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[PMID]: 25255260
[Au] Autor:Chohan MO; Bragina O; Kazim SF; Statom G; Baazaoui N; Bragin D; Iqbal K; Nemoto E; Yonas H
[Ad] Address:*Department of Neurosurgery, University of New Mexico Hospital, Albuquerque, New Mexico; ‡Department of Neurochemistry, Inge Grundke-Iqbal Floor, New York State Institute for Basic Research in Developmental Disabilities, Staten Island, New York; §Neural and Behavioral Science Graduate Program, State University of New York (SUNY) Downstate Medical Center, Brooklyn, New York.
[Ti] Title:Enhancement of neurogenesis and memory by a neurotrophic Peptide in mild to moderate traumatic brain injury.
[So] Source:Neurosurgery;76(2):201-15, 2015 Feb.
[Is] ISSN:1524-4040
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND: Traumatic brain injury (TBI) is a risk factor for Alzheimer disease (AD), a neurocognitive disorder with similar cellular abnormalities. We recently discovered a small molecule (Peptide 6) corresponding to an active region of human ciliary neurotrophic factor, with neurogenic and neurotrophic properties in mouse models of AD and Down syndrome. OBJECTIVE: To describe hippocampal abnormalities in a mouse model of mild to moderate TBI and their reversal by Peptide 6. METHODS: TBI was induced in adult C57Bl6 mice using controlled cortical impact with 1.5 mm of cortical penetration. The animals were treated with 50 nmol/d of Peptide 6 or saline solution for 30 days. Dentate gyrus neurogenesis, dendritic and synaptic density, and AD biomarkers were quantitatively analyzed, and behavioral tests were performed. RESULTS: Ipsilateral neuronal loss in CA1 and the parietal cortex and increase in Alzheimer-type hyperphosphorylated tau and A-ß were seen in TBI mice. Compared with saline solution, Peptide 6 treatment increased the number of newborn neurons, but not uncommitted progenitor cells, in dentate gyrus by 80%. Peptide 6 treatment also reversed TBI-induced dendritic and synaptic density loss while increasing activity in tri-synaptic hippocampal circuitry, ultimately leading to improvement in memory recall on behavioral testing. CONCLUSION: Long-term treatment with Peptide 6 enhances the pool of newborn neurons in the dentate gyrus, prevents neuronal loss in CA1 and parietal cortex, preserves the dendritic and synaptic architecture in the hippocampus, and improves performance on a hippocampus-dependent memory task in TBI mice. These findings necessitate further inquiry into the therapeutic potential of small molecules based on neurotrophic factors. ABBREVIATIONS: AD, Alzheimer diseaseBrdU, bromodeoxyuridineBrdU-IR, bromodeoxyuridine immunoreactiveBrdU-NeuN-IR, BrdU-NeuN immunoreactive cellsCCI, controlled cortical impactCNTF, ciliary neurotrophic factorDG, dentate gyrusGCL, granular cell layerLIF, leukemia inhibitory factorMAP2, microtubule-associated protein 2MWM, Morris water mazeSEM, standard error of the meanTBI, traumatic brain injury.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1501
[Cu] Class update date: 150117
[Lr] Last revision date:150117
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1227/NEU.0000000000000577

  2 / 255017 MEDLINE  
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[PMID]: 25548230
[Au] Autor:Gorbacheva V; Fan R; Wang X; Baldwin WM; Fairchild RL; Valujskikh A
[Ad] Address:Glickman Urological Institute, Cleveland Clinic, Cleveland, OH 44195; and Department of Immunology, Cleveland Clinic, Cleveland, OH 44195....
[Ti] Title:IFN-γ Production by Memory Helper T Cells Is Required for CD40-Independent Alloantibody Responses.
[So] Source:J Immunol;194(3):1347-56, 2015 Feb 1.
[Is] ISSN:1550-6606
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Cognate T-B cell interactions and CD40-CD154 costimulation are essential for productive humoral immunity against T-dependent Ags. We reported that memory CD4 T cells can deliver help to B cells and induce pathogenic IgG alloantibodies in the absence of CD40-CD154 interactions. To determine cytokine requirements for CD40-independent help, we used CD40(-/-) mice containing differentiated subsets of donor-reactive memory Th cells as heart allograft recipients. Th1 and Th17, but not Th2, memory CD4 T cells elicited high titers of anti-donor Ab. Abs induced by Th17 memory CD4 T cells had decreased reactivity against donor MHC class I molecules and inferior ability to cause complement deposition in heart allografts compared with Abs induced by Th1 cells, suggesting a requirement for IFN-γ during CD40-independent help. IFN-γ neutralization inhibited helper functions of memory CD4 T cells in both CD40(-/-) recipients and wild type recipients treated with anti-CD154 mAb. Our results suggest that IFN-γ secreted by pre-existing memory helper cells determines both isotype and specificity of donor-reactive alloantibodies and can thus affect allograft pathology. This information may be valuable for identifying transplant patients at risk for de novo development of pathogenic alloantibodies and for preventing alloantibody production in T cell-sensitized recipients.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1501
[Cu] Class update date: 150117
[Lr] Last revision date:150117
[Js] Journal subset:AIM; IM
[St] Status:In-Data-Review
[do] DOI:10.4049/jimmunol.1401573

