBJECTIVE: To investigate the role and possible mechanism of astrocyte extracellular vesicles (AS-EVs) and lipopolysaccharide-preconditioned astrocyte extracellular vesicles (LPAS-EVs) in glutamate-induced neuronal injury. METHODS: Astrocyte was cultured in vitro and induced activation model was established by lipopolysaccharide. The supernatant of cells of two groups was collected and extracellular vesicles were extracted by hypervelocity centrifuges, and then identified. PC12 cells were used for preliminary experiments. First, we investigated the effects of AS-EVs and LPAS-EVs on PC12 cell proliferation, and then established the PC12 cells and primary neurons injury model induced by glutamate. Experiment was divided into four groups: PBS group (PBS of the same volume as EVs groups, 24 hours), glutamate group (10 mmol/L glutamate, 24 hours), AS-EVs group (200 mg/L AS-EVs, 24 hours + 10 mmol/L glutamate, 24 hours), and LPAS-EVs group (200 mg/L LPAS-EVs, 24 hours + 10 mmol/L glutamate, 24 hours). The survival rate of PC12 cells was determined by CCK-8 assay. Western blot assay was used to detect the expression of apoptosis related proteins Bax and Bcl-2. RESULTS AND CONCLUSION: (1) Astrocyte was extracted and lipopolysaccharide-induced astrocyte activation model was established successfully. (2) AS-EVs and LPAS-EVs were successfully extracted, which met the morphological standards of extracellular vesicles and showed positive expression of related markers. (3) AS-EVs and LPAS-EVs had no significant effect on PC12 cells proliferation. (4) Compared with glutamate group, AS-EVs and LPAS-EVs could improve the survival rate of PC12 cells, and the effect of LPAS-EVs was stronger than that of AS-EVs (all P < 0.05, n=3). (5) AS-EVs and LPAS-EVs could inhibit the pro-apoptotic protein Bax expression and promote the expression of anti-apoptotic protein Bcl-2 (all P < 0.01, n=3), and then inhibited apoptosis of PC12 cells and primary neurons, thus playing a neuroprotective role, and the effect of LPAS-EVs was stronger than that of AS-EVs (all P < 0.05). (6) The results conclude that extracellular vesicles derived from astrocytes can inhibit the apoptosis of neurons injured by glutamate, which has a neuroprotective effect, and this effect is enhanced after being stimulated by lipopolysaccharide. [ABSTRACT FROM AUTHOR]

Objective To investigate the clinicopathological features of central nervous system diffuse and multifocal lesions in the cerebral white matter. Methods The clinical and radiological data of 27 cases of diffuse and multifocal lesions in the cerebral white matter were collected from January 2015 to December 2020. The pathological features of these cases were retrospectively analyzed. Results All cases ranged from 10 to 73 years old, female 12 cases, male 15 cases. Clinical manifestations included dyskinesia and paresthesia (17 cases), headache and dizziness (10 cases), cognitive decline and language dysfunction (3 cases each), sleep disorder, visual impairment and epilepsy seizure (2 cases each). They showed diffuse and multifocal lesions in the cerebral white matter involving three or more lobes. Twenty⁃four cases performed stereotactic puncture, and 3 others accepted craniotomy. Pathological findings included 11 tumoral lesions, such as diffuse glioma 8 cases, lymphomatosis cerebri 2 cases, intravascular large B cell lymphoma one case; as well as 16 cases non⁃tumor lesions, such as idiopathic inflammatory demyelinating diseases 10 cases, primary angiitis of central nervous system 3 cases, progressive multifocal leukoencephalopathy one case, leukoencephalopathy with cerebral calcifications and cysts one case, and adult⁃onset leukoencephalopathy with axonal spheroids and pigmented glia one case. Conclusions Diffuse and multifocal lesions of the cerebral white matter includes tumor and non⁃tumoral diseases with no specific clinical manifestations. Stereotactic puncture is needed to reach a correct clinicopathological diagnosis, and ensure the precision treatment. doi:10.3969/j.issn.1672⁃6731.2021.04.007

Copyright of Food Research & Development is the property of Food Research & Development Editorial Department and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Central nervous system immune diseases include multiple sclerosis (MS), neuromyelitis optica spectrum disorders (NMOSDs), myelin oligodendrocyte glycoprotein - IgG associated disorders (MOGAD) and anti - N - methyl - D - aspartate receptor (NMDAR) encephalitis. The pathogenesis of these diseases is complex, and a variety of central nervous system and peripheral cells are involved. Single-cell omics has achieved high-resolution detection of the expression profile at the level of single-cell through a series of sequencing techniques to analyze cell heterogeneity and functional phenotype. This review will summarize the single cell sequencing (SCS) and its applications in the above-mentioned diseases. [ABSTRACT FROM AUTHOR]

