Trigeminal neuralgia (TN) is characterized by recurrent facial acupuncture like, electric shock like, burning like pain and other common clinical cranial nerve diseases in the trigeminal nerve distribution area. Around the world, people who are 40 or more are at risk. The incidence rate of TN of female is slightly higher than that of male and most of the affecting areas are on the right side unilaterally, which affects maxillary nerve and mandibular nerve, yet seldom ophthalmic nerve. Although controversy exists in the pathogenesis of TN, the most accepted theory is microvascular compression, which forces on the demyelination of the sensory axon of the trigeminal nerve root. Additionally, slight touch, conversation and chewing may cause intolerable pain. The diagnosis of TN mainly depends on clinical manifestation. The treatment mainly includes medicine, operation, and some supplementary methods. Among them, antiepileptics and tricyclic antidepressants are the first-line treatment. Surgical treatment is mainly used for patients with TN who have failed in drug treatment or have intolerable side effects. The methods of operation include destructive or non-destructive operation. Deep brain stimulation (DBS) and motor cortex stimulation (MCS) are new therapeutic techniques emerged recently. This method is expected to alleviate the refractory TN with poor drug control or ineffective conventional surgical treatment. At present,this method has not been approved for clinical treatment. Of course, more clinical data collection processes are in progress.

Intracranial metastasis of liver cancer is rare, and diplopia as the first manifestation is even more rare. This article aims to introduce a patient with sudden diplopia in a middle-aged man. Physical examination revealed left abductor nerve palsy, craniocerebral magnetic resonance imaging (MRI) showed intracranial metastatic tumor, and positron emission tomography-computer tomography (PET-CT) tracing of the original lesion detected the primary liver cancer. This paper provides clinical data for intracranial metastasis of primary liver cancer and the possible pathogenesis and mechanism of sudden diplopia.

Ischemic cerebral stroke is a leading cause of death and disability globally. At present, thrombolytics, such as recombinant tissue-type plasminogen activator, are the only effective treatment for acute stroke. However, usage of thrombolytics has a strict therapeutic window and cannot be applied to a number of patients. Despite the promising effects of some neuroprotectants in preclinical studies, they failed in clinical trials as a result of poor pharmacokinetic properties, particularly with regard to solubility and permeability across the blood-brain barrier (BBB). Approaches for delivering these drugs by nanotechnologies may overcome these pharmacokinetic deficits and enhance their neuroprotective effects. However, issues such as potential side effects and biosafety properties currently limit clinical application of these approaches. In this article, we reviewed recent progress of nanotechnology-based interventions for stroke treatment, and in particular, summarized novel materials applied to synthesize nanocarriers, encapsulation with neuroprotectants, and factors impacting nanodrug bioactivities to provide a theoretical basis for the development of anti-stroke drugs.

Post-polio syndrome (PPS) is a neurologic disorder characterized by an accumulation of symptoms, most often muscle weakness, fatigue, and pain, decades after the initial polio. Diagnosis of PPS is based on the presence of a lower motor neuron disorder which is supported by neuro-physiological findings, as well as exclusion of other disorders as causes of new symptoms. The pathogenesis of PPS is still disputed. Rehabilitation for patients with PPS should take a comprehensive approach. Evaluation of the need for orthoses is often required.

