Neuroimmunomodulation最新文献

{"title":"Association of Exposure to Particulate Matters and Multiple Sclerosis: A Systematic Review and Meta-Analysis.","authors":"Fatemeh Lotfi,&nbsp;Marjan Mansourian,&nbsp;Omid Mirmoayyeb,&nbsp;Soroush Najdaghi,&nbsp;Vahid Shaygannejad,&nbsp;Nafiseh Esmaeil","doi":"10.1159/000516559","DOIUrl":"https://doi.org/10.1159/000516559","url":null,"abstract":"<p><p>The association between air pollution and multiple sclerosis (MS) is not entirely clear. This meta-analysis was aimed at determining the correlation between particulate matter (PM)2.5, PM10, and MS incidence/relapse. The literature search was performed in EMBASE, Web of Science, PubMed, and the gray literature. Sixteen articles were retrieved, and ten articles were included and evaluated. Three measures of association were used for the meta-analysis: odds ratio (cross-sectional and case-control studies), incidence rate ratio, or hazard ratio (cohort studies). Meta-analysis of those 3 studies on PM2.5 indicated that exposure to PM2.5 was associated with MS relapse and incidence ([95% confidence interval; CI] 1.178 [1.102, 1.279]), p > 0.05. Also, assessment of risk ratio for all studies showed a correlation between PMs (PM10 and PM2.5) and MS incidence and relapse ([95% CI] 1.28, [1.13-1.43]) p < 0.05. Collectively, we found that PM exposure (PM10 and PM2.5) in MS patients associates with the occurrence and relapse of disease.</p>","PeriodicalId":19133,"journal":{"name":"Neuroimmunomodulation","volume":null,"pages":null},"PeriodicalIF":2.4,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000516559","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39237450","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Functional Roles of Curcumin on Astrocytes in Neurodegenerative Diseases.","authors":"Amir Mohammadi,&nbsp;Abasalt Hosseinzadeh Colagar,&nbsp;Ayeh Khorshidian,&nbsp;Seyed Mohammad Amini","doi":"10.1159/000517901","DOIUrl":"https://doi.org/10.1159/000517901","url":null,"abstract":"<p><p>Progressive abnormality and loss of axons and neurons in the central nervous system (CNS) cause neurodegenerative diseases (NDs). Protein misfolding and its collection are the most important pathological features of NDs. Astrocytes are the most plentiful cells in the mammalian CNS (about 20-40% of the human brain) and have several central functions in the maintenance of the health and correct function of the CNS. Astrocytes have an essential role in the preservation of brain homeostasis, and it is not surprising that these multifunctional cells have been implicated in the onset and progression of several NDs. Thus, they become an exciting target for the study of NDs. Over almost 15 years, it was revealed that curcumin has several therapeutic effects in a wide variety of diseases' treatment. Curcumin is a valuable ingredient present in turmeric spice and has several essential roles, including those which are anticarcinogenic, hepatoprotective, thrombosuppressive, cardioprotective, anti-arthritic, anti-inflammatory, antioxidant, chemopreventive, chemotherapeutic, and anti-infectious. Furthermore, curcumin can suppress inflammation; promote angiogenesis; and treat diabetes, pulmonary problems, and neurological dysfunction. Here, we review the effects of curcumin on astrocytes in NDs, with a focus on Alzheimer's disease, Parkinson's disease, multiple scleroses, Huntington's disease, and amyotrophic lateral sclerosis.</p>","PeriodicalId":19133,"journal":{"name":"Neuroimmunomodulation","volume":null,"pages":null},"PeriodicalIF":2.4,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39395666","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Silencing of TRIM44 Inhibits Inflammation and Alleviates Traumatic Brain Injury in Rats by Downregulating TLR4-NF-κB Signaling.","authors":"Lin Zhu,&nbsp;Ce Dong,&nbsp;Xiongfei Yue,&nbsp;Pengzhen Ge,&nbsp;Guozhen Zheng,&nbsp;Zhanying Ye,&nbsp;Baogen Pan","doi":"10.1159/000524536","DOIUrl":"https://doi.org/10.1159/000524536","url":null,"abstract":"<p><strong>Background: </strong>Neuroinflammation subsequent to traumatic brain injury (TBI) is important for the recovery of patients and is associated with neurodegenerative changes post-TBI. The tripartite motif containing 44 (TRIM44) protein is an E3 ligase involved in the regulation of immune function with no previously known link to TBI. This study explores the connection between TRIM44 and TBI.