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[PMID]: 25913858
[Au] Autor:Mukai J; Tamura M; Fénelon K; Rosen AM; Spellman TJ; Kang R; MacDermott AB; Karayiorgou M; Gordon JA; Gogos JA
[Ad] Address:Department of Physiology and Cellular Biophysics, College of Physicians and Surgeons, Columbia University, New York, NY 10032, USA....
[Ti] Title:Molecular substrates of altered axonal growth and brain connectivity in a mouse model of schizophrenia.
[So] Source:Neuron;86(3):680-95, 2015 May 6.
[Is] ISSN:1097-4199
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:22q11.2 deletion carriers show specific cognitive deficits, and ∼30% of them develop schizophrenia. One of the disrupted genes is ZDHHC8, which encodes for a palmitoyltransferase. We show that Zdhhc8-deficient mice have reduced palmitoylation of proteins that regulate axonal growth and branching. Analysis of axonal projections of pyramidal neurons from both Zdhhc8-deficient and Df(16)A(+/-) mice, which model the 22q11.2 deletion, revealed deficits in axonal growth and terminal arborization, which can be prevented by reintroduction of active ZDHHC8 protein. Impaired terminal arborization is accompanied by a reduction in the strength of synaptic connections and altered functional connectivity and working memory. The effect of ZDHHC8 is mediated in part via Cdc42-dependent modulation of Akt/Gsk3ß signaling at the tip of the axon and can be reversed by pharmacologically decreasing Gsk3ß activity during postnatal brain development. Our findings provide valuable mechanistic insights into the cognitive and psychiatric symptoms associated with a schizophrenia-predisposing mutation.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1505
[Cu] Class update date: 150516
[Lr] Last revision date:150516
[Js] Journal subset:IM
[St] Status:In-Data-Review

  2 / 261077 MEDLINE  
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[PMID]: 25444819
[Au] Autor:Singh S; Yang G; Byrareddy SN; Barry MA; Sastry KJ
[Ad] Address:Department of Immunology, The University of Texas M.D. Anderson Cancer Center, Houston, TX, United States....
[Ti] Title:Natural killer T cell and TLR9 agonists as mucosal adjuvants for sublingual vaccination with clade C HIV-1 envelope protein.
[So] Source:Vaccine;32(51):6934-40, 2014 Dec 5.
[Is] ISSN:1873-2518
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:The vast majority of HIV-1 infections occur at mucosa during sexual contact. It may therefore be advantageous to provide mucosal barrier protection against this entry by mucosal vaccination. While a number of mucosal routes of vaccination are possible, many like enteric oral vaccines or intranasal vaccines have significant impediments that limit vaccine efficacy or pose safety risks. In contrast, immunogens applied to the sublingual region of the mouth could provide a simple route for mucosal vaccination. While sublingual immunization is appealing, this site does not always drive strong immune responses, particularly when using protein antigens. To address this issue, we have tested the ability of two mucosal adjuvants: alpha-galactosylceramide (αGalCer) that is a potent stimulator of natural killer T cells and CpG-oligodeoxynucleotide (CpG-ODN) a TLR9 agonist for their ability to amplify immune responses against clade C gp140 HIV-1 envelope protein antigen. Immunization with envelope protein alone resulted in a weak T cell and antibody responses. In contrast, CD4(+) and CD8(+) T cells responses in systemic and mucosal tissues were significantly higher in mice immunized with gp140 in the presence of either αGalCer or CpG-ODN and these responses were further augmented when the two adjuvants were used together. While both the adjuvants effectively increased gp140-specific serum IgG and vaginal IgA antibody levels, combining both significantly improved these responses. Memory T cell responses 60 days after immunization revealed αGalCer to be more potent than CpG-ODN and the combination of the αGalCer and CpG-ODN adjuvants was more effective than either alone. Serum and vaginal washes collected 60 days after immunization with gp140 with both αGalCer and CpG-ODN adjuvants had significant neutralization activity against Tier 1 and Tier 2 SHIVs. These data support the utility of the sublingual route for mucosal vaccination particularly in combination with αGalCer and CpG-ODN adjuvants.
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Em] Entry month:1501
[Cu] Class update date: 150516
[Lr] Last revision date:150516
[Js] Journal subset:IM
[St] Status:In-Process