Some primary or secondary diseases of the central nervous system are closely related tohuman immune system. Autoimmune diseases such as multiple Takayasu arteritis (MTA) can causeintracranial vascular lesions. The disorder of autoimmune system can cause limbic encephalitis (LE) andautoimmune hypophysitis (AH). Patients with immunodeficiency disease are prone to opportunisticinfections of the nervous system and malignant lymphoma. At present, the pathogenesis of many immune⁃related diseases in neurosurgery are not clear, and there is a lack of "golden standard" for diagnosis. Someimmune⁃related diseases in neurosurgery, such as human immunodeficiency virus (HIV) encephalopathy andparaneoplastic neurological syndrome (PNS), have low incidence and high clinical misdiagnosis rate. Mostof the immune⁃related diseases in neurosurgery have their own characteristics in terms of pathophysiology,clinical and imaging feature, etc. Understanding these characteristics will be of great help to the diagnosisand differential diagnosis of relevant clinical diseases. This paper intends to briefly describe the commonimmune ⁃ related diseases in neurosurgery, so as to improve clinicians' understanding of immune ⁃ relateddiseases in neurosurgery and even save more patients' lives. DOI：10.3969/j.issn.1672⁃6731.2020.02.010

Phosphodiesterases (PDE) are involved in the regulation of cellular physiological processes and neurological functions, including neuronal plasticity, synapto-genesis, synaptic transmission, memory formation and cognitive functions by catalyzing the hydrolysis of intracellular cyclic adenosine monophosphate (cAMP) and cyclic guanosine monophosphate (cGMP). Many basic and clinical studies have shown that PDE4 inhibitors block or ameliorate the occurrence and development of central nervous system (CNS) diseases by inhibiting cAMP hydrolysis, increasing cAMP content and enhancing its downstream effects. PDE4 inhibitors have long-term potentiation effect, which can enhance phosphorylation of cAMP response element binding protein (CREB) and upregulate expression of memory related Arc genes in hippocampal neurons, thereby improving cognitive impairment and Alzheimer's disease-like symptoms. They can also delay the occurrence and development of Parkinson's disease by reducing the cytotoxicity induced by α-syn and increasing the effect of miR-124-3p on cell functions. Alteration of PDE4 activity is the molecular basis for psychosis and some cognitive disorders, therefore it is considered as a therapeutic target for schizophrenia. PDE4 inhibitors play a role in depression by inhibiting the advanced glycation end product receptor (RAGE), TLR4 and NLRP3 pathways in the hippocampus, reducing the activation of microglia and the production of IL-1β, down-regulating HMGB1/RAGE signaling pathway and inhibiting inflammatory factors. PDE4 inhibitor plays a role in the treatment of autism spectrum disorder by reducing the damage of cerebellar glial cells, increasing nociceptive threshold, and improving mutual learning and memory deficits. PDE4 inhibitors might be used in the treatment of fragile X syndrome by regulating the level of cAMP and affecting the expression of fragile X mental retardation protein (FMRP). PDE4 inhibitors can also promote the differentiation of oligodendrocyte progenitor cells and enhance myelination, which has potential in the treatment of multiple sclerosis. PDE4 is also related to bipolar disorder, which may be one of the therapeutic targets. At present, several PDE4 inhibitors are in clinical trials for the treatment of CNS diseases. This article reviews and discusses the progress on basic research and clinical trials of PDE4 inhibitors in CNS diseases, providing a reference for the prevention and treatment of CNS diseases and the development of new drugs.

At present, there is a lack of imaging methods to monitor demyelination and myelin regeneration of central nervous system demyelinating diseases. All kinds of MRI techniques are used to measure demyelination indirectly and are vulnerable to other interference factors. PET is an imaging technique that can image central nervous system diseases at the molecular level. It can realize real-time imaging of function, metabolism, biochemistry and make up for the limitations of MRI. PET myelin imaging tracers have developed rapidly in recent years. There are currently three types of PET tracers targeting myelin: congo red derivatives, diphenylethylene derivatives and sulforaphane derivatives. The new multimodal medical imaging technology PET/MRI combines the advantages of PET molecular level imaging and MRI high soft tissue resolution to realize real-time fusion of anatomical structure and functional, metabolic, biochemical images. In the future, it may become an effective means to monitor demyelinating lesions of the central nervous system. [ABSTRACT FROM AUTHOR]