</p><p><strong>Methods: </strong>After induction of TBI in rats by control cortex injury, TRIM44 expressions were determined with quantitative real-time reverse transcription polymerase chain reaction and Western blot, and Toll-like receptor 4 (TLR4)-NF-κB signaling was examined by the expression of TLR4, p65 phosphorylation, and the specific NF-κB transcription activity. The effects of TRIM44 knockdown on inflammation, neurological function, and TLR4-NF-κB signaling in TBI rats were revealed by the detection of proinflammatory cytokines and TLR4-NF-κB signaling molecules, modified neurological severity score, brain water content, and Evans blue permeability.</p><p><strong>Results: </strong>We found that TRIM44 expression was significantly increased following TBI induction along with TLR4-NF-κB activation. Silencing of TRIM44 suppressed proinflammatory cytokine production, improved neurological outcomes, alleviated brain edema, and inhibited TLR4-NF-κB signaling in TBI rats.</p><p><strong>Conclusion: </strong>Our findings suggest that suppressing TRIM44 or modulation of relevant pathways may be a therapeutic strategy for TBI.</p>","PeriodicalId":19133,"journal":{"name":"Neuroimmunomodulation","volume":null,"pages":null},"PeriodicalIF":2.4,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10476631","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of Long Noncoding RNA H19 on Isoflurane-Induced Cognitive Dysregulation by Promoting Neuroinflammation.","authors":"Yanhu Ge,&nbsp;Duomao Lin,&nbsp;Boqun Cui,&nbsp;Liang Zhang,&nbsp;Shurong Li,&nbsp;Zhaoqi Wang,&nbsp;Jun Ma","doi":"10.1159/000519124","DOIUrl":"https://doi.org/10.1159/000519124","url":null,"abstract":"<p><strong>Introduction: </strong>Isoflurane (ISO) may cause neuronal apoptosis and synaptic disorder during development, and damage long-term learning and memory function. This observation aimed to study the function of H19 in vitro and in vivo tests and the further mechanism was identified.</p><p><strong>Methods: </strong>ISO cell models and rat models were established and reactive oxygen species (ROS) identified. The viability and apoptosis of HT22 cells were detected by the MTT and flow cytometer. Morris water maze test was conducted to analyze the neurotoxicity of ISO on spatial learning and memory ability. Quantitative PCR was the method to verify the expression of H19. The concentration of inflammatory indicators was identified by enzyme-linked immunosorbent assay.</p><p><strong>Results: </strong>1.5% and 2% ISO led to the neurotoxicity of HT22 cells and increased expression of H19. Silenced H19 meliorated these adverse impacts of ISO. Interference of H19 exerted neuroprotective roles by repressing modified neurological severity score, inhibiting escape latency, elevating distance and time of target area, and controlling ROS and inflammation. MiR-17-5p might be a promising competing endogenous RNA of H19. The expression of miR-17-5p was reduced in the ISO group and reversed by the absence of H19.</p><p><strong>Conclusion: </strong>Our results of in vitro and in vivo assay indicated that the absence of HT22 is a neuroprotective regulator of cognition and inflammation by accumulating miR-17-5p.</p>","PeriodicalId":19133,"journal":{"name":"Neuroimmunomodulation","volume":null,"pages":null},"PeriodicalIF":2.4,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39938635","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Nodakenetin Alleviates Inflammatory Pain Hypersensitivity by Suppressing NF-κB Signal Pathway.","authors":"Yiqin Lin,&nbsp;Yingle Chen,&nbsp;Jingyang Zeng,&nbsp;Shunyuan Li","doi":"10.1159/000525690","DOIUrl":"https://doi.org/10.1159/000525690","url":null,"abstract":"<p><strong>Background: </strong>Inflammatory pain mediated by nuclear factor kappa-B (NF-κB) signal pathway has become an increasingly important clinical issue in the last decade. As a potent antioxidant, Nodakenetin has been shown to have a prominent inhibitory effect on inflammation. However, the therapeutic effects and underlying pharmacological mechanisms of Nodakenetin for inflammatory pain remain unclear.