  3 / 261077 MEDLINE  
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[PMID]: 25523827
[Au] Autor:Boska MD; Dash PK; Knibbe J; Epstein AA; Akhter SP; Fields N; High R; Makarov E; Bonasera S; Gelbard HA; Poluektova LY; Gendelman HE; Gorantla S
[Ti] Title:Associations between brain microstructures, metabolites, and cognitive deficits during chronic HIV-1 infection of humanized mice.
[So] Source:Mol Neurodegener;9:58, 2014.
[Is] ISSN:1750-1326
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: Host-species specificity of the human immunodeficiency virus (HIV) limits pathobiologic, diagnostic and therapeutic research investigations to humans and non-human primates. The emergence of humanized mice as a model for viral infection of the nervous system has overcome such restrictions enabling research for HIV-associated end organ disease including behavioral, cognitive and neuropathologic deficits reflective of neuroAIDS. Chronic HIV-1 infection of NOD/scid-IL-2Rgcnull mice transplanted with human CD34+ hematopoietic stem cells (CD34-NSG) leads to persistent viremia, profound CD4+ T lymphocyte loss and infection of human monocyte-macrophages in the meninges and perivascular spaces. Murine cells are not infected with virus. METHODS: Changes in mouse behavior were measured, starting at 8 weeks after viral infection. These were recorded coordinate with magnetic resonance spectroscopy metabolites including N-acetylaspartate (NAA), creatine and choline. Diffusion tensor magnetic resonance imaging (DTI) was recorded against multispectral immunohistochemical staining for neuronal markers that included microtubule associated protein-2 (MAP2), neurofilament (NF) and synaptophysin (SYN); for astrocyte glial fibrillary acidic protein (GFAP); and for microglial ionized calcium binding adaptor molecule 1 (Iba-1). Oligodendrocyte numbers and integrity were measured for myelin associated glycoprotein (MAG) and myelin oligodendrocyte glycoprotein (MOG) antigens. RESULTS: Behavioral abnormalities were readily observed in HIV-1 infected mice. Longitudinal open field activity tests demonstrated lack of habituation indicating potential for memory loss and persistent anxiety in HIV-1 infected mice compared to uninfected controls. End-point NAA and creatine in the cerebral cortex increased with decreased MAG. NAA and glutamate decreased with decreased SYN and MAG. Robust inflammation reflected GFAP and Iba-1 staining intensities. DTI metrics were coordinate with deregulation of NF, Iba-1, MOG and MAG levels in the whisker barrel and MAP2, NF, MAG, MOG and SYN in the corpus callosum. CONCLUSIONS: The findings are consistent with some of the clinical, biochemical and pathobiologic features of human HIV-1 nervous system infections. This model will prove useful towards investigating the mechanisms of HIV-1 induced neuropathology and in developing novel biomarkers and therapeutic strategies for disease.
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Entry month:1501
[Cu] Class update date: 150516
[Lr] Last revision date:150516
[Js] Journal subset:IM
[St] Status:In-Process
[do] DOI:10.1186/1750-1326-9-58

  4 / 261077 MEDLINE  
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[PMID]: 25057146
[Au] Autor:Cao G; Harris KM
[Ad] Address:The Center for Learning and Memory, University of Texas at Austin, Austin, Texas.
[Ti] Title:Augmenting saturated LTP by broadly spaced episodes of theta-burst stimulation in hippocampal area CA1 of adult rats and mice.
[So] Source:J Neurophysiol;112(8):1916-24, 2014 Oct 15.
[Is] ISSN:1522-1598
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Hippocampal long-term potentiation (LTP) is a model system for studying cellular mechanisms of learning and memory. Recent interest in mechanisms underlying the advantage of spaced over massed learning has prompted investigation into the effects of distributed episodes of LTP induction. The amount of LTP induced in hippocampal area CA1 by one train (1T) of theta-burst stimulation (TBS) in young Sprague-Dawley rats was further enhanced by additional bouts of 1T given at 1-h intervals. However, in young Long-Evans (LE) rats, 1T did not initially saturate LTP. Instead, a stronger LTP induction paradigm using eight trains of TBS (8T) induced saturated LTP in hippocampal slices from both young and adult LE rats as well as adult mice. The saturated LTP induced by 8T could be augmented by another episode of 8T following an interval of at least 90 min. The success rate across animals and slices in augmenting LTP by an additional episode of 8T increased significantly with longer intervals between the first and last episodes, ranging from 0% at 30- and 60-min intervals to 13-66% at 90- to 180-min intervals to 90-100% at 240-min intervals. Augmentation above initially saturated LTP was blocked by the N-methyl-D-aspartate (NMDA) glutamate receptor antagonist D-2-amino-5-phosphonovaleric acid (D-APV). These findings suggest that the strength of induction and interval between episodes of TBS, as well as the strain and age of the animal, are important components in the augmentation of LTP.
[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: 150516
[Lr] Last revision date:150516
[Js] Journal subset:IM
[St] Status:In-Process
[do] DOI:10.1152/jn.00297.2014