BACKGROUND: In the diseases process of the central nervous system, pathogenic factors stimulate microglia cells to over-activate and secrete inflammatory factors, which lead to further injury of neurons. Whether the deacetylase inhibitor sodium butyrate can reduce the over-activation and inflammatory effects of microglia cells caused by fluorosis is worthy of further study. OBJECTIVE: To investigate the effects of sodium butyrate on fluorine-induced over-activation of microglia in the brain and the expression of inflammatory factors interleukin-1β, interleukin-6 and tumor necrosis factor-α. METHODS: Microglia cells (BV-2) were routinely cultured in F12/DMEM medium containing 10% fetal bovine serum. CCK-8 method was used to observe the effects of sodium fluoride, sodium butyrate and their combination on the viability of BV-2 cells in logarithmic growth phase. The morphology of BV-2 cells after treatment with sodium fluoride, sodium butyrate and their combination, mRNA and protein expressions of interleukin-1β, interleukin-6 and tumor necrosis factor-α were observed by inverted microscope, RT-qPCR and western blot assay. RESULTS AND CONCLUSION: (1) CCK8 results showed that 25×10-6 sodium fluoride could reduce the viability of BV-2 cells, and 0.25 mmol/L sodium butyrate could increase the viability of BV-2 cells. Sodium butyrate 0.25 mmol/L could reverse the decreased viability of 25×10-6 sodium fluoride on BV-2 cells. (2) RTqPCR and western blot assay results showed that 0.25 mmol/L sodium butyrate could antagonize the over-expression of interleukin-1β, interleukin-6 and tumor necrosis factor-α induced by 25×10-6 sodium fluoride. (3) It indicates that sodium butyrate, in a certain dose, can reduce the inflammatory response mediated by fluorium-induced microglia cells. [ABSTRACT FROM AUTHOR]

Astrocyte-neuron transformation (ANT) is an important discovery in neuroscience field in the 21st century. Astrocytes are the largest number of glial cells and originate from the same precursor cells as neurons. Their potential to transform into neurons has brought new hope for the treatment of various neurological diseases characterized by neuronal damage or loss. There have been many successful experiments on the transformation of astrocyte-neuron in vitro, but the exploration in vivo is just beginning. Transcription factors, drugs, and microRNAs have been found to induce this transformation in animal models. Meanwhile, astrocyte-neuron transformation can be induced by pathological conditions such as Alzheimer’s disease, spinal cord injury, focal stroke, and Parkinson’s disease. In this paper, we systematically review the current status of studies on the transformation of astrocytes into neurons in normal and related disease animal models, and sort out the possible mechanisms of astrocytes’ reprogramming, neuronal transformation, then supplement and integration into damaged neural circuits. [ABSTRACT FROM AUTHOR]

Nervous system diseases are associated with complexity and diversity. As a result, the prognosis of patients deeply depends on physicians' clinical experience and their diagnosis and treatment level. With the exponential growth of medical big data and the development of statistical analysis tools, more researchers discover the pathogenesis of diseases and assist clinical process through the mining of big data, so as to improve the diagnosis, treatment, and prognosis of nervous system diseases. This paper elaborates the application of three kinds of medical big data in nervous system diseases, including structured data, radiomics, and bioinformatics. [ABSTRACT FROM AUTHOR]

Cerebral amyloid angiopathy associated with inflammation (CAA-I) is a rare subtype of cerebral amyloid angiopathy (CAA), and is increasingly recognized by neurologists. CAA-I is characterized by the pathological hallmarks of both CAA and vasculitis. The main clinical manifestations contain cognitive decline, seizures, headaches and so on, which present great clinical heterogeneity. Cranial MRI plays an important role in the diagnosis and evaluation of CAA -I, by which white matter hyperintensity (WMH) and multiple cerebral microbleeds (CMBs) could be usually found. CAA-I responds well to immunosuppressive therapy. All the characteristics above are different from CAA somehow. This paper aims to review the advances in pathophysiology, pathology, clinical manifestations, laboratory examination and treatment of CAA-I. [ABSTRACT FROM AUTHOR]