Objective: bipolar cells (BCs) communicate with amacrine and ganglion cells of the retina via both transient and sustained neurotransmitter release in ribbon synapses. Reconstructing the published quantitative release data from electrical soma stimulation (voltage clamp experiments) of rat rod BCs were used to develop two simple models to predict the number of released vesicles as time series. In the experiment, the currents coming to the AII amacrine cell originating from releasing vesicles from the rod BC were recorded using paired-recordings in whole-cell voltage-clamp method. Method: one of the models is based directly on terminal transmembrane voltage, so-called ‘modelV’, whereas the temporally exacter modelCa includes changes of intracellular calcium concentrations at terminals. Result: the intracellular calcium concentration method replicates a 0.43 ms signal delay for the transient release to pulsatile stimulation as a consequence of calcium channel dynamics in the presynaptic membrane, while the modelV has no signal delay. Both models produce the quite similar results in low stimuli amplitudes. However, for large stimulation intensities that may be done during extracellular stimulations in retinal implants, the modelCa predicts that the reversal potential of calcium limits the number of transiently released vesicles. Adding sodium and potassium ion channels to the axon of the cell enable to study the impact of spikes on the transient release in BC ribbons. Conclusion: a spike elicited by somatic stimulation causes the rapid release of all vesicles that are available for transient release, while a non-spiking BC with a similar morphometry needs stronger stimuli for any transient vesicle release. During extracellular stimulation, there was almost no difference in transient release between the active and passive cells because in both cases the terminal membrane of the cell senses the same potentials originating from the microelectrode. An exception was found for long pulses when the spike has the possibility to generate a higher terminal voltage than the passive cell. Simulated periodic 5 Hz stimulation showed a reduced transient release of 3 vesicles per stimulus, which is a recovery effect.

Objective: lobectomy is an effective therapy for patients with Sturge-Weber syndrome (SWS). Perioperative complications often play a critical role for SWS patients’ rehabilitation. This study aimed to explore and the factors of perioperative complications in SWS patients. Methods: we reviewed retrospectively the clinical profile of totally 60 SWS patients who received surgically treatments in Sanbo Brain Hospital, Capital Medical University, from March 2009 to April 2018. Univariate analyses were used to identify the potential predictors of perioperative complications.Results: the average hospitalization time of 60 patients was (35.57±10.79)d. After surgery, 54 (90.00%) patients reached Engle I level. The most common postoperative complications were fever (83.33%), motor function damage (38.33%) and hyponatremia (55.00%). Univariate analyses revealed that mental retardation, seizure types and surgery types could be the predictive factors for postoperative complications. Conclusion: postoperative complications are common in SWS patients. Prediction of the severity can help doctors know what kind of special care SWS patients need to help them for further rehabilitation.

Neuromyelitis optica spectrum disorders (NMOSD) is a demyelinating disease mainly involving the optic nerve and spinal cord. It has recurrent and aggravating attacks and high disability rate. Most patients have a stepwise progression, resulting in complete blindness or paraplegia. NMOSD lesions contain not only the optic nerve and spinal cord, but also other neurological and non-neurological symptoms, which has clinical heterogeneity. The discovery of aquaporin-4-immunoglobulin G (AQP4-IgG) attributed it to autoimmune ion-channel disease, and rituximab (RTX) has achieved good clinical efficacy in the treatment of NMOSD. Myelin oligodendrocyte glycoprotein (MOG) antibodies have been found in some AQP4-IgG-negative NMOSD patients, which have different clinical and immunological features, posing new challenges to the diagnosis and treatment of NMOSD, which may require re-design and testing of new immune-targeted drugs.

N-methyl-D-aspartate glutamate receptors (NMDARs) play crucial roles in the pathogenesis of neuronal injuries following a stroke insult; therefore, a plethora of preclinical studies focus on better understanding functions of NMDARs and their associated signaling pathways. Over the past decades, NMDARs have been found to exert dual effects in neuronal deaths signaling and neuronal survival signaling during cerebral ischemia. Moreover, many complex intracellular signaling pathways downstream of NMDAR activation have been elucidated, which provide novel targets for developing much-needed neuro-protectants for patients with stroke. In this review, we will discuss the recent progress in understanding the underlying mechanisms of stroke related to NMDAR activation and the potential therapeutic strategies based on these discoveries.

Glioma is the most common and destructive tumor of primary brain tumor types in the central nervous system. After comprehensive treatment including surgical treatment, radiation therapy and chemical drug treatment, the survival period of the glioma patients is still very short. In recent years, cancer immunotherapy methods have achieved great success in the treatment of solid tumors, but the application in the treatment of gliomas has not been universal yet. This review discussed the immunotherapy and latest progress in glioma study, hoping to bring new ideas for treatment of gliomas.

