No genetic causal associations between periodontitis and brain atrophy or cognitive impairment: evidence from a comprehensive bidirectional Mendelian randomization study.

BACKGROUND: Observational studies have explored the relationships of periodontitis with brain atrophy and cognitive impairment, but these findings are limited by reverse causation, confounders and have reported conflicting results. Our study aimed to investigate the causal associations of periodontitis with brain atrophy and cognitive impairment through a comprehensive bidirectional Mendelian randomization (MR) research. METHODS: We incorporated two distinct genome-wide association study (GWAS) summary datasets as an exploration cohort and a replication cohort for periodontitis. Four and eight metrics were selected for the insightful evaluation of brain atrophy and cognitive impairment, respectively. The former involved cortical thickness and surface area, left and right hippocampal volumes, with the latter covering assessments of cognitive performance, fluid intelligence scores, prospective memory, and reaction time for mild cognitive impairment to Alzheimer's disease (AD), Lewy body dementia, vascular dementia and frontotemporal dementia for severe situations. Furthermore, supplementary analyses were conducted to examine the associations between the longitudinal rates of change in brain atrophy and cognitive function metrics with periodontitis. The main analysis utilized the inverse variance weighting (IVW) method and evaluated the robustness of the results through a series of sensitivity analyses. For multiple tests, associations with p-values < 0.0021 were considered statistically significant, while p-values ≥ 0.0021 and < 0.05 were regarded as suggestive of significance. RESULTS: In the exploration cohort, forward and reverse MR results revealed no causal associations between periodontitis and brain atrophy or cognitive impairment, and only a potential causal association was found between AD and periodontitis (IVW: OR = 0.917, 95% CI from 0.845 to 0.995, P = 0.038). Results from the replication cohort similarly corroborated the absence of a causal relationship. In the supplementary analyses, the longitudinal rates of change in brain atrophy and cognitive function were also not found to have causal relationships with periodontitis. CONCLUSIONS: The MR analyses indicated a lack of substantial evidence for a causal connection between periodontitis and both brain atrophy and cognitive impairment.

Intraneural hemangioma of spinal nerve roots: a Case Report and literature review.

Intraneural hemangiomas are rare benign neoplasms. We report the case of a 53­year­old female with a hemangioma in a spinal nerve root. The patient presented with muscular atropy of the right arm wihout obvious predisposing factors one year ago. MRI demonstrated a heterogeneously enhanced lesion adjacent to the right C4/5 intervertebral foramen. The lesion was considered to be a schwannoma preoperatively. Histologically, the lesion was abundant with intervening malformed vascular mass lined by simple squamous epithelial cells, and CD31 was positively stained at these epithelial cells by immunohistochemistry. The patient underwent microsurgical resection and recovered without complications.

[Research Progress on the Application of Goel Technique in Craniovertebral Junction Anomalies].

Craniovertebral junction anomalies are a group of diseases characterized by the pathological changes of occipital bone,atlantoaxial bone,cerebellar tonsil,surrounding soft tissue,and nervous system,which are caused by a variety of factors.Chiari malformation is a common type of craniovertebral junction anomalies,the conventional surgical therapy of which is posterior fossa decompression.Currently,scholars represented by Goel have proposed a new theory on the classification,pathogenesis,and treatment of Chiari malformation based on posterior atlantoaxial fixation (Goel technique).This article introduces the progress in Goel technique,aiming to provide reference for the clinical work.

Curcumin suppress inflammatory response in traumatic brain injury via p38/MAPK signaling pathway.

Traumatic brain injury (TBI) is a common disease worldwide with a high mortality and disability rate and is closely related to the inflammatory response. However, the molecular mechanisms during the pathophysiological responses are not completely understood. This study was conducted to investigate the protective effect of curcumin on TBI and the molecular mechanisms of the p38/MAPK signal pathway. We found that curcumin remarkably ameliorated secondary brain injury after TBI, including effects on the neurological severity score and inflammation. After injection of curcumin, the neurological function score of mice decreased significantly. Curcumin exhibited antiinflammatory pharmacological effects, as reflected by inhibition of inflammatory factors (e.g., interleukin [IL]-1ß, IL-6, and tumor necrosis factor [TNF]-α). Additionally, curcumin notably reduced the expression of p-p38 according to western blotting and immunohistochemical analyses. In conclusion, curcumin remarkably alleviated posttraumatic inflammation and thus shows potential for treating inflammation associated with TBI.