</p><p><strong>Methods: </strong>Intraplanar injection of complete Freund's adjuvant (CFA) was used to establish a model of chronic inflammation pain in C57BL/6 mice. The chronic neuropathic pain model was conducted by the sciatic nerve ligation surgery. QRT-PCR was performed to estimate the RNA levels of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6). Western blot was used to demonstrated the protein levels of phospho-IkappaBα (IκBα), p50, and p65 in HEK293T cells.</p><p><strong>Results: </strong>The bioactive components of the traditional Chinese medicine Notopterygium forbesii boiss mainly include Nodakenetin, isoimperatorin, and pregnenolone. Nodakenetin significantly alleviated CFA-induced inflammatory pain but showed no significant therapeutic effect on surgically induced neuralgia in a mouse model. In contrast, isoimperatorin and pregnenolone did not relieve CFA-induced inflammatory pain. Mechanistically, Nodakenetin inhibited IL-1β-induced activation of the NF-κB pathway and phosphorylation of IκBα in HEK293T cells. Furthermore, Nodakenetin treatment suppressed the expression of IL-6, TNF-α, and IL-1β in mouse bone marrow-derived macrophages.</p><p><strong>Conclusion: </strong>Nodakenetin alleviates inflammatory pain induced by CFA injection in vivo and modulates NF-κB signal pathway in vitro.</p>","PeriodicalId":19133,"journal":{"name":"Neuroimmunomodulation","volume":null,"pages":null},"PeriodicalIF":2.4,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10762175","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Autoantibodies against Central Nervous System Antigens and the Serum Levels of IL-32 in Patients with Schizophrenia.","authors":"Fatemeh Keshavarz,&nbsp;Marziyeh Soltani,&nbsp;Kobra Mokhtarian,&nbsp;Pezhman Beshkar,&nbsp;Jafar Majidi,&nbsp;Fatemeh Azadegan-Dehkordi,&nbsp;Maryam Anjomshoa,&nbsp;Nader Bagheri","doi":"10.1159/000526425","DOIUrl":"https://doi.org/10.1159/000526425","url":null,"abstract":"<p><strong>Background: </strong>Schizophrenia is a disease of the nervous system, and immune system disorders can affect its pathogenesis. Activation of microglia, proinflammatory cytokines, disruption of the blood-brain barrier due to inflammation, activation of autoreactive B cells, and consequently the production of autoantibodies against system antigens are among the immune processes involved in neurological diseases. Interleukin-32 (IL-32) is a proinflammatory cytokine that is essential in activating innate and adaptive immune responses. This study aimed to measure the serum level of IL-32 as well as the frequency of autoantibody positivity against several nervous system antigens in patients with schizophrenia.</p><p><strong>Material and methods: </strong>This study was conducted on 40 patients with schizophrenia and 40 healthy individuals in the control group. Serum IL-32 levels were measured by ELISA. The frequency of autoantibodies against Hu, Ri, Yo, Tr, CV2, amphiphysin, SOX1, Zic4, ITPR1, CARP, glutamic acid decarboxylase GAD, recoverin, titin, and ganglioside antigens was measured by the indirect immunofluorescence method.</p><p><strong>Results: </strong>Serum IL-32 levels in patients with schizophrenia were significantly higher compared to the control group. The frequency of autoantibodies against GAD and RI antigens in patients with schizophrenia was significantly higher than in the control group. Autoantibodies were positive in 8 patients for GAD antigen and 5 patients for RI antigen. Autoantibodies were also positive in 2 patients for CV2, 1 patient for Hu, and 1 patient for CARP. Negative results were reported for other antigens.</p><p><strong>Conclusion: </strong>Our findings suggest that elevated the serum IL-32 level and autoantibodies against GAD and RI antigens may be a reflection of immune system dysregulation in patients with schizophrenia.