Glioma is the tumor with the highest incidence in the brain, and it is eager to seek new and effective treatment. The interaction of ubiquitination and deubiquitination regulates many cell activities in organisms, and participates in tumor occurrence, development, migration, invasion and other processes. This article summarized the progress of E3 ubiquitination ligase smad ubiquitination regulatory factor 2 (Smurf2) and glioma-related signaling pathways to assist clinical diagnosis and treatment of glioma.

Objective: to investigate the effect of improving prehospital hypotension and hypoxemia on the prognosis of different subgroups of patients with traumatic brain injury (TBI). Methods: medical staff were trained about the prehospital first aid for 2 months to fully master the methods of improving prehospital hypotension and hypoxemia, then the prognosis of TBI patients pre- and post-training for 12 months was collected and recorded. The prognostic differences of different TBI subgroups were discussed through data analysis. Results: after the training, the proportion of prehospital hypotension and hypoxemia in TBI patients decreased by 77% (8.5% vs. 1.9%) and 63% (9.9% vs. 3.6%, P < 0.05), respectively. However, only the prognosis of moderate and severe TBI patients was improved, the proportion of patients with “good prognosis” increased by 14% (61.4% vs. 70.5%, respectively) and 62% (35.6% vs. 58%), and no significant effect showed in mild and critical TBI patients.Conclusion: reducing the incidence of prehospital hypoxemia and hypotension can improve the prognosis of moderate and severe TBI patients, while no significant effect on mild and critical TBI patients.

Human umbilical cord mesenchymal stem cells (HuMSCs) have the multi-differentiation potential to differentiate into various types of cells without immune rejection. They are considered to be an ideal source of neural stem cells and also an ideal cell carrier for gene therapy. Because of the invasive growth of brain gliomas, most of them have no obvious boundaries with normal brain tissues. It is difficult to completely remove them by surgery and the remaining cells become the main source of tumor recurrence. In recent years, gene therapy has become a new method for the treatment of gliomas. The vector carrying the target gene is introduced into HuMSCs in a certain way to correct gene defects or play other roles. The differentiation potential of HuMSCs makes it an ideal source of nerve cells to play a greater role in gene therapy of glioma. Therefore, this article reviews the current status and prospects of HuMSCs as cell carriers in the treatment of glioma.

Objective: to investigate the clinical and pathological characteristics of bronchial cyst of the posterior mediastinum misdiagnosed as a ganglioneuroma, and to improve the level of their diagnosis, differential diagnosis, and treatment. Methods: the clinical data and pathological findings of a young woman misdiagnosed with a ganglioneuroma was collected and analyzed, and the relevant literature were reviewed. Results: the patient had no specific clinical symptoms. The right posterior mediastinum was accidentally found due to a physical examination for COVID-19. The enhanced chest computed tomography (CT) showed a ganglioneuroma. After a thoracoscopic resection of the lesion, a pathological diagnosis revealed a posterior mediastinal bronchial cyst. Conclusion: bronchial cyst of the mediastinum is rare and their clinical symptoms are atypical and can be easily diagnosed as a ganglioneuroma. It can be preliminarily judged by laboratory and imaging examination and confirmed by pathological examination. The main treatment is surgical resection.