[Recurrence Rate and Risk Factors of Atypical Meningioma:a Meta-analysis].

Objective To systematically review the overall status of postoperative recurrence in patients with atypical meningiomas. Methods China National Knowledge Infrastructure,Wanfang Database,Chinese Biomedical Literature Database,VIP Database,PubMed,Embase,Web of Science,and Cochrane Library were searched for collection of the relevant literature on the recurrence of atypical meningioma from database establishment to July 2021.Two investigators independently screened the literature,extracted data,and assessed the risk of bias of the included studies,and then performed a meta-analysis by using R 5.0. Results A total of 29 studies involving 3122 patients were included in this study.The meta-analysis showed that the overall postoperative recurrence rate of atypical meningioma was 38%.The subgroup analysis showed that the tumor recurrence rate of patients ≥60 years old and<60 years old was 51% and 40%,respectively,with no significant difference.The tumor recurrence rates in male and female patients were 42% and 44%,respectively,which showed no significant difference.The recurrence rates of the patients with parasagittal meningiomas,brain tissue infiltration,Ki-67>8%,mitotic count ≥6/10 high-power fields,and tissue necrosis were 52%,47%,63%,53%,and 69%,respectively.The recurrence rate after subtotal tumor resection was as high as 58%,and the patients who received radiotherapy had higher tumor recurrence rate than that those who did not receive radiotherapy (38% vs.29%,P=0.007). Conclusions The current evidence demonstrates that atypical meningioma has a high recurrence rate after surgery.It is essential to pay more attention and take corresponding measures to improve the tumor-free survival rate of the patients.

ZNF436 promotes tumor cell proliferation through transcriptional activation of BCL10 in glioma.

Transcriptional factors (TFs) are key regulators in orchestrating gene transcription during cancer development. However, their roles in glioma remain elusive. Here, we analyzed the differential expression of TFs and identified ZNF436 is upregulated in glioblastoma and Lower Grade Glioma patients. High expression of ZNF436 is positively associated with poor overall survival and regulated by CREB1 in glioma cells. Knockdown of ZNF436 significantly abolished glioma cells proliferation in vitro. RNA sequencing revealed that ZNF436 regulates cell cycle and controlling BCL10 expression. Overexpression of BCL10 promoted glioma cells growth and rescued the malignant behavior in ZNF436-knockdown cells. High levels of BCL10 also result in a worse prognosis in glioma patients. Taken together, our findings identify the CREB1/ZNF436/BCL10 axis represents a novel, potential therapeutic target for glioma interventions.

SLC1A2 mediates refractory temporal lobe epilepsy with an initial precipitating injury by targeting the glutamatergic synapse pathway.

This study aimed to identify the genes related to epilepsy and their effects on epilepsy, as well as the underlying mechanism. Using microarray analysis, differentially expressed genes (DEGs) were screened out and then used to build weighted gene coexpression networks using WGCNA. Module membership and evaluation of gene significance (GS) were adopted to detect hub genes. The DAVID online tool was used to understand the function of modules and target genes. The Licl-pilocarpine chronic rat epilepsy model was used to simulate mesial temporal lobe epilepsy with an initial precipitating injury. Hippocampal expression of the proteins solute carrier family 1 member 2 (SLC1A2), glial fibrillary acidic protein, interleukin-1ß (IL-1ß), tumor necrosis factor α (TNF-α), and N-methyl-d-aspartic acid receptor (NMDAR) was determined by ELISA and Western blot. Nissl staining was used to measure neuronal loss. Immunohistochemistry was performed to assess the percentage of positive cells to reflect the distribution of NMDAR1. Here, 3232 potential genes highly correlated with epilepsy were selected from the screened DEGs, among which SLC1A2 was related to brain development and its expression was significantly decreased in epilepsy patients. According to Gene Ontology and KEGG analysis, SLC1A2 mediates epilepsy through the glutamatergic synapse pathway. Tissue experiments suggested that Slc1a2 could genuinely ameliorate epilepsy through the glutamatergic synapse pathway, mitigate neuronal loss, and suppress astrocytosis and inflammatory responses. Our study suggested that low hippocampal content of SLC1A2 is a potential biomarker of epilepsy and may affect the function of neurons through the glutamatergic synapse pathway. © 2018 IUBMB Life, 71(1):213-222, 2019.

