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[PMID]: 25481013
[Au] Autor:Wang Q; Xiao B; Cui S; Song H; Qian Y; Dong L; An H; Cui Y; Zhang W; He Y; Zhang J; Yang J; Zhang F; Hu G; Gong X; Yan Z; Zheng Y; Wang X
[Ad] Address:Department of Physiology, Department of Neurobiology, Key Laboratory for Neurodegenerative Disorders of the Ministry of Education, Capital Medical University, Beijing 100069, PR China. Beijing Institute for Brain Disorders, Beijing 100069, PR China....
[Ti] Title:Triptolide treatment reduces Alzheimer's disease (AD)-like pathology through inhibition of BACE1 in a transgenic mouse model of AD.
[So] Source:Dis Model Mech;7(12):1385-95, 2014 Dec.
[Is] ISSN:1754-8411
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:The complex pathogenesis of Alzheimer's disease (AD) involves multiple contributing factors, including amyloid ß (Aß) peptide accumulation, inflammation and oxidative stress. Effective therapeutic strategies for AD are still urgently needed. Triptolide is the major active compound extracted from Tripterygium wilfordii Hook.f., a traditional Chinese medicinal herb that is commonly used to treat inflammatory diseases. The 5-month-old 5XFAD mice, which carry five familial AD mutations in the ß-amyloid precursor protein (APP) and presenilin-1 (PS1) genes, were treated with triptolide for 8 weeks. We observed enhanced spatial learning performances, and attenuated Aß production and deposition in the brain. Triptolide also inhibited the processing of amyloidogenic APP, as well as the expression of ßAPP-cleaving enzyme-1 (BACE1) both in vivo and in vitro. In addition, triptolide exerted anti-inflammatory and anti-oxidative effects on the transgenic mouse brain. Triptolide therefore confers protection against the effects of AD in our mouse model and is emerging as a promising therapeutic candidate drug for AD.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1412
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1242/dmm.018218

  2 / 1249683 MEDLINE  
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[PMID]: 25177766
[Au] Autor:Lavallée-Adam M; Rauniyar N; McClatchy DB; Yates JR
[Ad] Address:Department of Chemical Physiology, The Scripps Research Institute , 10550 N. Torrey Pines Rd., La Jolla, California 92037, United States.
[Ti] Title:PSEA-Quant: A Protein Set Enrichment Analysis on Label-Free and Label-Based Protein Quantification Data.
[So] Source:J Proteome Res;13(12):5496-509, 2014 Dec 5.
[Is] ISSN:1535-3907
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The majority of large-scale proteomics quantification methods yield long lists of quantified proteins that are often difficult to interpret and poorly reproduced. Computational approaches are required to analyze such intricate quantitative proteomics data sets. We propose a statistical approach to computationally identify protein sets (e.g., Gene Ontology (GO) terms) that are significantly enriched with abundant proteins with reproducible quantification measurements across a set of replicates. To this end, we developed PSEA-Quant, a protein set enrichment analysis algorithm for label-free and label-based protein quantification data sets. It offers an alternative approach to classic GO analyses, models protein annotation biases, and allows the analysis of samples originating from a single condition, unlike analogous approaches such as GSEA and PSEA. We demonstrate that PSEA-Quant produces results complementary to GO analyses. We also show that PSEA-Quant provides valuable information about the biological processes involved in cystic fibrosis using label-free protein quantification of a cell line expressing a CFTR mutant. Finally, PSEA-Quant highlights the differences in the mechanisms taking place in the human, rat, and mouse brain frontal cortices based on tandem mass tag quantification. Our approach, which is available online, will thus improve the analysis of proteomics quantification data sets by providing meaningful biological insights.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1412
[Cu] Class update date: 141206
[Lr] Last revision date:141206
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1021/pr500473n

