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[PMID]: 27017423
[Au] Autor:Cooper CM; Briggs RW; Farris EA; Bartlett J; Haley RW; Odegard TN
[Ad] Address:Department of Psychiatry, University of Texas Southwestern Medical Center, Dallas, TX, USA. Electronic address: crystal.cooper@utsouthwestern.edu....
[Ti] Title:Memory and functional brain differences in a national sample of U.S. veterans with Gulf War Illness.
[So] Source:Psychiatry Res;250:33-41, 2016 Apr 30.
[Is] ISSN:1872-7123
[Cp] Country of publication:Ireland
[La] Language:eng
[Ab] Abstract:Roughly 26-32% of U. S. veterans who served in the 1991 Persian Gulf War report suffering from chronic health problems. Memory complaints are regularly reported by ill Gulf War veterans (GWV), but limited data verify their complaints. This study investigated episodic memory and brain function in a nationally representative sample of GWV, using a face-name memory task and functional magnetic resonance imaging during encoding. A syndrome classification system was used to subdivide ill GWV into the three major Gulf War Illness syndrome types, "impaired cognition" (GWV-1), "confusion ataxia" (GWV-2), and "central pain" (GWV-3). Memory and brain function of ill GWV were contrasted to deployed and nondeployed well GWV controls (GWV-C). Ill GWV exhibited impaired memory function relative to GWV-C but the patterns of functional brain differences varied. Brain activation differentiated the GWV-C from the ill GWV. The different syndrome types also differed from one another in several brain regions. Additionally, the current study was the first to observe differences in brain function between deployed and nondeployed GWV-C. These results provide (1) evidence of memory impairment in ill GWV and differentiate the syndrome types at a functional neurobiological level, and (2) the role of deployment in the war on brain function.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1604
[Js] Journal subset:IM
[St] Status:In-Data-Review

  2 / 280032 MEDLINE  
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[PMID]: 27063650
[Au] Autor:Felgentreff K; Baxi SN; Lee YN; Dobbs K; Henderson LA; Csomos K; Tsitsikov EN; Armanios M; Walter JE; Notarangelo LD
[Ad] Address:Division of Immunology, Boston Children's Hospital, Harvard Medical School, Boston, MA, USA....
[Ti] Title:Ligase-4 Deficiency Causes Distinctive Immune Abnormalities in Asymptomatic Individuals.
[So] Source:J Clin Immunol;36(4):341-53, 2016 May.
[Is] ISSN:1573-2592
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:PURPOSE: DNA Ligase 4 (LIG4) is a key factor in the non-homologous end-joining (NHEJ) DNA double-strand break repair pathway needed for V(D)J recombination and the generation of the T cell receptor and immunoglobulin molecules. Defects in LIG4 result in a variable syndrome of growth retardation, pancytopenia, combined immunodeficiency, cellular radiosensitivity, and developmental delay. METHODS: We diagnosed a patient with LIG4 syndrome by radiosensitivity testing on peripheral blood cells, and established that two of her four healthy siblings carried the same compound heterozygous LIG4 mutations. An extensive analysis of the immune phenotype, cellular radiosensitivity, telomere length, and T and B cell antigen receptor repertoire was performed in all siblings. RESULTS: In the three genotypically affected individuals, variable severities of radiosensitivity, alterations of T and B cell counts with an increased percentage of memory cells, and hypogammaglobulinemia, were noticed. Analysis of T and B cell antigen receptor repertoires demonstrated increased usage of alternative microhomology-mediated end-joining (MHMEJ) repair, leading to diminished N nucleotide addition and shorter CDR3 length. However, overall repertoire diversity was preserved. CONCLUSIONS: We demonstrate that LIG4 syndrome presents with high clinical variability even within the same family, and that distinctive immunologic abnormalities may be observed also in yet asymptomatic individuals.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1604
[Cu] Class update date: 160423
[Lr] Last revision date:160423
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1007/s10875-016-0266-5