Traumatic bifrontoparietal extradural hematomas with detachment of superior sagittal sinus: a case report and review of the literature.

A 45-year-old man suffered bifrontoparietal extradural hematoma resulting from head injury, which cause superior sagittal sinus detachment from its subperiosteal loggia. We present the patient who was treated by early surgical evacuation of the hematoma with an excellent outcome and we also perform a review of the current literature.

Defining optimal cutoff value of MGMT promoter methylation by ROC analysis for clinical setting in glioblastoma patients.

Resistance to temozolomide (TMZ) chemotherapy poses a significant challenge in the treatment of glioblastoma (GBM). Hypermethylation in O6-methylguanine-DNA methyltransferase (MGMT) promoter is thought to play a critical role in this resistance. Pyrosequencing (PSQ) has been shown to be accurate and robust for MGMT promoter methylation testing. The unresolved issue is the determination of a cut-off value for dichotomization of quantitative MGMT PSQ results into "MGMT methylated" and "MGMT unmethylated" patient subgroups as a basis for further treatment decisions. In this study, receiver operating characteristic (ROC) curve analysis was used to identify an optimal cutoff of MGMT promoter methylation by testing mean percentage of methylation of 4 CpG islands (76-79) within MGMT exon 1. The area under the ROC (AUC) as well as the best cutoff to classify the methylation were calculated. Positive likelihood ratio (LR+) was chosen as a diagnostic parameter for defining an optimal cut-off. Meanwhile, we also analyzed whether mean percentage of methylation at the investigated CpG islands could be regarded as a marker for evaluating prognostication. ROC analysis showed that the optimal threshold was 12.5% (sensitivity: 60.87%; specificity: 76%) in response to the largest LR+ 2.54. 12.5% was established to distinguish MGMT promoter methylation, which was confirmed using validation set. According to the cutoff value, the MGMT promoter methylation was found in 58.3% of GBM. Mean methylation level of the investigated CpG sites strong correlated with overall survival (OS), which means GBM patients with a high level of methylation survived longer than those with low level of methylation(log-rank test, P = 0.017). In conclusion, ROC curve analysis enables the best cutoff for discriminating MGMT promoter methylation status. LR+ can be used as a key factor that evaluates cutoff. The promoter methylation level of MGMT by PSQ in GBM patients had prognostic value.

Myeloperoxidase Nuclear Imaging for Epileptogenesis.

PURPOSE: To determine if myeloperoxidase (MPO) is involved in epileptogenesis and if molecular nuclear imaging can be used to noninvasively map inflammatory changes in epileptogenesis. MATERIALS AND METHODS: The animal and human studies were approved by the institutional review boards. Pilocarpine-induced epileptic mice were treated with 4-aminobenzoic acid hydrazide (n = 46), a specific irreversible MPO inhibitor, or saline (n = 42). Indium-111-bis-5-hydroxytryptamide-diethylenetriaminepentaacetate was used to image brain MPO activity (n = 6 in the 4-aminobenzoic acid hydrazide and saline groups; n = 5 in the sham group) by using single photon emission computed tomography/computed tomography. The role of MPO in the development of spontaneous recurrent seizures was assessed by means of clinical symptoms and biochemical and histopathologic data. Human brain specimens from a patient with epilepsy and a patient without epilepsy were stained for MPO. The Student t test, one-way analysis of variance, and Mann-Whitney and Kruskal-Wallis tests were used. Differences were regarded as significant if P was less than .05. RESULTS: MPO and leukocytes increased in the brain during epileptogenesis (P < .05). Blocking MPO delayed spontaneous recurrent seizures (99.6 vs 142 hours, P = .016), ameliorated the severity of spontaneous recurrent seizures (P < .05), and inhibited mossy fiber sprouting (Timm index, 0.31 vs 0.03; P = .003). Matrix metalloproteinase activity was upregulated during epileptogenesis in an MPO-dependent manner (1.44 vs 0.94 U/mg, P = .049), suggesting that MPO acts upstream of matrix metalloproteinases. MPO activity was mapped during epileptogenesis in vivo in the hippocampal regions. Resected temporal lobe tissue from a human patient with refractory epilepsy but not the temporal lobe tissue from a patient without seizures demonstrated positive MPO immunostaining, suggesting high translational potential for this imaging technology. CONCLUSION: The findings of this study highlight an important role for MPO in epileptogenesis and show MPO to be a potential therapeutic target and imaging biomarker for epilepsy.