  3 / 255017 MEDLINE  
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[PMID]: 25539474
[Au] Autor:Storkel HL
[Ad] Address:University of Kansas , Lawrence, KS , USA.
[Ti] Title:Learning from input and memory evolution: Points of vulnerability on a pathway to mastery in word learning.
[So] Source:Int J Speech Lang Pathol;17(1):1-12, 2015 Feb.
[Is] ISSN:1754-9515
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Abstract Word learning consists of at least two neurocognitive processes: learning from input during training and memory evolution during gaps between training sessions. Fine-grained analysis of word learning by normal adults provides evidence that learning from input is swift and stable, whereas memory evolution is a point of potential vulnerability on the pathway to mastery. Moreover, success during learning from input is linked to positive outcomes from memory evolution. These two neurocognitive processes can be overlaid on to components of clinical treatment with within-session variables (i.e. dose form and dose) potentially linked to learning from input and between-session variables (i.e. dose frequency) linked to memory evolution. Collecting data at the beginning and end of a treatment session can be used to identify the point of vulnerability in word learning for a given client and the appropriate treatment component can then be adjusted to improve the client's word learning. Two clinical cases are provided to illustrate this approach.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1501
[Cu] Class update date: 150117
[Lr] Last revision date:150117
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.3109/17549507.2014.987818

  4 / 255017 MEDLINE  
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[PMID]: 24362528
[Au] Autor:Ren T; Takahashi Y; Liu X; Loughran TP; Sun SC; Wang HG; Cheng H
[Ad] Address:1] Penn State Hershey Cancer Institute, Penn State University College of Medicine, Hershey, PA, USA [2] Department of Microbiology and Immunology, Penn State University College of Medicine, Hershey, PA, USA....
[Ti] Title:HTLV-1 Tax deregulates autophagy by recruiting autophagic molecules into lipid raft microdomains.
[So] Source:Oncogene;34(3):334-45, 2015 Jan 15.
[Is] ISSN:1476-5594
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:The retroviral oncoprotein Tax from human T-cell leukemia virus type 1 (HTLV-1), an etiological factor that causes adult T-cell leukemia and lymphoma, has a crucial role in initiating T-lymphocyte transformation by inducing oncogenic signaling activation. We here report that Tax is a determining factor for dysregulation of autophagy in HTLV-1-transformed T cells and Tax-immortalized CD4 memory T cells. Tax facilitated autophagic process by activating inhibitor of κB (IκB) kinase (IKK) complex, which subsequently recruited an autophagy molecular complex containing Beclin1 and Bif-1 to the lipid raft microdomains. Tax engaged a crosstalk between IKK complex and autophagic molecule complex by directly interacting with both complexes, promoting assembly of LC3+ autophagosomes. Moreover, expression of lipid raft-targeted Bif-1 or Beclin1 was sufficient to induce formation of LC3+ autophagosomes, suggesting that Tax recruitment of autophagic molecules to lipid rafts is a dominant strategy to deregulate autophagy in the context of HTLV-1 transformation of T cells. Furthermore, depletion of autophagy molecules such as Beclin1 and PI3 kinase class III resulted in impaired growth of HTLV-1-transformed T cells, indicating a critical role of Tax-deregulated autophagy in promoting survival and transformation of virally infected T cells.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1501
[Cu] Class update date: 150117
[Lr] Last revision date:150117
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1038/onc.2013.552