Objective: to screen the genes differentially expressed in autism using bioinformatics methods, and to explore their functional enrichment, related signaling pathways and the tissue-specific expression of hub genes. Methods: the autism expression profile chip numbered GSE77103 in the Gene Expression Omnibus (GEO) database was selected for examination. R language and related R packages were used for the screening and visualization of the differentially expressed genes. Gene Ontology (GO) function enrichment and Kyoto Encyclopedia of Genes and Genomes (KEGG) signaling pathway analysis of the differential genes were carried out using the relevant R package of R language. The database STRING was used to construct the interaction network of the proteins encoded by the differentially expressed genes, and the software Cytoscape was used to screen the hub genes in the network. The selected hub genes were imported into the BioGPS database to analyze the tissue-specific expression of the hub genes. Results: six hundred and sixty differentially expressed genes were screened out. Three hundred and seventy-three up-regulated genes and 287 down-regulated genes in the peripheral blood mononuclear cells of autistic children were compared with the peripheral blood mononuclear cells of healthy children. GO functional enrichment results showed that biological processes (BP) were mainly involved in viral response, negative regulation of viral genome replication, negative regulation of multiple biological processes, negative regulation of viral life cycle, and defense responses to viruses. Cell components (CC) were involved in vesicles, lysosomal membranes, lysosomal lumen, etc.; molecular functions (MF) were involved in regulating glutathione transferase activity, peroxidase activity, oxidoreductase activity, Glutathione peroxidase and transferase activity, etc. The results of KEGG signaling pathway analysis showed that the differentially expressed genes were related to the lysosomal pathway, the glutathione metabolism pathway and the arachidonic acid metabolism pathway. The hub genes screened by cytoHubba were: interferon regulatory factor 7 (IRF7), interferon stimulated exonuclease gene 15 (ISG15), XIAP associated factor 1 (XAF1), MX dynamin like GTPase 1 (MX1), interferon induced protein with tetratricopeptide repeats 1 (IFIT1), interferon induced protein with tetratricopeptide repeats 5 (IFIT5), 2’-5’-oligoadenylate synthetase 3 (OAS3), interferon induced protein 44 (IFI44), HECT and the RLD domain containing E3 ubiquitin protein ligase 5 (HERC5), interferon stimulated exonuclease gene 20 (ISG20). Conclusion: there are genes that are differentially expressed in the peripheral blood mononuclear cells of autistic toddlers and healthy toddlers. IRF7, ISG15, XAF1, MX1, IFIT1, IFIT5, OAS3, IFI44, HERC5, ISG20 are the hub regulatory genes of autism.

Objective: allergic granulomatous vasculitis is relatively rare in clinic. We aimed to analyze the clinical characteristics of allergic granulomatous vasculitis. Methods: collecting allergic granulomatous vasculitis patients in Taihe Hospital from January 2017 to June 2020, sorting out their general information, system involvement and clinical examination results, and analyzing their clinical characteristics. Results: a total of 5 patients diagnosed with allergic granulomatous vasculitis were collected, all with multiple organ involvement, including the skin, respiratory system, circulatory system, digestive system, urinary system, and nervous system. Respiratory system involvement was mainly due to decreased lung function; 60% manifested as obstructive ventilatory dysfunction. Lung biopsy showed a large amount of eosinophil infiltration in the interstitium of the alveolar septum, and eosinophil and fibrin-like exudation in the alveolar cavity. The circulatory system was mainly affected by myocardial damage, and patient two (P2) had pericardial effusion. 60% of nervous system involvement was central nervous system involvement, and 40% was peripheral nerve involvement. Skin system involvement accounted for 60%. Urinary system involvement was mainly manifested as hematuria and proteinuria. Digestive system involvement was mainly manifested as gastritis, gastric ulcer and other diseases. Conclusion: allergic granulomatous vasculitis is clinically rare. The clinical manifestations are atypical and often involve damage to multiple systems. Clinicians need to fully understand the characteristics of the disease and make comprehensive judgments based on the onset process and examination results to avoid misdiagnosis.

Schizophrenia (SCZ) is the most common serious mental illness with a high disability rate and heavy social and family burdens. At present, there is no clear etiology and pathogenesis of schizophrenia. Studies have shown that the occurrence of schizophrenia may be related to the abnormality of the hypothalamic-pituitary-adrenal (HPA) axis. The LIM-homeobox gene 3 (LHX3) and early growth response 1 (EGR1) can affect pituitary function. Because the synapsin 2 (SYN2) gene polymorphism regulates the activity of LHX3 and EGR1, it may cause the occurrence of schizophrenia. This article will review the possible involvement of SYN2 gene polymorphism in the pathogenesis of schizophrenia via regulating the activity of LHX3 and EGR1, then to affect the HPA axis.