Quality appraisal of clinical practice guidelines on glioma.

Clinical practice guidelines (CPGs) play an important role in healthcare. The guideline development process should be precise and rigorous to ensure that the results are reproducible and not vague. To determine the quality of guidelines, the Appraisal of Guidelines and Research and Evaluation (AGREE) instrument was developed and introduced. The aim of the present study was to assess the methodological quality of clinical practice guidelines on glioma. Eight databases (including MEDLINE and Embase) were searched till to August, 2013. The methodological quality of the guidelines was assessed by four authors independently using the AGREE II instrument. Fifteen relevant guidelines were included from 940 citations. The overall agreement among reviewers was moderate (intra-class correlation coefficient = 0.83; 95% confidence interval [CI], 0.66-0.92). The mean scores were moderate for the domains "scope and purpose" (59.54) and "clarity of presentation" (65.46); however, there were low scores for the domains "stakeholder involvement" (43.80), "rigor of development" (39.01), "applicability" (31.89), and "editorial independence" (30.83). Only one third of the guidelines described the systematic methods for searching, and nearly half of the (47%) guidelines did not give a specific recommendation. Only four of 15 described a procedure for updating the guideline; meanwhile, just six guidelines in this field can be considered to be evidence-based. The quality and transparency of the development process and the consistency in the reporting of glioma guidelines need to be improved. And the quality of reporting of guidelines was disappointing. Many other methodological disadvantages were identified. In the future, glioma CPGs should be based on the best available evidence and rigorously developed and reported. Greater efforts are needed to provide high-quality guidelines that serve as a useful and reliable tool for clinical decision-making in this field.

Research progress and prospects of benefit-risk assessment methods for umbilical cord mesenchymal stem cell transplantation in the clinical treatment of spinal cord injury.

Over the past decade, we have witnessed the development of cell transplantation as a new strategy for repairing spinal cord injury (SCI). However, due to the complexity of the central nervous system (CNS), achieving successful clinical translation remains a significant challenge. Human umbilical cord mesenchymal stem cells (hUMSCs) possess distinct advantages, such as easy collection, lack of ethical concerns, high self-renewal ability, multilineage differentiation potential, and immunomodulatory properties. hUMSCs are promising for regenerating the injured spinal cord to a significant extent. At the same time, for advancing SCI treatment, the appropriate benefit and risk evaluation methods play a pivotal role in determining the clinical applicability of treatment plans. Hence, this study discusses the advantages and risks of hUMSCs in SCI treatment across four dimensions-comprehensive evaluation of motor and sensory function, imaging, electrophysiology, and autonomic nervous system (ANS) function-aiming to improve the rationality of relevant clinical research and the feasibility of clinical translation.

Analysis and validation of aging-related genes in prognosis and immune function of glioblastoma.

BACKGROUND: Glioblastoma (GBM) is a common malignant brain tumor with poor prognosis and high mortality. Numerous reports have identified the correlation between aging and the prognosis of patients with GBM. The purpose of this study was to establish a prognostic model for GBM patients based on aging-related gene (ARG) to help determine the prognosis of GBM patients. METHODS: 143 patients with GBM from The Cancer Genomic Atlas (TCGA), 218 patients with GBM from the Chinese Glioma Genomic Atlas (CGGA) of China and 50 patients from Gene Expression Omnibus (GEO) were included in the study. R software (V4.2.1) and bioinformatics statistical methods were used to develop prognostic models and study immune infiltration and mutation characteristics. RESULTS: Thirteen genes were screened out and used to establish the prognostic model finally, and the risk scores of the prognostic model was an independent factor (P < 0.001), which indicated a good prediction ability. In addition, there are significant differences in immune infiltration and mutation characteristics between the two groups with high and low risk scores. CONCLUSION: The prognostic model of GBM patients based on ARGs can predict the prognosis of GBM patients. However, this signature requires further investigation and validation in larger cohort studies.

Demyelinating diseases: myeloperoxidase as an imaging biomarker and therapeutic target.