  3 / 1249683 MEDLINE  
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[PMID]: 25385825
[Au] Autor:Mutnal MB; Hu S; Schachtele SJ; Lokensgard JR
[Ad] Address:Neuroimmunology Laboratory, Center for Infectious Diseases and Microbiology Translational Research, Department of Medicine, University of Minnesota, Minneapolis, MN 55455....
[Ti] Title:Infiltrating Regulatory B Cells Control Neuroinflammation following Viral Brain Infection.
[So] Source:J Immunol;193(12):6070-80, 2014 Dec 15.
[Is] ISSN:1550-6606
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Previous studies have demonstrated the existence of a subset of B lymphocytes, regulatory B cells (Bregs), which modulate immune function. In this study, in vivo and in vitro experiments were undertaken to elucidate the role of these Bregs in controlling neuroinflammation following viral brain infection. We used multicolor flow cytometry to phenotype lymphocyte subpopulations infiltrating the brain, along with in vitro cocultures to assess their anti-inflammatory and immunoregulatory roles. This distinctive subset of CD19(+)CD1d(hi)CD5(+) B cells was found to infiltrate the brains of chronically infected animals, reaching highest levels at the latest time point tested (30 d postinfection). B cell-deficient Jh(-/-) mice were found to develop exacerbated neuroimmune responses as measured by enhanced accumulation and/or retention of CD8(+) T cells within the brain, as well as increased levels of microglial activation (MHC class II). Conversely, levels of Foxp3(+) regulatory T cells were found to be significantly lower in Jh(-/-) mice when compared with wild-type (Wt) animals. Further experiments showed that in vitro-generated IL-10-secreting Bregs (B10) were able to inhibit cytokine responses from microglia following stimulation with viral Ags. These in vitro-generated B10 cells were also found to promote proliferation of regulatory T cells in coculture studies. Finally, gain-of-function experiments demonstrated that reconstitution of Wt B cells into Jh(-/-) mice restored neuroimmune responses to levels exhibited by infected Wt mice. Taken together, these results demonstrate that Bregs modulate T lymphocyte as well as microglial cell responses within the infected brain and promote CD4(+)Foxp3(+) T cell proliferation in vitro.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1412
[Cu] Class update date: 141206
[Lr] Last revision date:141206
[Js] Journal subset:AIM; IM
[St] Status:In-Data-Review
[do] DOI:10.4049/jimmunol.1400654

  4 / 1249683 MEDLINE  
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[PMID]: 25300859
[Au] Autor:Ohkuri T; Ghosh A; Kosaka A; Zhu J; Ikeura M; David M; Watkins SC; Sarkar SN; Okada H
[Ad] Address:Department of Neurological Surgery, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania. Department of Brain Tumor, University of Pittsburgh Cancer Institute, Pittsburgh, Pennsylvania....
[Ti] Title:STING Contributes to Antiglioma Immunity via Triggering Type I IFN Signals in the Tumor Microenvironment.
[So] Source:Cancer Immunol Res;2(12):1199-208, 2014 Dec.
[Is] ISSN:2326-6074
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Although type I IFNs play critical roles in antiviral and antitumor activity, it remains to be elucidated how type I IFNs are produced in sterile conditions of the tumor microenvironment and directly affect tumor-infiltrating immune cells. Mouse de novo gliomas show increased expression of type I IFN messages, and in mice, CD11b(+) brain-infiltrating leukocytes (BIL) are the main source of type I IFNs that are induced partially in a STING (stimulator of IFN genes)-dependent manner. Consequently, glioma-bearing Sting(Gt) (/Gt) mice showed shorter survival and lower expression levels of Ifns compared with wild-type mice. Furthermore, BILs of Sting(Gt) (/Gt) mice showed increased CD11b(+) Gr-1(+) immature myeloid suppressor and CD25(+) Foxp3(+) regulatory T cells (Treg) and decreased IFNγ-producing CD8(+) T cells. CD4(+) and CD8(+) T cells that received direct type I IFN signals showed lesser degrees of regulatory activity and increased levels of antitumor activity, respectively. Finally, intratumoral administration of a STING agonist (cyclic diguanylate monophosphate; c-di-GMP) improved the survival of glioma-bearing mice associated with enhanced type I IFN signaling, Cxcl10 and Ccl5, and T-cell migration into the brain. In combination with subcutaneous OVA peptide vaccination, c-di-GMP increased OVA-specific cytotoxicity of BILs and prolonged their survival. These data demonstrate significant contributions of STING to antitumor immunity via enhancement of type I IFN signaling in the tumor microenvironment and suggest a potential use of STING agonists for the development of effective immunotherapy, such as the combination with antigen-specific vaccinations. Cancer Immunol Res; 2(12); 1199-208. ©2014 AACR.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1412
[Cu] Class update date: 141206
[Lr] Last revision date:141206
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1158/2326-6066.CIR-14-0099