BACKGROUND: Brain tissue is the most complex structure of human development. Many human brain diseases are difficult to reproduce in animals, so the establishment of an in vitro model of brain development has a very important research value. In recent years, with the rapid development of the field of stem cells, an artificial tissue culture technology has emerged, that is, through the three-dimensional culture in vitro, stem cells from a single cell are produced into a complex structure resembling whole organs, which is called organoids. OBJECTIVE: To review the research progress of brain organ in recent years from the aspects of the current situation of brain organ culture, pathogenesis, histological characteristics and application in nervous system diseases, and analyze the research defects of brain organ in order to provide reference for the research in related fields. METHODS: CNKI, Wanfang, and PubMed databases were searched by the first author for related studies published from January 1998 to June 2019. The keywords were "organoids, cerebral organoids, embryonic stem cells, induced pluripotent stem cells, neurogenesis, cerebral cortex, development, neurodegenerative disease" in Chinese, and 'organoids, cerebral organoids, embryonic stem cells, induced pluripotent stem cells, neurogenesis, cerebral cortex, development, neurological diseases, self-organization' in English. Finally, 45 eligible artides were included in result analysis. RESULTS AND CONCLUSION: The cerebral organoids can be effectively developed in vitro by using the self-organization of pluripotent stem cells and adding nerve-inducing factors. As a new biological culture technology, cerebral organoids have great research and application value in investigating development of living tissue, the mechanism of disease formation, tissue replacement therapy and drug experiments. [ABSTRACT FROM AUTHOR]

Some primary or secondary diseases of the central nervous system are closely related to human immune system. Autoimmune diseases such as multiple Takayasu arteritis (MTA) can cause intracranial vascular lesions. The disorder of autoimmune system can cause limbic encephalitis (LE) and autoimmune hypophysitis (AH). Patients with immunodeficiency disease are prone to opportunistic infections of the nervous system and malignant lymphoma. At present, the pathogenesis of many immune-related diseases in neurosurgery are not clear, and there is a lack of "golden standard" for diagnosis. Some immune-related diseases in neurosurgery, such as human immunodeficiency virus (HIV) encephalopathy and paraneoplastic neurological syndrome (PNS), have low incidence and high clinical misdiagnosis rate. Most of the immune-related diseases in neurosurgery have their own characteristics in terms of pathophysiology, clinical and imaging feature, etc. Understanding these characteristics will be of great help to the diagnosis and differential diagnosis of relevant clinical diseases. This paper intends to briefly describe the common immune-related diseases in neurosurgery, so as to improve clinicians' understanding of immune - related diseases in neurosurgery and even save more patients' lives. [ABSTRACT FROM AUTHOR]

Stem cell-derived extracellular vesicles can regulate functions of targeting cells in lesions and have fewer risks in treating diseases. In central nervous injury lesions, stem cell-derived extracellular vesicles can promote neurogenesis and angiogenesis and regulate nervous inflammation, which promotes the recovery of the nerve injury. Stem cell-derived extracellular vesicles can ease Aβ protein-related neuron damage in Alzheimers disease. Stem cell-derived extracellular vesicles also can deliver microRNA and chemotherapeutic agents to neuroglioma cells. This review introduces recent advances in using stem cell-derived extracellular vesicles in treating central nervous system diseases. [ABSTRACT FROM AUTHOR]

Central nervous system diseases are complicated, and general examinations are lack of accuracy because they are easily influenced by subjective factors of patients. Objective results from optical coherence tomography (OCT) can detect the changes of ocular posterior structures, and then further reflect the neuronal degeneration. The aim of this review is to discuss the application of OCT in central nervous system diseases and look for new biomarkers. DOI: 10.3969/j.issn.1672-6731.2017.05.013

Objective To investigate the clinical characteristics of nervous system involvement in patients with primary Sjogren’s syndrome (pSS). Methods Data of 32 pSS patients with nervous system involvement collected from Tianjin Medical University General Hospital and Peking Union Medical College Hospital were retrospectively analyzed. The demographic characteristics, clinical symptoms, laboratory parameters and imaging results were evaluated and analyzed. Results In 32 patients with pSS, there were 30 (93.8%) females and 2 (6.2%) males, with the average age 46±12 years. The neurological impairment was the first symptom in 16 (50%) patients, and sicca symptoms was the first symptom in the rest patients. Thirteen (40.6%) patients developed isolated peripheral nervous system (PNS) damages, 10 (31.3%) patients developed isolated central nervous system (CNS) damages, and 9 (40.6%) patients showed both (CNS-PNS). The most common lesion of PNS was polyneuropathy (6, 18.8%). The most common lesion of CNS was optic neuromyelitis pedigree disease (NMODS, 6, 18.8%). Patients with PNS lesion were more likely to have Reynolds phenomenon than those with CNS lesion (P=0.046). The prevalence of interstitial lung disease (ILD) was significantly higher in pSS patients with PNS and CNS-PNS damages than patients with CNS lesion (P=0.013). Conclusion Polyneuropathy and NMODS are the most common damages in pSS patients with PNS and CNS lesions respectively. Patients with PNS lesions are more likely to have ILD. [ABSTRACT FROM AUTHOR]