PURPOSE: To evaluate myeloperoxidase (MPO) as a newer therapeutic target and bis-5-hydroxytryptamide-diethylenetriaminepentaacetate-gadolinium (Gd) (MPO-Gd) as an imaging biomarker for demyelinating diseases such as multiple sclerosis (MS) by using experimental autoimmune encephalomyelitis (EAE), a murine model of MS. MATERIALS AND METHODS: Animal experiments were approved by the institutional animal care committee. EAE was induced in SJL mice by using proteolipid protein (PLP), and mice were treated with either 4-aminobenzoic acid hydrazide (ABAH), 40 mg/kg injected intraperitoneally, an irreversible inhibitor of MPO, or saline as control, and followed up to day 40 after induction. In another group of SJL mice, induction was performed without PLP as shams. The mice were imaged by using MPO-Gd to track changes in MPO activity noninvasively. Imaging results were corroborated by enzymatic assays, flow cytometry, and histopathologic analyses. Significance was computed by using the t test or Mann-Whitney U test. RESULTS: There was a 2.5-fold increase in myeloid cell infiltration in the brain (P = .026), with a concomitant increase in brain MPO level (P = .0087). Inhibiting MPO activity with ABAH resulted in decrease in MPO-Gd-positive lesion volume (P = .012), number (P = .009), and enhancement intensity (P = .03) at MR imaging, reflecting lower local MPO activity (P = .03), compared with controls. MPO inhibition was accompanied by decreased demyelination (P = .01) and lower inflammatory cell recruitment in the brain (P < .0001), suggesting a central MPO role in inflammatory demyelination. Clinically, MPO inhibition significantly reduced the severity of clinical symptoms (P = .0001) and improved survival (P = .0051) in mice with EAE. CONCLUSION: MPO may be a key mediator of myeloid inflammation and tissue damage in EAE. Therefore, MPO could represent a promising therapeutic target, as well as an imaging biomarker, for demyelinating diseases and potentially for other diseases in which MPO is implicated.

Immunoglobulin G4-Related Spinal Intramedullary Inflammatory Pseudotumor: A Case Report and Literature Review.

Immunoglobulin G4-related disease (IgG4-RD) is an autoimmune disease that affects several organs. An inflammatory pseudotumor is a histologically proven benign tumor-like lesion that most commonly involves the lung and orbit. It is rare in the central nervous system, but rarest in the spinal canal. In this report, we present a case of IgG4-related intramedullary spinal inflammatory pseudotumor, along with a literature review. A 29-year-old male was transferred to the Department of Neurosurgery of Lanzhou University Second Hospital with progressive quadriparesis after numbness and weakness in both lower limbs for 50 days. Enhanced magnetic resonance imaging (MRI) of the spine revealed an isointense signal on T1-weighted images and a hyperintense signal on T2-weighted images from an enhanced mass located at the thoracic vertebrae region, for which a schwannoma was highly suspected. Then, a posterior median approach was adopted. The lesion was resected. The patient received further glucocorticoid after the diagnosis of an IgG4-related inflammatory pseudotumor was established, and the patient's symptoms improved, such as quadriparesis and lower limb weakness. This case highlights the importance of considering IgG4-related inflammatory pseudotumor as a differential diagnosis in patients with lesions involving the spinal intramedullary compartment and lower limb weakness when other more threatening causes have been excluded. IgG4-related inflammatory pseudotumor is etiologically unclear and prognostically unpredictable, and imaging may not help establish the diagnosis of IgG4-related inflammatory pseudotumor due to its resemblance to malignant tumors, and total resection might not be warranted. Glucocorticoid and surgery are usually the first-line treatments used.

Effects and mechanism of myeloperoxidase on microglia in the early stage of intracerebral hemorrhage.

Objectives: (1) To clarify the dynamic relationship between the expression of myeloperoxidase (MPO) and microglial activation of intracerebral hemorrhage (ICH), (2) to explore the effect of inhibition of MPO on microglial activation, and (3) to observe the improvement in the neurobehavior of mice with inhibition of MPO. Methods: C57 BL/6 mice and CX3CR1 + /GFP mice were used to establish a phosphate-buffered saline (PBS) group, an ICH group, and a 4-aminobenzoic acid hydrazide (ABAH) group. Longa score, open field locomotion, hind-limb clasping test, immunohistochemistry, immunofluorescence, blood routine detection, and flow cytometry were used. Results: The neurobehavior of the mice was significantly impaired following ICH (P < 0.01); the expression of MPO was significantly increased following ICH, and reached a peak value at 6 h post-injury (P < 0.001). Moreover, the microglial activation increased significantly following ICH, and reached a peak level at 24 h post-injury (P < 0.01). Following inhibition of MPO, the activation of microglia in the ICH group decreased significantly (P < 0.001). Moreover, the neurobehavior of the ICH group was significantly improved with MPO inhibition (P < 0.05). Conclusion: MPO may be an upstream molecule activated by microglia and following inhibition of MPO can improve secondary injury resulting from ICH.