  5 / 1249683 MEDLINE  
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[PMID]: 25434001
[Au] Autor:Lee YS; Hall SM; Ramos-Colon C; Remesic M; LeBaron L; Nguyen A; Rankin D; Porreca F; Lai J; Hruby VJ
[Ad] Address:Department of Chemistry and Biochemistry, University of Arizona, Tucson, AZ 85721, USA. Electronic address: yeon@email.arizona.edu....
[Ti] Title:Modification of amphipathic non-opioid dynorphin A analogues for rat brain bradykinin receptors.
[So] Source:Bioorg Med Chem Lett;25(1):30-3, 2015 Jan 1.
[Is] ISSN:1464-3405
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:It has been shown that under chronic pain or nerve injury conditions, up-regulated dynorphin A (Dyn A) interacts with bradykinin receptors (BRs) to cause hyperalgesia in the spinal cord. Thus BRs antagonist can modulate hyperalgesia by blocking Dyn A's interaction with the BRs in the central nervous system. In our earlier structure-activity relationship (SAR) study, [des-Arg(7)]-Dyn A-(4-11) 13 was discovered as a minimum pharmacophore for rat brain BRs with its antagonist activity (anti-hyperalgesic effect) in in vivo tests using naïve or injured animals. We have pursued further modification on the [des-Arg(7)]-Dyn A analogues and identified a key insight into the pharmacophore of the rat brain BRs: amphipathicity.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1412
[Cu] Class update date: 141206
[Lr] Last revision date:141206
[Js] Journal subset:IM
[St] Status:In-Data-Review

  6 / 1249683 MEDLINE  
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[PMID]: 25448683
[Au] Autor:Vito ST; Austin AT; Banks CN; Inceoglu B; Bruun DA; Zolkowska D; Tancredi DJ; Rogawski MA; Hammock BD; Lein PJ
[Ad] Address:Department of Entomology, College of Agricultural and Environmental Sciences, University of California-Davis, Davis, CA 95616, United States. Electronic address: stvito@ucdavis.edu....
[Ti] Title:Post-exposure administration of diazepam combined with soluble epoxide hydrolase inhibition stops seizures and modulates neuroinflammation in a murine model of acute TETS intoxication.
[So] Source:Toxicol Appl Pharmacol;281(2):185-94, 2014 Dec 1.
[Is] ISSN:1096-0333
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Tetramethylenedisulfotetramine (TETS) is a potent convulsant poison for which there is currently no approved antidote. The convulsant action of TETS is thought to be mediated by inhibition of type A gamma-aminobutyric acid receptor (GABAAR) function. We, therefore, investigated the effects of post-exposure administration of diazepam, a GABAAR positive allosteric modulator, on seizure activity, death and neuroinflammation in adult male Swiss mice injected with a lethal dose of TETS (0.15mg/kg, ip). Administration of a high dose of diazepam (5mg/kg, ip) immediately following the second clonic seizure (approximately 20min post-TETS injection) effectively prevented progression to tonic seizures and death. However, this treatment did not prevent persistent reactive astrogliosis and microglial activation, as determined by GFAP and Iba-1 immunoreactivity and microglial cell morphology. Inhibition of soluble epoxide hydrolase (sEH) has been shown to exert potent anti-inflammatory effects and to increase survival in mice intoxicated with other GABAAR antagonists. The sEH inhibitor TUPS (1mg/kg, ip) administered immediately after the second clonic seizure did not protect TETS-intoxicated animals from tonic seizures or death. Combined administration of diazepam (5mg/kg, ip) and TUPS (1mg/kg, ip, starting 1h after diazepam and repeated every 24h) prevented TETS-induced lethality and influenced signs of neuroinflammation in some brain regions. Significantly decreased microglial activation and enhanced reactive astrogliosis were observed in the hippocampus, with no changes in the cortex. Combining an agent that targets specific anti-inflammatory mechanisms with a traditional antiseizure drug may enhance treatment outcome in TETS intoxication.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1412
[Cu] Class update date: 141206
[Lr] Last revision date:141206
[Js] Journal subset:IM
[St] Status:In-Data-Review