  3 / 280032 MEDLINE  
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[PMID]: 26947191
[Au] Autor:Miles B; Connick E
[Ad] Address:Division of Infectious Diseases, University of Colorado Denver, Aurora CO 80045, USA.
[Ti] Title:TFH in HIV Latency and as Sources of Replication-Competent Virus.
[So] Source:Trends Microbiol;24(5):338-44, 2016 May.
[Is] ISSN:1878-4380
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:During untreated disease, HIV replication is concentrated within T follicular helper cells (TFH). Heightened permissiveness, the presence of highly infectious virions on follicular dendritic cells (FDCs), low frequencies of virus-specific cytotoxic T lymphocytes (CTLs) in B cell follicles, expansions in TFH, and TFH dysfunction, all likely promote replication in TFH. Limited data suggest that memory TFH play a role in the latent or subclinical reservoir of HIV during antiretroviral therapy (ART), potentially for many of the same reasons. A better understanding of the role of memory TFH and FDC-bound virions in promoting recrudescent viremia in the setting of ART cessation is essential. Studies that target follicular virus reservoirs are needed to determine their role in HIV latency and to suggest successful cure strategies.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1604
[Cu] Class update date: 160423
[Lr] Last revision date:160423
[Js] Journal subset:IM
[St] Status:In-Data-Review

  4 / 280032 MEDLINE  
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[PMID]: 27100200
[Au] Autor:Xia D; Kelleher RJ; Shen J
[Ad] Address:Department of Neurology, Brigham & Women's Hospital, Harvard Medical School, Boston, MA 02115, USA; Center for Human Genetic Research, Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA.
[Ti] Title:Loss of Aß43 Production Caused by Presenilin-1 Mutations in the Knockin Mouse Brain.
[So] Source:Neuron;90(2):417-22, 2016 Apr 20.
[Is] ISSN:1097-4199
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:We recently reported that homozygous Presenilin-1 (Psen1) knockin (KI) mice carrying the familial Alzheimer's disease (FAD) mutation L435F or C410Y recapitulate the phenotypes of Psen1(-/-) mice. Production and steady-state levels of Aß40 and Aß42 are undetectable in KI/KI brains and reduced in KI/+ brains, though the Aß42/Aß40 ratio is slightly increased in KI/+ brains. Moreover, the FAD mutation impairs synaptic function, learning and memory, and age-dependent neuronal survival in the adult brain. Here we extend our analysis of the effects of the L435F and C410Y mutations to the generation of Aß43. Similar to Aß40 and Aß42, production of Aß43 is undetectable in KI/KI brains and reduced in KI/+ brains. These results support our previous conclusions that the L435F and C410Y mutations cause loss of Presenilin function and γ-secretase activity, including impaired Aß production in the brain. This Matters Arising Response paper addresses the Veugelen et al. (2016) Matters Arising paper, published concurrently in Neuron.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1604
[Cu] Class update date: 160423
[Lr] Last revision date:160423
[Js] Journal subset:IM
[St] Status:In-Data-Review

  5 / 280032 MEDLINE  
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[PMID]: 27103520
[Au] Autor:Sidhu VK; Huang BX; Desai A; Kevala K; Kim HY
[Ad] Address:Laboratory of Molecular Signaling, DICBR, NIAAA, NIH, Bethesda, MD, USA....
[Ti] Title:Role of DHA in aging-related changes in mouse brain synaptic plasma membrane proteome.
[So] Source:Neurobiol Aging;41:73-85, 2016 May.
[Is] ISSN:1558-1497
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Aging has been related to diminished cognitive function, which could be a result of ineffective synaptic function. We have previously shown that synaptic plasma membrane proteins supporting synaptic integrity and neurotransmission were downregulated in docosahexaenoic acid (DHA)-deprived brains, suggesting an important role of DHA in synaptic function. In this study, we demonstrate aging-induced synaptic proteome changes and DHA-dependent mitigation of such changes using mass spectrometry-based protein quantitation combined with western blot or messenger RNA analysis. We found significant reduction of 15 synaptic plasma membrane proteins in aging brains including fodrin-α, synaptopodin, postsynaptic density protein 95, synaptic vesicle glycoprotein 2B, synaptosomal-associated protein 25, synaptosomal-associated protein-α, N-methyl-D-aspartate receptor subunit epsilon-2 precursor, AMPA2, AP2, VGluT1, munc18-1, dynamin-1, vesicle-associated membrane protein 2, rab3A, and EAAT1, most of which are involved in synaptic transmission. Notably, the first 9 proteins were further reduced when brain DHA was depleted by diet, indicating that DHA plays an important role in sustaining these synaptic proteins downregulated during aging. Reduction of 2 of these proteins was reversed by raising the brain DHA level by supplementing aged animals with an omega-3 fatty acid sufficient diet for 2 months. The recognition memory compromised in DHA-depleted animals was also improved. Our results suggest a potential role of DHA in alleviating aging-associated cognitive decline by offsetting the loss of neurotransmission-regulating synaptic proteins involved in synaptic function.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1604
[Cu] Class update date: 160423
[Lr] Last revision date:160423
[Js] Journal subset:IM
[St] Status:In-Data-Review