</p>","PeriodicalId":19133,"journal":{"name":"Neuroimmunomodulation","volume":null,"pages":null},"PeriodicalIF":2.4,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10401196","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"New Editor-in-Chief's Note: The Past and the Future.","authors":"Rainer H Straub","doi":"10.1159/000521574","DOIUrl":"https://doi.org/10.1159/000521574","url":null,"abstract":"By studying the history of a scientific journal, we can learn more about the scientific culture of a research field and we can start to understand how it changed and what it is now. Samuel M. McCann† and James M. Lipton† (served: 1994–2001), George P. Chrousos (2002–2006), and Wilson Savino (2007–2021) were the distinguished Editors-in-Chief of Neuroimmunomodulation, giants of the science of neuro-endocrine-immune interrelations. The late Sam McCann wrote in the first Neuroimmunomodulation Editorial in Volume 1, Issue 1, 1994 [1]:","PeriodicalId":19133,"journal":{"name":"Neuroimmunomodulation","volume":null,"pages":null},"PeriodicalIF":2.4,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39642810","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Animal Model of Neonatal Immune Challenge by Lipopolysaccharide: A Study of Sex Influence in Behavioral and Immune/Neurotrophic Alterations in Juvenile Mice.","authors":"Larissa Maria Frota Cristino,&nbsp;Adriano José Maia Chaves Filho,&nbsp;Charllyany Sabino Custódio,&nbsp;Silvânia Maria Mendes Vasconcelos,&nbsp;Francisca Cléa F de Sousa,&nbsp;Lia Lira O Sanders,&nbsp;David Freitas de Lucena,&nbsp;Danielle S Macedo","doi":"10.1159/000522055","DOIUrl":"https://doi.org/10.1159/000522055","url":null,"abstract":"<p><strong>Introduction: </strong>The prenatal/perinatal exposure to infections may trigger neurodevelopmental alterations that lead to neuropsychiatric disorders such as autism spectrum disorder (ASD). Previous evidence points to long-term behavioral consequences, such as autistic-like behaviors in rodents induced by lipopolysaccharide (LPS) pre- and postnatal (PN) exposure during critical neurodevelopmental periods. Additionally, sex influences the prevalence and symptoms of ASD. Despite this, the mechanisms underlying this influence are poorly understood. We aim to study sex influences in behavioral and neurotrophic/inflammatory alterations triggered by LPS neonatal exposure in juvenile mice at an approximate age of ASD diagnosis in humans.</p><p><strong>Methods: </strong>Swiss male and female mice on PN days 5 and 7 received a single daily injection of 500 μg/kg LPS from Escherichia coli or sterile saline (control group). We conducted behavioral determinations of locomotor activity, repetitive behavior, anxiety-like behavior, social interaction, and working memory in animals on PN25 (equivalent to 3-5 years old of the human). To determine BDNF levels in the prefrontal cortex and hippocampus, we used animals on PN8 (equivalent to a human term infant) and PN25. In addition, we evaluated iba-1 (microglia marker), TNFα, and parvalbumin expression on PN25.</p><p><strong>Results: </strong>Male juvenile mice presented repetitive behavior, anxiety, and working memory deficits. Females showed social impairment and working memory deficits. In the neurochemical analysis, we detected lower BDNF levels in brain areas of female mice that were more evident in juvenile mice. Only LPS-challenged females presented a marked hippocampal expression of the microglial activation marker, iba-1, and increased TNFα levels, accompanied by a lower parvalbumin expression.</p><p><strong>Discussion/conclusion: </strong>Male and female mice presented distinct behavioral alterations. However, LPS-challenged juvenile females showed the most prominent neurobiological alterations related to autism, such as increased microglial activation and parvalbumin impairment. Since these sex-sensitive alterations seem to be age-dependent, a better understanding of changes induced by the exposure to specific risk factors throughout life represents essential targets for developing strategies for autism prevention and precision therapy.