  5 / 255017 MEDLINE  
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[PMID]: 25590029
[Au] Autor:Noori N; Bangash MY; Motaghinejad M; Hosseini P; Noudoost B
[Ad] Address:Department of Food Hygiene, Faculty of Veterinary Medicine, University of Tehran, Tehran, Iran....
[Ti] Title:Kefir protective effects against nicotine cessation-induced anxiety and cognition impairments in rats.
[So] Source:Adv Biomed Res;3:251, 2014.
[Is] ISSN:2277-9175
[Cp] Country of publication:India
[La] Language:eng
[Ab] Abstract:BACKGROUND: Nicotine as one of the potent psychostimulant drugs is characterized by its parasympathomimetic activity. Upon the abrupt discontinuation of nicotine intake, a number of symptoms such as anxiety, depression and cognition impairment develop. Kefir as a food supplement is rich in tryptophan. In this study, we have evaluated the effects of Kefir on nicotine cessation-induced anxiety, depression and cognition impairment. MATERIALS AND METHODS: Forty adult male rats were divided into four groups. All the groups received 6 mg/kg/day of nicotine for 17 days and then the negative control groups got 5 mg/kg/day of normal saline. The positive control groups were given 40 mg/kg/day of Sertraline HCl for 7 days. The group treated with Cow Milk Kefir (CMK) and Soy Milk Kefir (SMK) received 5 mg/kg/day for 7 days. On the 25(th) day, Elevated Plus Maze (EPM), Open Field Test (OFT) and Forced Swim Test (FST) were used to investigate anxiety and depression. In addition, Moris Water Maze was applied to evaluate learning and memory in the animals between the 20(th) and 25(th) days. RESULTS: The results showed that administration of CMK, SMK and Sertraline had higher anti-depression and anxiolytic effects on nicotine withdrawal-induced depression and anxiety in rats (P < 0.05). Moreover, CMK and SMK improved learning and memory impairment results in the nicotine withdrawal period (P < 0.05). CONCLUSION: This study revealed that Kefir had a potential effect on the treatment of nicotine cessation-induced depression, anxiety and cognition impairment in the animal model. Kefir may be useful for adjunct therapy for nicotine abandonment treatment protocols.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1501
[Cu] Class update date: 150117
[Lr] Last revision date:150117
[Da] Date of entry for processing:150115
[St] Status:PubMed-not-MEDLINE
[do] DOI:10.4103/2277-9175.146377

  6 / 255017 MEDLINE  
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[PMID]: 25586207
[Au] Autor:Lv H; Xu X; Liu H; Liu R; Liu Q; Banerjee W; Sun H; Long S; Li L; Liu M
[Ad] Address:Lab of Nano-fabrication and Novel Devices Integration, Institute of Microelectronics, Chinese Academy of Sciences, Beijing 100029, China....
[Ti] Title:Evolution of conductive filament and its impact on reliability issues in oxide-electrolyte based resistive random access memory.
[So] Source:Sci Rep;5:7764, 2015.
[Is] ISSN:2045-2322
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:The electrochemical metallization cell, also referred to as conductive bridge random access memory, is considered to be a promising candidate or complementary component to the traditional charge based memory. As such, it is receiving additional focus to accelerate the commercialization process. To create a successful mass product, reliability issues must first be rigorously solved. In-depth understanding of the failure behavior of the ECM is essential for performance optimization. Here, we reveal the degradation of high resistance state behaves as the majority cases of the endurance failure of the HfO2 electrolyte based ECM cell. High resolution transmission electron microscopy was used to characterize the change in filament nature after repetitive switching cycles. The result showed that Cu accumulation inside the filament played a dominant role in switching failure, which was further supported by measuring the retention of cycle dependent high resistance state and low resistance state. The clarified physical picture of filament evolution provides a basic understanding of the mechanisms of endurance and retention failure, and the relationship between them. Based on these results, applicable approaches for performance optimization can be implicatively developed, ranging from material tailoring to structure engineering and algorithm design.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1501
[Cu] Class update date: 150117
[Lr] Last revision date:150117
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1038/srep07764