  7 / 1249683 MEDLINE  
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[PMID]: 25466916
[Au] Autor:Burbridge TJ; Xu HP; Ackman JB; Ge X; Zhang Y; Ye MJ; Zhou ZJ; Xu J; Contractor A; Crair MC
[Ad] Address:Department of Neurobiology, Yale University School of Medicine, New Haven, CT 06510, USA....
[Ti] Title:Visual circuit development requires patterned activity mediated by retinal acetylcholine receptors.
[So] Source:Neuron;84(5):1049-64, 2014 Dec 3.
[Is] ISSN:1097-4199
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The elaboration of nascent synaptic connections into highly ordered neural circuits is an integral feature of the developing vertebrate nervous system. In sensory systems, patterned spontaneous activity before the onset of sensation is thought to influence this process, but this conclusion remains controversial, largely due to the inherent difficulty recording neural activity in early development. Here, we describe genetic and pharmacological manipulations of spontaneous retinal activity, assayed in vivo, that demonstrate a causal link between retinal waves and visual circuit refinement. We also report a decoupling of downstream activity in retinorecipient regions of the developing brain after retinal wave disruption. Significantly, we show that the spatiotemporal characteristics of retinal waves affect the development of specific visual circuits. These results conclusively establish retinal waves as necessary and instructive for circuit refinement in the developing nervous system and reveal how neural circuits adjust to altered patterns of activity prior to experience.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1412
[Cu] Class update date: 141206
[Lr] Last revision date:141206
[Js] Journal subset:IM
[St] Status:In-Data-Review

  8 / 1249683 MEDLINE  
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[PMID]: 25401692
[Au] Autor:Gascon E; Lynch K; Ruan H; Almeida S; Verheyden JM; Seeley WW; Dickson DW; Petrucelli L; Sun D; Jiao J; Zhou H; Jakovcevski M; Akbarian S; Yao WD; Gao FB
[Ad] Address:Department of Neurology, University of Massachusetts Medical School, Worcester, Massachusetts, USA....
[Ti] Title:Alterations in microRNA-124 and AMPA receptors contribute to social behavioral deficits in frontotemporal dementia.
[So] Source:Nat Med;20(12):1444-51, 2014 Dec.
[Is] ISSN:1546-170X
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Neurodegenerative diseases, such as frontotemporal dementia (FTD), are often associated with behavioral deficits, but the underlying anatomical and molecular causes remain poorly understood. Here we show that forebrain-specific expression of FTD-associated mutant CHMP2B in mice causes several age-dependent neurodegenerative phenotypes, including social behavioral impairments. The social deficits were accompanied by a change in AMPA receptor (AMPAR) composition, leading to an imbalance between Ca(2+)-permeable and Ca(2+)-impermeable AMPARs. Expression of most AMPAR subunits was regulated by the brain-enriched microRNA miR-124, whose abundance was markedly decreased in the superficial layers of the cerebral cortex of mice expressing the mutant CHMP2B. We found similar changes in miR-124 and AMPAR levels in the frontal cortex and induced pluripotent stem cell-derived neurons from subjects with behavioral variant FTD. Moreover, ectopic miR-124 expression in the medial prefrontal cortex of mutant mice decreased AMPAR levels and partially rescued behavioral deficits. Knockdown of the AMPAR subunit Gria2 also alleviated social impairments. Our results identify a previously undescribed mechanism involving miR-124 and AMPARs in regulating social behavior in FTD and suggest a potential therapeutic avenue.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1412
[Cu] Class update date: 141206
[Lr] Last revision date:141206
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1038/nm.3717