Objective: to evaluate the clinical efficacy and safety of ultra-early lumbar puncture drainage of cerebrospinal fluid (CSF) in patients with aneurysmal subarachnoid hemorrhage (SAH). Methods: patients (n=140) with aneurysmal SAH were randomly divided into observation group (n=70) and control group (n=70). After admission, CSF was drained by ultra-early lumbar puncture in the observation group and intermittent lumbar puncture after aneurysm operation in the control group. The incidences of early aneurysm rupture, acute hydrocephalus and delayed hydrocephalus were compared between the two groups. Results: there was no significant difference in the incidence of early-ruptured aneurysm and acute hydrocephalus between the two groups, but the incidence of delayed hydrocephalus in the observation group was significantly lower than that in the control group. Conclusion: ultra-early lumbar puncture drainage of CSF in aneurysmal SAH can effectively reduce the incidence of long-term delayed hydrocephalus and it is a safe and effective treatment.

Schizophrenia (SCZ) is a serious mental illness whose etiology and pathogenesis are not yet clear. The level of miRNA may be a crucial factor in the occurrence and development of SCZ. This study found that miR-495 may regulate the susceptibility gene of SCZ and that proteolipid protein 1 (PLP1) as a risk gene for schizophrenia may be involved in its pathogenesis. In this article we review the research progress related to hsa-miR-495-3p (miR-495), PLP1, and schizophrenia.

Schizophrenia (SCZ) is a serious mental illness with unknown etiology, high recurrence rate and high disability rate, which has caused a great burden to individuals and society. There is no clear etiology and pathogenesis. Methylation of N6-methyladenosine (m6A) can regulate the nervous and mental system, and affect the function of the nervous system. Proteolipid protein 1 (PLP1) is a risk gene for schizophrenia. In this study we review the research progress on the pathogenesis of schizophrenia, m6A methylation, and PLP1 gene.

Cogan’s syndrome is rare. The purpose of this article is to describe a Cogan’s syndrome case characterized by bilateral internal carotid artery occlusion and to review the literature. Treatment remedies: we showed a patient with vertigo, nausea and retching, blurred vision, unclear speech. And the whole cerebral angiogram of the patient showed bilateral internal carotid artery occlusion without obvious neurological deficit. After differential diagnosis, compared with classic Cogan’s syndrome, granulomatous polyvasculitis (GPA), rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), the patient was considered as Cogan’s syndrome. Post treatment evaluating: the patient did not significantly improve vertigo after vascular bypass therapy. Conclusions: Cogan’s syndrome may cause severe vascular occlusion. The patient had no clinical symptoms; and the chronic occlusion caused by vascular inflammation may be the reason, so that there was enough time for compensation.

Objective: to describe the clinical features of Holmes tremor (HT) in the head and neck region caused by midbrain and thalamus hemorrhage. Methods: we collected the clinical history and examination data of a patient with HT in the head and neck region. Results: the patient had HT in the head and neck region with dizziness. Brain computed tomography (CT) showed midbrain and thalamus hemorrhage. Conclusion: HT in the head and neck region as a delayed complication of midbrain and thalamus stroke are rare in clinic. When patients have a tremor in the head and neck region after midbrain or thalamus stroke, HT should be considered.

Parkinson’s disease (PD) is a common age-related neurodegenerative disease characterized by movement disorders. The hallmark pathological lesions of PD are the formation of Lewy pathology in selected populations of neurons throughout the nervous system. Braak and his colleagues created a staging system for PD describing the connection between Lewy pathology and disease severity. They proposed that Lewy pathology might be initially triggered by exogenous pathogens targeting the enteric or olfactory nervous system, then spread in a prion-like propagation manner from the peripheral nerves to the lower brainstem and midbrain, before finally reaching higher cortical structures, causing a sequential occurrence of the non-motor and motor symptoms, depending on the lesioned neurons. However, emerging evidence also supports a functional threshold hypothesis proposed by Engelender and Isacson in which Lewy pathology may occur parallelly in the central and peripheral nervous systems and the symptoms only begin when the functional reserve of the affected neurons (and their connecting brain regions) is unable to allow for network compensation. Consequently, early symptoms of PD reflect the loss of function in the least compensated systems, such as the enteric and olfactory nervous systems, rather than the spread of Lewy pathology from the peripheral to the central nervous systems. The current review article provides a comprehensive overview of the evidence supporting a merged mechanism that the neurodegeneration in PD happens to those neurons that are not only intrinsically vulnerable but also affected by the spread of Lewy pathology.