Clinical Impact of the Histopathological Index and Neuroimaging Features Status in Primary Central Nervous System Diffuse Large B-Cell Lymphoma: A Single-Center Retrospective Analysis of 51 Cases.

Primary central nervous system diffuse large B-cell lymphoma (PCNS-DLBCL) is an uncommon non-Hodgkin lymphoma subtype, and its clinical and pathological characteristics remain unclear. PCNS-DLBCL patient data were retrospectively evaluated to determine clinical and pathological characteristics and prognostic factors. Furthermore, prognoses were calculated by Kaplan-Meier and Cox regression models based on clinical observations. In total, 51 immunocompetent patients were enrolled. The median age was 55 (range, 16-82) years, and the male-to-female ratio was 3:2. Headache (n = 19; 37%) and the frontal lobe (n = 16; 31%) were the most common presenting symptom and location, respectively. The median follow-up was 33 (range, 3-86) months, and the median overall survival (OS) and progression-free survival (PFS) were 18 months [95% confidence interval (CI), 21.2-34.2] and 15 months (95% CI, 16.9-28.7), respectively. Ki-67, cluster of differentiation-3, and deep brain involvement were independent prognostic markers. Moreover, multifocal lesions and deep brain involvement were unfavorable independent prognostic markers for PFS. This study indicates that targeted drug development for adverse prognostic factors is possible and provides guidance for clinical treatment decision-making.

Myeloperoxidase: a new target for the treatment of stroke?

Myeloperoxidase is an important inflammatory factor in the myeloid system, primarily expressed in neutrophils and microglia. Myeloperoxidase and its active products participate in the occurrence and development of hemorrhagic and ischemic stroke, including damage to the blood-brain barrier and brain. As a specific inflammatory marker, myeloperoxidase can be used in the evaluation of vascular disease occurrence and development in stroke, and a large amount of experimental and clinical data has indicated that the inhibition or lack of myeloperoxidase has positive impacts on stroke prognosis. Many studies have also shown that there is a correlation between the overexpression of myeloperoxidase and the risk of stroke. The occurrence of stroke not only refers to the first occurrence but also includes recurrence. Therefore, myeloperoxidase is significant for the clinical evaluation and prognosis of stroke. This paper reviews the potential role played by myeloperoxidase in the development of vascular injury and secondary brain injury after stroke and explores the effects of inhibiting myeloperoxidase on stroke prognosis. This paper also analyzes the significance of myeloperoxidase etiology in the occurrence and development of stroke and discusses whether myeloperoxidase can be used as a target for the treatment and prediction of stroke.

OLFML2A Downregulation Inhibits Glioma Proliferation Through Suppression of Wnt/ß-Catenin Signaling.

Glioma is a highly heterogeneous and lethal tumor with an extremely poor prognosis. Through analysis of TCGA data, we identified that OLFML2A is a key promotor of gliomagenesis. However, the molecular function of OLFML2A and its underlying mechanism of action in glioma remain unclear. In this study, we found that OLFML2A expression was significantly upregulated in glioma specimens and positively correlated with pathological grades in glioma patients. Moreover, Kaplan-Meier survival analysis of TCGA data revealed that glioma patients with higher OLFML2A expression had shorter overall survival. Importantly, OLFML2A knockdown in glioma cells inhibited cell proliferation and promoted apoptosis. Mechanistically, OLFML2A downregulation inhibits Wnt/ß-catenin signaling by upregulating amyloid precursor protein (APP) expression and reducing stabilized ß-catenin levels, leading to the repression of MYC, CD44, and CSKN2A2 expression. Furthermore, OLFML2A downregulation suppressed the growth of transplanted glioma subcutaneously and intracranially by inhibiting Wnt/ß-catenin pathway-dependent cell proliferation. By uncovering the oncogenic effects in human and rodent gliomas, our data support OLFML2A as a potential therapeutic target for glioma.