  7 / 255017 MEDLINE  
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[PMID]: 25585693
[Au] Autor:Mai VH; Moradpour A; Senzier PA; Pasquier C; Wang K; Rozenberg MJ; Giapintzakis J; Mihailescu CN; Orfanidou CM; Svoukis E; Breza A; Lioutas ChB; Franger S; Revcolevschi A; Maroutian T; Lecoeur P; Aubert P; Agnus G; Salot R; Albouy PA; Weil R; Alamarguy D; March K; Jomard F; Chrétien P; Schneegans O
[Ad] Address:1] Laboratoire de Génie Électrique de Paris, CNRS-UMR 8507, Universités UPMC et Paris-Sud, Supélec, F-91192 Gif-sur-Yvette, France [2] Institut d'Électronique Fondamentale, CNRS-UMR 8622, Université Paris-Sud, 91405 Orsay, France....
[Ti] Title:Memristive and neuromorphic behavior in a LixCoO2 nanobattery.
[So] Source:Sci Rep;5:7761, 2015.
[Is] ISSN:2045-2322
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:The phenomenon of resistive switching (RS), which was initially linked to non-volatile resistive memory applications, has recently also been associated with the concept of memristors, whose adjustable multilevel resistance characteristics open up unforeseen perspectives in cognitive computing. Herein, we demonstrate that the resistance states of LixCoO2 thin film-based metal-insulator-metal (MIM) solid-state cells can be tuned by sequential programming voltage pulses, and that these resistance states are dramatically dependent on the pulses input rate, hence emulating biological synapse plasticity. In addition, we identify the underlying electrochemical processes of RS in our MIM cells, which also reveal a nanobattery-like behavior, leading to the generation of electrical signals that bring an unprecedented new dimension to the connection between memristors and neuromorphic systems. Therefore, these LixCoO2-based MIM devices allow for a combination of possibilities, offering new perspectives of usage in nanoelectronics and bio-inspired neuromorphic circuits.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1501
[Cu] Class update date: 150117
[Lr] Last revision date:150117
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1038/srep07761

  8 / 255017 MEDLINE  
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[PMID]: 25228141
[Au] Autor:Delpech JC; Madore C; Joffre C; Aubert A; Kang JX; Nadjar A; Layé S
[Ad] Address:1] INRA, Nutrition et Neurobiologie Intégrée, UMR 1286, Bordeaux, France [2] Univ. Bordeaux, Nutrition et Neurobiologie Intégrée, UMR 1286, Bordeaux, France....
[Ti] Title:Transgenic Increase in n-3/n-6 Fatty Acid Ratio Protects Against Cognitive Deficits Induced by an Immune Challenge through Decrease of Neuroinflammation.
[So] Source:Neuropsychopharmacology;40(3):525-36, 2015 Feb.
[Is] ISSN:1740-634X
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Polyunsaturated fatty acids (PUFAs) display immunomodulatory properties in the brain, n-3 PUFAs being able to reduce inflammation whereas n-6 PUFAs are more pro-inflammatory. It has been extensively demonstrated that exposure to a peripheral immune challenge leads to the production and release of inflammatory mediators in the brain in association with cognitive deficits. The question arises whether n-3 PUFA supplementation could downregulate the brain inflammatory response and subsequent cognitive alterations. In this study, we used a genetically modified mouse line carrying the fat-1 gene from the roundworm Caenorhabditis elegans, encoding an n-3 PUFA desaturase that catalyzes conversion of n-6 into n-3 PUFA. Consequently, these mice display endogenously elevated n-3 PUFA tissue contents. Fat-1 mice or wild-type (WT) littermates were injected peripherally with lipopolysaccharide (LPS), a bacterial endotoxin, to induce an inflammatory episode. Our results showed that LPS altered differently the phenotype of microglia and the expression of cytokines and chemokines in Fat-1 and WT mice. In Fat-1 mice, pro-inflammatory factors synthesis was lowered compared with WT mice, whereas anti-inflammatory mechanisms were favored 24 h after LPS treatment. Moreover, LPS injection impaired spatial memory in WT mice, whereas interestingly, the Fat-1 mice showed normal cognitive performances. All together, these data suggest that the central n-3 PUFA increase observed in Fat-1 mice modulated the brain innate immune system activity, leading to the protection of animals against LPS-induced pro-inflammatory cytokine production and subsequent spatial memory alteration.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1501
[Cu] Class update date: 150117
[Lr] Last revision date:150117
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1038/npp.2014.196