Objective: autism spectrum disorder (ASD), a serious disorder that begins early in life, continues throughout the lifespan. Children with ASD who are diagnosed early are more responsive to therapeutic interventions and have less social and language impairment than children diagnosed later; however, current diagnostic measures are mostly applied to children older than one year and lack the appropriate biological markers for early diagnosis of ASD. Using bioinformatic analysis, this study explores the molecular information mechanism of ASD. Method: in this study, we used dataset GSE6575 from Gene Expression Omnibus (GEO) to analyze the mRNA expression profile of ASD, including 35 ASD samples and 12 normal control samples looking for different genes and we did enrichment analysis of those genes. We then used the STRING database to construct a protein–protein interaction (PPI) network of differential genes. Finally, Cytoscape plug-in cytoHubba was used to search for hub genes. The diagnostic value of the hub genes was verified by subject operating characteristic curves. Result: we looked for 50 different genes and did an enrichment analysis of those genes. The results of the enrichment analysis showed that these differential genes were mainly concentrated in the response to viruses, the immune regulation of inflammation and energy metabolism. Using Cytoscape plug-in cytoHubba, we found ten different genes. We drew ROC curves for all ten genes among which two genes, interleukin 2 receptor subunit beta (IL2Rβ) and perforin 1 (PRF1), had good sensitivity and specificity for the early diagnosis of autism. The areas under the ROC curves were 0.855, 0.830 for IL2Rβ, PRF1. Conclusion: data analysis using the GEO database can provide new insights into the etiology of ASD as well as some possible biomarkers and therapeutic targets for early diagnosis and treatment of ASD.

Anxiety disorder is a common and serious mental disorder. At present, the pathogenesis of anxiety disorder includes hypothalamus-pituitary-adrenal (HPA) axis, neuroimmune, and brain-gut axis disorders, among others. This paper discusses the correlation between anxiety disorder and the hypothalamus-pituitary-endocrine axis and finds that immune inflammation can be used as a “bridge” between the hypothalamus-pituitary-endocrine axis and anxiety disorder.

Parkinson’s disease (PD) is a common neurodegenerative disease, characterized clinically by both motor and non-motor symptoms. Pathologically, PD is hallmarked by the loss of dopaminergic neurons in the substantia nigra (SN) and the formation of α-synuclein (α-syn) containing inclusion bodies (Lewy pathology) in the surviving neurons. Diagnosis of PD is still based on clinical features. However, owing to the complexity, heterogeneity, and overlapping of its symptoms with other Parkinsonian disorders, correct diagnosis of PD remains a challenge, especially in the early stages. Therefore, there is an urgent need for biomarkers that can help correctly diagnose PD, differentiate PD from other Parkinsonian disorders, monitor the progression of the disease, and evaluate the therapeutic efficacy. Various molecules have been investigated for their utility in diagnosing PD, among which α-syn is the most extensively investigated one due to its close implication in the etiology and pathogenesis of PD and related diseases. During the past decade, various species of α-syn, including total, oligomeric, and phosphorylated α-syn in various tissues, have been investigated for their utility as a potential biomarker for PD diagnosis and differential diagnosis. Various forms of α-syn in body fluids, including cerebrospinal fluid (CSF), blood plasma, and saliva, are among the ones that are extensively investigated, since the body fluids are relatively accessible compared to the peripheral tissues. The aim of this review is to summarize the progress of studies on the utility of α-syn in body fluid as a biomarker for PD diagnosis and differential diagnosis.