  5 / 261077 MEDLINE  
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[PMID]: 24685143
[Au] Autor:Zahodne LB; Nowinski CJ; Gershon RC; Manly JJ
[Ad] Address:1Cognitive Neuroscience Division,Department of Neurology and Taub Institute for Research on Alzheimer's Disease and The Aging Brain,Columbia University College of Physicians and Surgeons,New York,New York....
[Ti] Title:Which psychosocial factors best predict cognitive performance in older adults?
[So] Source:J Int Neuropsychol Soc;20(5):487-95, 2014 May.
[Is] ISSN:1469-7661
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Negative affect (e.g., depression) is associated with accelerated age-related cognitive decline and heightened dementia risk. Fewer studies examine positive psychosocial factors (e.g., emotional support, self-efficacy) in cognitive aging. Preliminary reports suggest that these variables predict slower cognitive decline independent of negative affect. No reports have examined these factors in a single model to determine which best relate to cognition. Data from 482 individuals 55 and older came from the normative sample for the NIH Toolbox for the Assessment of Neurological and Behavioral Function. Negative and positive psychosocial factors, executive functioning, working memory, processing speed, and episodic memory were measured with the NIH Toolbox Emotion and Cognition modules. Confirmatory factor analysis and structural equation modeling characterized independent relations between psychosocial factors and cognition. Psychosocial variables loaded onto negative and positive factors. Independent of education, negative affect and health status, greater emotional support was associated with better task-switching and processing speed. Greater self-efficacy was associated with better working memory. Negative affect was not independently associated with any cognitive variables. Findings support the conceptual distinctness of negative and positive psychosocial factors in older adults. Emotional support and self-efficacy may be more closely tied to cognition than other psychosocial variables.
[Mh] MeSH terms primary: Aging/physiology
Aging/psychology
Cognition/physiology
Emotions
Psychology
[Mh] MeSH terms secundary: Adolescent
Adult
Aged
Aged, 80 and over
Child
Child, Preschool
Factor Analysis, Statistical
Female
Humans
Male
Middle Aged
Statistics as Topic
Young Adult
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Em] Entry month:1504
[Cu] Class update date: 150516
[Lr] Last revision date:150516
[Js] Journal subset:IM
[Da] Date of entry for processing:140528
[St] Status:MEDLINE
[do] DOI:10.1017/S1355617714000186

  6 / 261077 MEDLINE  
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[PMID]: 25414002
[Au] Autor:Raslau FD; Mark IT; Klein AP; Ulmer JL; Mathews V; Mark LP
[Ad] Address:From the Department of Radiology (F.D.R.), University of Kentucky, Lexington, Kentucky....
[Ti] Title:Memory part 2: the role of the medial temporal lobe.
[So] Source:AJNR Am J Neuroradiol;36(5):846-9, 2015 May.
[Is] ISSN:1936-959X
[Cp] Country of publication:United States
[La] Language:eng
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1505
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.3174/ajnr.A4169

  7 / 261077 MEDLINE  
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[PMID]: 25572530
[Au] Autor:Janetsian SS; Linsenbardt DN; Lapish CC
[Ad] Address:Department of Psychology, Indiana University-Purdue University Indianapolis, 402 N. Blackford, LD 124, Indianapolis, IN, 46202, USA, sjanetsi@iupui.edu.
[Ti] Title:Memory impairment and alterations in prefrontal cortex gamma band activity following methamphetamine sensitization.
[So] Source:Psychopharmacology (Berl);232(12):2083-95, 2015 Jun.
[Is] ISSN:1432-2072
[Cp] Country of publication:Germany
[La] Language:eng
[Ab] Abstract:RATIONALE: Repeated methamphetamine (MA) use leads to increases in the incentive motivational properties of the drug as well as cognitive impairments. These behavioral alterations persist for some time following abstinence, and neuroadaptations in the structure and function of the prefrontal cortex (PFC) are particularly important for their expression. However, there is a weak understanding of the changes in neural firing and oscillatory activity in the PFC evoked by repeated drug use, thus complicating the development of novel treatment strategies for addiction. OBJECTIVES: The purpose of the current study was to assess changes in cognitive and brain function following MA sensitization. METHODS: Sensitization was induced in rats, then temporal and recognition memory were assessed after 1 or 30 days of abstinence. Electrophysiological recordings from the medial PFC were also acquired from rats whereupon simultaneous measures of oscillatory and spiking activity were examined. RESULTS: Impaired temporal memory was observed after 1 and 30 days of abstinence. However, recognition memory was only impaired after 1 day of abstinence. An injection of MA profoundly decreased neuronal firing rate and the anesthesia-induced slow oscillation (SO) in both sensitized (SENS) and control (CTRL) rats. Strong correlations were observed between the SO and gamma band power, which was altered in SENS animals. A decrease in the number of neurons phase-locked to the gamma oscillation was also observed in SENS animals. CONCLUSIONS: The changes observed in PFC function may play an integral role in the expression of the altered behavioral phenotype evoked by MA sensitization.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1505
[Cu] Class update date: 150515
[Lr] Last revision date:150515
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1007/s00213-014-3840-7