  9 / 1249683 MEDLINE  
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[PMID]: 25055809
[Au] Autor:Admon R; Nickerson LD; Dillon DG; Holmes AJ; Bogdan R; Kumar P; Dougherty DD; Iosifescu DV; Mischoulon D; Fava M; Pizzagalli DA
[Ad] Address:Center for Depression, Anxiety and Stress Research,McLean Hospital/Harvard Medical School Belmont,MA,USA....
[Ti] Title:Dissociable cortico-striatal connectivity abnormalities in major depression in response to monetary gains and penalties.
[So] Source:Psychol Med;45(1):121-31, 2015 Jan.
[Is] ISSN:1469-8978
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: Individuals with major depressive disorder (MDD) are characterized by maladaptive responses to both positive and negative outcomes, which have been linked to localized abnormal activations in cortical and striatal brain regions. However, the exact neural circuitry implicated in such abnormalities remains largely unexplored. METHOD: In this study 26 unmedicated adults with MDD and 29 matched healthy controls (HCs) completed a monetary incentive delay task during functional magnetic resonance imaging (fMRI). Psychophysiological interaction (PPI) analyses probed group differences in connectivity separately in response to positive and negative outcomes (i.e. monetary gains and penalties). RESULTS: Relative to HCs, MDD subjects displayed decreased connectivity between the caudate and dorsal anterior cingulate cortex (dACC) in response to monetary gains, yet increased connectivity between the caudate and a different, more rostral, dACC subregion in response to monetary penalties. Moreover, exploratory analyses of 14 MDD patients who completed a 12-week, double-blind, placebo-controlled clinical trial after the baseline fMRI scans indicated that a more normative pattern of cortico-striatal connectivity pre-treatment was associated with greater improvement in symptoms 12 weeks later. CONCLUSIONS: These results identify the caudate as a region with dissociable incentive-dependent dACC connectivity abnormalities in MDD, and provide initial evidence that cortico-striatal circuitry may play a role in MDD treatment response. Given the role of cortico-striatal circuitry in encoding action-outcome contingencies, such dysregulated connectivity may relate to the prominent disruptions in goal-directed behavior that characterize MDD.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1412
[Cu] Class update date: 141206
[Lr] Last revision date:141206
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1017/S0033291714001123

  10 / 1249683 MEDLINE  
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[PMID]: 25383518
[Au] Autor:Dias C; Feng J; Sun H; Shao NY; Mazei-Robison MS; Damez-Werno D; Scobie K; Bagot R; LaBonté B; Ribeiro E; Liu X; Kennedy P; Vialou V; Ferguson D; Peña C; Calipari ES; Koo JW; Mouzon E; Ghose S; Tamminga C; Neve R; Shen L; Nestler EJ
[Ad] Address:Fishberg Department of Neuroscience and Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, New York 10029, USA....
[Ti] Title:ß-catenin mediates stress resilience through Dicer1/microRNA regulation.
[So] Source:Nature;516(7529):51-5, 2014 Dec 4.
[Is] ISSN:1476-4687
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:ß-catenin is a multi-functional protein that has an important role in the mature central nervous system; its dysfunction has been implicated in several neuropsychiatric disorders, including depression. Here we show that in mice ß-catenin mediates pro-resilient and anxiolytic effects in the nucleus accumbens, a key brain reward region, an effect mediated by D2-type medium spiny neurons. Using genome-wide ß-catenin enrichment mapping, we identify Dicer1-important in small RNA (for example, microRNA) biogenesis--as a ß-catenin target gene that mediates resilience. Small RNA profiling after excising ß-catenin from nucleus accumbens in the context of chronic stress reveals ß-catenin-dependent microRNA regulation associated with resilience. Together, these findings establish ß-catenin as a critical regulator in the development of behavioural resilience, activating a network that includes Dicer1 and downstream microRNAs. We thus present a foundation for the development of novel therapeutic targets to promote stress resilience.
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Entry month:1412
[Cu] Class update date: 141206
[Lr] Last revision date:141206
[Js] Journal subset:IM
[St] Status:In-Process
[do] DOI:10.1038/nature13976


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