Objective: to describe the clinical features of a case of infective endocarditis caused by Staphylococcus lugdunensis, followed by cerebral embolism, spleen embolism and tendon rupture. Methods: the clinical data of a 22-year-old female patient with aphasia hemiplegia and abdominal pain were collected. Relevant examinations such as routine blood test, myocardial enzyme spectrum, electrocardiogram (ECG), cardiac color Doppler ultrasound, brain magnetic resonance, abdominal computed tomography (CT) and blood culture were completed, and anti infection treatment was carried out according to the drug sensitivity test. Results: brain magnetic resonance imaging (MRI) showed cerebral infarction in the left basal ganglia, cardiac color Doppler ultrasound showed mitral valve vegetation and abscess formation, and abdominal CT showed splenic infarction. After anti infection treatment, the patient’s condition gradually improved, but the patient had sudden arrhythmia in the recovery period. Color Doppler ultrasound showed rupture of the mitral tendinous cord and valve prolapse. The condition was improved after surgical treatment. Conclusion: the first manifestation of Staphylococcus lugdunensis infection is cerebral infarction, which is relatively rare in the clinic setting. The main manifestation of this case is aphasia hemiplegia with abdominal pain. Blood culture and identification show Staphylococcus lugdunensis, which is rare in adolescent patients. The infection has a rapid onset, rapid progress and causes serious valve damage. Timely strain identification and drug sensitivity test are conducive to accurate diagnosis and treatment. Valve surgery is often necessary.

Multiple system atrophy (MSA) is a rapidly progressive neurodegenerative disorder characterized by a variable combination of autonomic failure, parkinsonism with poor response to levodopa, cerebellar ataxia and pyramidal symptoms. The pathological hallmark of MSA is the oligodendrocytic glial cytoplasmic inclusions (GCIs) consisting of α-synuclein, and so MSA, together with Parkinson’s disease (PD) and dementia with Lewy bodies (DLB), is an α-synucleinopathy. Currently few effective biomarkers have been identified for the diagnosis or prognosis of MSA, and there is no established therapy to delay its progression. In this review, we discuss the epidemiology, neuropathology, genetics, clinical presentation and diagnostic biomarkers of MSA, as well as recent advances in its treatment.

Abstract Autism spectrum disorders (ASD) area group of neurodevelopmental disorders that affect up to 1.5% of population in the world. Recent largescale genomic studies show that genetic causes of ASD are very heterogeneous. Gene ontology, pathwayanalysis and animal model studies have revealed several potential converging mechanisms including postsynaptic dysfunction of excitatory synapses. In this review, we focus on the structural and functional specializations of dendritic spines, and describe their defects in ASD.We use Fragile X syndrome, Rett syndrome and Phelan-McDermid syndrome, three of the most studied neurodevelopmental disorders with autism features, as examples to demonstrate the significant contribution made by mouse models towards the understanding of monogenic ASD. We envision that the development and application of new technologies to study the function of dendritic spines in valid animal models will eventually lead to innovative treatments for ASD.

Glioma, the most common primary intracranial tumor, has high morbidity and mortality. The detection of circulating tumor cells (CTCs) is an important part of the liquid biopsy of gliomas. CTCs, carrying the genetic and biological information of tumor tissue, provide a new perspective and dimension for the study of tumor metastasis, progression, chemotherapy sensitivity and drug resistance. Cerebrospinal fluid (CSF) circulates through the ventricle and spinal cord cistern, which can better maintain the original information of tumor cells compared with the complicated environments of tissues and plasma. Study on the dynamic changes of CTCs in the CSF of the central nervous system (CNS) is relatively rare. However, the analysis of CTCs in CSF can be used to guide the treatment of gliomas and reveal the pathophysiological and genetic mechanisms of tumor cell metastasis to the CSF. This paper reviews the progress in the research on CTC detection in gliomas.