  9 / 255017 MEDLINE  
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[PMID]: 25139064
[Au] Autor:Colizzi M; Fazio L; Ferranti L; Porcelli A; Masellis R; Marvulli D; Bonvino A; Ursini G; Blasi G; Bertolino A
[Ad] Address:1] Group of Psychiatric Neuroscience, Department of Basic Medical Sciences, Neuroscience and Sense Organs, University of Bari 'Aldo Moro', Bari, Italy [2] Department of Psychosis Studies, Institute of Psychiatry, King's College London, London, UK....
[Ti] Title:Functional genetic variation of the cannabinoid receptor 1 and cannabis use interact on prefrontal connectivity and related working memory behavior.
[So] Source:Neuropsychopharmacology;40(3):640-9, 2015 Feb.
[Is] ISSN:1740-634X
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Cannabinoid signaling is involved in different brain functions and it is mediated by the cannabinoid receptor 1 (CNR1), which is encoded by the CNR1 gene. Previous evidence suggests an association between cognition and cannabis use. The logical interaction between genetically determined cannabinoid signaling and cannabis use has not been determined. Therefore, we investigated whether CNR1 variation predicts CNR1 prefrontal mRNA expression in postmortem prefrontal human tissue. Then, we studied whether functional variation in CNR1 and cannabis exposure interact in modulating prefrontal function and related behavior during working memory processing. Thus, 208 healthy subjects (113 males) were genotyped for the relevant functional SNP and were evaluated for cannabis use by the Cannabis Experience Questionnaire. All individuals performed the 2-back working memory task during functional magnetic resonance imaging. CNR1 rs1406977 was associated with prefrontal mRNA and individuals carrying a G allele had reduced CNR1 prefrontal mRNA levels compared with AA subjects. Moreover, functional connectivity MRI demonstrated that G carriers who were also cannabis users had greater functional connectivity in the left ventrolateral prefrontal cortex and reduced working memory behavioral accuracy during the 2-back task compared with the other groups. Overall, our results indicate that the deleterious effects of cannabis use are more evident on a specific genetic background related to its receptor expression.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1501
[Cu] Class update date: 150117
[Lr] Last revision date:150117
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1038/npp.2014.213

  10 / 255017 MEDLINE  
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[PMID]: 25120077
[Au] Autor:Hida H; Mouri A; Mori K; Matsumoto Y; Seki T; Taniguchi M; Yamada K; Iwamoto K; Ozaki N; Nabeshima T; Noda Y
[Ad] Address:Division of Clinical Sciences and Neuropsychopharmacology, Graduate School of Pharmacy, Meijo University, Nagoya, Japan....
[Ti] Title:Blonanserin Ameliorates Phencyclidine-Induced Visual-Recognition Memory Deficits: the Complex Mechanism of Blonanserin Action Involving D3-5-HT2A and D1-NMDA Receptors in the mPFC.
[So] Source:Neuropsychopharmacology;40(3):601-13, 2015 Feb.
[Is] ISSN:1740-634X
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Blonanserin differs from currently used serotonin 5-HT2A/dopamine-D2 receptor antagonists in that it exhibits higher affinity for dopamine-D2/3 receptors than for serotonin 5-HT2A receptors. We investigated the involvement of dopamine-D3 receptors in the effects of blonanserin on cognitive impairment in an animal model of schizophrenia. We also sought to elucidate the molecular mechanism underlying this involvement. Blonanserin, as well as olanzapine, significantly ameliorated phencyclidine (PCP)-induced impairment of visual-recognition memory, as demonstrated by the novel-object recognition test (NORT) and increased extracellular dopamine levels in the medial prefrontal cortex (mPFC). With blonanserin, both of these effects were antagonized by DOI (a serotonin 5-HT2A receptor agonist) and 7-OH-DPAT (a dopamine-D3 receptor agonist), whereas the effects of olanzapine were antagonized by DOI but not by 7-OH-DPAT. The ameliorating effect was also antagonized by SCH23390 (a dopamine-D1 receptor antagonist) and H-89 (a protein kinase A (PKA) inhibitor). Blonanserin significantly remediated the decrease in phosphorylation levels of PKA at Thr(197) and of NR1 (an essential subunit of N-methyl-D-aspartate (NMDA) receptors) at Ser(897) by PKA in the mPFC after a NORT training session in the PCP-administered mice. There were no differences in the levels of NR1 phosphorylated at Ser(896) by PKC in any group. These results suggest that the ameliorating effect of blonanserin on PCP-induced cognitive impairment is associated with indirect functional stimulation of the dopamine-D1-PKA-NMDA receptor pathway following augmentation of dopaminergic neurotransmission due to inhibition of both dopamine-D3 and serotonin 5-HT2A receptors in the mPFC.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1501
[Cu] Class update date: 150117
[Lr] Last revision date:150117
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1038/npp.2014.207


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