  8 / 261077 MEDLINE  
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[PMID]: 25283790
[Au] Autor:Arnett AB; Pennington BF; Willcutt EG; DeFries JC; Olson RK
[Ad] Address:Department of Psychology, University of Denver, Denver, CO, USA....
[Ti] Title:Sex differences in ADHD symptom severity.
[So] Source:J Child Psychol Psychiatry;56(6):632-9, 2015 Jun.
[Is] ISSN:1469-7610
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:BACKGROUND: Males show higher rates of attention deficit hyperactivity disorder (ADHD) than do females. Potential explanations include genuine etiological differences or artifact. METHODS: 2,332 twin and sibling youth participated in behavioral and cognitive testing. Partially competing models of symptom severity distribution differences, the mean difference, and variance difference models, were tested within a randomly selected subsample. The Delta method was used to test for mediation of sex differences in ADHD symptom severity by processing speed, inhibition and working memory. RESULTS: The combined mean difference and variance difference models fully explained the sex difference in ADHD symptom severity. Cognitive endophenotypes mediated 14% of the sex difference effect. CONCLUSIONS: The sex difference in ADHD symptom severity is valid and may be due to differing genetic and cognitive liabilities between the sexes.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1505
[Cu] Class update date: 150515
[Lr] Last revision date:150515
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1111/jcpp.12337

  9 / 261077 MEDLINE  
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[PMID]: 24408959
[Au] Autor:Muntané G; Horvath JE; Hof PR; Ely JJ; Hopkins WD; Raghanti MA; Lewandowski AH; Wray GA; Sherwood CC
[Ad] Address:Department of Anthropology, The George Washington University, Washington, DC 20052, USA....
[Ti] Title:Analysis of synaptic gene expression in the neocortex of primates reveals evolutionary changes in glutamatergic neurotransmission.
[So] Source:Cereb Cortex;25(6):1596-607, 2015 Jun.
[Is] ISSN:1460-2199
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Increased relative brain size characterizes the evolution of primates, suggesting that enhanced cognition plays an important part in the behavioral adaptations of this mammalian order. In addition to changes in brain anatomy, cognition can also be regulated by molecular changes that alter synaptic function, but little is known about modifications of synapses in primate brain evolution. The aim of the current study was to investigate the expression patterns and evolution of 20 synaptic genes from the prefrontal cortex of 12 primate species. The genes investigated included glutamate receptors, scaffolding proteins, synaptic vesicle components, as well as factors involved in synaptic vesicle release and structural components of the nervous system. Our analyses revealed that there have been significant changes during primate brain evolution in the components of the glutamatergic signaling pathway in terms of gene expression, protein expression, and promoter sequence changes. These results could entail functional modifications in the regulation of specific genes related to processes underlying learning and memory.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1505
[Cu] Class update date: 150515
[Lr] Last revision date:150515
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1093/cercor/bht354

  10 / 261077 MEDLINE  
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[PMID]: 24363266
[Au] Autor:Villalta JI; Landi SM; Fló A; Della-Maggiore V
[Ad] Address:Department of Physiology and Biophysics, School of Medicine, University of Buenos Aires, C1121ABG Buenos Aires, Argentina....
[Ti] Title:Extinction interferes with the retrieval of visuomotor memories through a mechanism involving the sensorimotor cortex.
[So] Source:Cereb Cortex;25(6):1535-43, 2015 Jun.
[Is] ISSN:1460-2199
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Savings is a fundamental property of learning. In motor adaptation, it refers to the improvement in learning observed when adaptation to a perturbation A (A1) is followed by re-adaptation to the same perturbation (A2). A common procedure to equate the initial level of error across sessions consists of restoring native sensorimotor coordinates by inserting null-unperturbed-trials (N) just before re-adaptation (washout). Here, we hypothesized that the washout is not innocuous but interferes with the expression of the new memory at recall. To assess this possibility, we measured savings following the A1NA2 protocol, where A was a 40° visual rotation. In Experiment 1, we increased the time window between N and A2 from 1 min to 24 h. This manipulation increased the amount of savings during middle to late phases of adaptation, suggesting that N interfered with the retrieval of A. In Experiment 2, we used repetitive TMS to evaluate if this interference was partly mediated by the sensorimotor cortex (SM). We conclude that the washout does not just restore the unperturbed sensorimotor coordinates, but inhibits the expression of the recently acquired visuomotor map through a mechanism involving SM. Our results resemble the phenomenon of extinction in classical conditioning.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1505
[Cu] Class update date: 150515
[Lr] Last revision date:150515
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1093/cercor/bht346


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