</p>","PeriodicalId":19133,"journal":{"name":"Neuroimmunomodulation","volume":null,"pages":null},"PeriodicalIF":2.4,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10827304","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mild Traumatic Brain Injury Contributes to the Development of Delayed Neuroinflammation.","authors":"Arina Ponomarenko,&nbsp;Anna Tyrtyshnaia,&nbsp;Darya Ivashkevich,&nbsp;Igor Manzhulo","doi":"10.1159/000519011","DOIUrl":"https://doi.org/10.1159/000519011","url":null,"abstract":"<p><strong>Introduction: </strong>In recent years, according to the literature, the problem of mild traumatic brain injury (mTBI) has become more and more urgent. Compared to moderate to severe craniocerebral trauma, mTBI occurs in a far greater number of people. The delayed sequelae caused by a single mTBI or multiple mTBIs are a significant public health problem.</p><p><strong>Methods: </strong>A weight-drop model was used for the formation of mTBI. A metal rod weighing 337 g with a blunt tip of 3 mm diameter was uplifted at 8 cm height and held by a lever. The trauma was created by lowering the lever and the rod and free-dropping onto the rat skull. In the cerebral cortex of experimental animals, we analyzed the level of microglial activity (Iba-1-positive system) and the expression of pro-inflammatory markers (IL1β, IL6, and CD86). Also, the expression level of the endocannabinoid system receptor (cannabinoid receptor type 1 [CB1]) was assessed in brain samples.</p><p><strong>Results: </strong>Experiments have shown that mTBI increases (1) the amount of microglia (iba-1) activated by the pro-inflammatory pathway (CD86); (2) the level of pro-inflammatory cytokines IL1β and IL6; and (3) CB1R activity.</p><p><strong>Conclusion: </strong>Overall, the results of this study indicate that mTBI induces a sustained neuroinflammatory response.</p>","PeriodicalId":19133,"journal":{"name":"Neuroimmunomodulation","volume":null,"pages":null},"PeriodicalIF":2.4,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39465649","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Differential Expression of miR-381-3p in Alzheimer's Disease Patients and Its Role in Beta-Amyloid-Induced Neurotoxicity and Inflammation.","authors":"Meng Zhang,&nbsp;Yonglei Liu,&nbsp;Pingping Teng,&nbsp;Qing Yang","doi":"10.1159/000519780","DOIUrl":"https://doi.org/10.1159/000519780","url":null,"abstract":"<p><strong>Introduction: </strong>This study aimed to explore the diagnostic value and effect of miR-381-3p on Alzheimer's disease (AD).</p><p><strong>Methods: </strong>RT-qPCR was used for the measurement of miR-381-3p levels. Pearson correlation coefficient was used for the correlation analysis. Receiver operating characteristic (ROC) curve was constructed to assess the distinct ability of miR-381-3p for AD. SH-SY5Y cells were treated with Aβ25-35 to establish an AD cell model. The role of miR-381-3p on cell proliferation and apoptosis was detected. ELISA was applied to detect the protein levels of inflammatory cytokine expression. The target relationship of miR-381-3p with PTGS2 was verified by luciferase reporter gene assay.</p><p><strong>Results: </strong>Low expression of miR-381-3p was detected in the serum of AD patients and cell models. There was a negative association of serum miR-381-3p with the serum inflammatory cytokines. The ROC curve demonstrated the distinct ability of serum miR-381-3p for AD, with the AUC value of 0.898, with a sensitivity of 87.5%, and a specificity of 77.7%. Overexpression of miR-381-3p reversed the influence of Aβ25-35 on cell proliferation and apoptosis, but miR-381-3p downregulation exacerbated the influence. miR-381-3p overexpression inhibited the release of IL-6, IL-1β, and TNF-α induced by Aβ25-35 treatment, whereas miR-381-3p downregulation further promoted the release of inflammatory cytokines. PTGS2 was the target gene of miR-381-3p and was upregulated in AD cell models.</p><p><strong>Conclusion: </strong>miR-381-3p is less expressed in the serum of AD patients and has potential diagnostic values for AD. Overexpression of miR-381-3p may attenuate Aβ25-35-induced neurotoxicity and inflammatory responses via targeting PTGS2 in SH-SY5Y cells.</p>","PeriodicalId":19133,"journal":{"name":"Neuroimmunomodulation","volume":null,"pages":null},"PeriodicalIF":2.4,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39601216","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}