Characterized by "postural headche", spontaneous intracranial hypotension (SIH) is one of the few diseases of central nervous system (CNS) that can be completely cured with definitive diagnosis. However, if the headache attacks are not typically postural, it brings doctors much difficulties to diagnose and make more misdiagnosis or diagnostic errors. In recent years, rapidly developed imaging technologies contribute to early diagnosis in clinic and a lot of new treatment methods were emerged. Here we summarize the literatures about imaging and treatment methods in the past few years to help doctors increase the understanding of SIH. [ABSTRACT FROM AUTHOR]

Mitochondria is a highly dynamic organelle with coordinately fusion and fission, which is involved in in the regulation of physiological and pathological functions. The balance of mitochondrial dynamics is regulated by certain related proteins, such as dynamin- related protein 1 (Drp1), fission 1 (Fis1), mitofusin1 (Mfn1), mitofusin2 (Mfn2), optic atrophy 1 (OPA1), et al. A variety of inducible factors regulate the mitochondrial morphology and physiological functions by modulating the expression and activation of mitochondrial fusion and fission-associated proteins. Increasing evidences show that abnormal mitochondrial dynamics is involved in many central nervous system diseases, such as stroke, Alzheimer's disease, Parkinson's disease and so on, which indicate that unbalance of mitochondrial fission and fusion is one of mechanisms of central nervous systemdiseases. This paper reviews the current advances of abnormal mitochondrial dynamics relevant to neuronal dysfunction in central nervous system diseases, so as to provide some clues or references for the prevention and treatment of the related diseases. [ABSTRACT FROM AUTHOR]

doi：10.3969/j.issn.1672-6731.2014.01.014

DOI: 10.3969/j.issn.1672-6731.2015.06.015

Central nervous system diseases are complicated, and general examinations are lack of accuracy because they are easily influenced by subjective factors of patients. Objective results from optical coherence tomography (OCT) can detect the changes of ocular posterior structures, and then further reflect the neuronal degeneration. The aim of this review is to discuss the application of OCT in central nervous system diseases and look for new biomarkers. [ABSTRACT FROM AUTHOR]

Parkinson's disease (PD) is a neurodegenerative disease commonly happening in the middle - aged and old population, which involves central nervous system and exhibits a broad variety of clinical symptoms that are only partially treatable by pharmacological treatment. Rehabilitation is considered as an adjuvant therapy to pharmacological and surgical treatments for PD to maximize functional abilities and minimize secondary complications. This review outlines a rehabilitational, multidisciplinary team-based approach (physical therapy, occupational therapy, speech therapy, and so on) to the management of PD. [ABSTRACT FROM AUTHOR]

Objective To report the first case of central nervous system Whipple's disease (WD) with relatively good prognosis in China and present a brief review of central nervous system WD so as to improve the understanding of the diagnosis and treatment of this rare disease. Methods The clinical data of diagnosis, treatment and prognosis of one case of 35-year-old female was analysed in detail. Results Headache, hemiplesia and dementia were the main symptoms of this case and hypercranial pressure crisis occurred. During the course of disease, the patient successively presented paroxysmal extremity convulsion, right leg weakness, urinary incontinence, overeating, body mass increase. Despite of high dose of corticosteroid, penicillin and compound sulfamethoxazole were used, no effect was seen. Along with the increasing of intracranial pressure, cerebral hernia occurred. Cerebrospinal fluid examination indicated that glucose and chloride were normal while protein was obviously increased to 1700 mg/L. Electrocardiography (EEG) showed slow wave in right frontal and temporal lobes. Serial magnetic resonance imaging (MRI) revealed mutiple long T1 and long T2 signals mainly in right cerebral hemisphere, frontal parietal temporal lobes, semioval center and basal ganglion, with edema and irregular loose contrast and extended to left cerebral. Brain biopsy showed large pieces of necrosis at right fronto-temporal lobe with massive infiltration of lymphocytes and plasmocytes at perivascular and brain tissue, and exudation of glitter cells. Positive PAS and methenamine silver staining revealed bacterial particles inglitter cells. Central nervous system tumor, demyelinating disease and inflammatory pseudotumor were excluded. Both clinical symptoms and neuroimging recovered well after regular antibiotic therapy. Conclusion Central nervous system WD is a rare disease with complicated symptoms and imaging characters challenging diagnosis and treatment. The pathological findings may only indicate a special infection of central nervous system with unknown origin. The management is difficult. The misdiagnosis rate and fatality are high. It is important for clinicians to be aware of the features of this disease and make early decision to perform brain biopsy for diagnosis. Once it is diagnosed, normalized therapy should be given. DOI：10.3969/j.issn.1672-6731.2011.05.017