  6 / 280032 MEDLINE  
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[PMID]: 27097664
[Au] Autor:Vandenberghe R
[Ad] Address:Department of Neurosciences, Laboratory for Cognitive Neurology, KU Leuven, Leuven, Belgium. rik.vandenberghe@uz.kuleuven.ac.be.
[Ti] Title:Classification of the primary progressive aphasias: principles and review of progress since 2011.
[So] Source:Alzheimers Res Ther;8(1):16, 2016.
[Is] ISSN:1758-9193
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Highly influential recommendations published in 2011 for the classification of the primary progressive aphasias (PPA) distinguished three subtypes: the semantic variant, the nonfluent/agrammatic variant, and the logopenic variant. We review empirical evidence published after 2011 that bears relevance to the validity of the recommended classification scheme. The studies that we review principally rely on monocentric, memory clinic-based consecutive series of PPA patients. We review whether a data-driven analysis of neurolinguistic test scores confirms the subtyping that was based on expert consensus, whether the 2011 subtyping covers the diversity of PPA in a comprehensive manner, and whether the proposed subgroups differ along dimensions that are not explicitly part of the defining criteria, such as diffusion tractography. Data-driven mathematical analyses of neurolinguistic data in PPA broadly confirm the presence of separate clusters corresponding to the subtypes but also leave 15-30 % unclassified. A comprehensive description of PPA requires the addition of the mixed variant as a fourth subtype and needs to leave room for cases fulfilling the criteria for a root diagnosis of PPA but not those of any of the three subtypes. Finally, given the limited predictive value of the clinical phenotype for the underlying neuropathology, biomarkers of the underlying pathology are likely of clinical utility in PPA.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1604
[Cu] Class update date: 160423
[Lr] Last revision date:160423
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1186/s13195-016-0185-y

  7 / 280032 MEDLINE  
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[PMID]: 27001176
[Au] Autor:Lopes LT; Patrone LG; Li KY; Imber AN; Graham CD; Gargaglioni LH; Putnam RW
[Ad] Address:Dept of Animal Morphology and Physiology. São Paulo State University, FCAV, Jaboticabal, SP, Brazil....
[Ti] Title:Anatomical and functional connections between the locus coeruleus and the nucleus tractus solitarius in neonatal rats.
[So] Source:Neuroscience;324:446-68, 2016 Jun 2.
[Is] ISSN:1873-7544
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:This study was designed to investigate brain connections among chemosensitive areas in newborn rats. Rhodamine beads were injected unilaterally into the locus coeruleus (LC) or into the caudal part of the nucleus tractus solitarius (cNTS) in Sprague-Dawley rat pups (P7-P10). Rhodamine-labeled neurons were patched in brainstem slices to study their electrophysiological responses to hypercapnia and to determine if chemosensitive neurons are communicating between LC and cNTS regions. After 7-10days, retrograde labeling was observed in numerous areas of the brainstem, including many chemosensitive regions, such as the contralateral LC, cNTS and medullary raphe. Whole-cell patch clamp was done in cNTS. In 4 of 5 retrogradely labeled cNTS neurons that projected to the LC, firing rate increased in response to hypercapnic acidosis (15% CO2), even in synaptic blockade medium (SNB) (high Mg(2+)/low Ca(2+)). In contrast, 2 of 3 retrogradely labeled LC neurons that projected to cNTS had reduced firing rate in response to hypercapnic acidosis, both in the presence and absence of SNB. Extensive anatomical connections among chemosensitive brainstem regions in newborn rats were found and at least for the LC and cNTS, the connections involve some CO2-sensitive neurons. Such anatomical and functional coupling suggests a complex central respiratory control network, such as seen in adult rats, is already largely present in neonatal rats by at least day P7-P10. Since the NTS and the LC play a major role in memory consolidation, our results may also contribute to the understanding of the development of memory consolidation.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1604
[Cu] Class update date: 160423
[Lr] Last revision date:160423
[Js] Journal subset:IM
[St] Status:In-Data-Review

  8 / 280032 MEDLINE  
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[PMID]: 27082990
[Au] Autor:Deep SN; Baitharu I; Sharma A; Gurjar AK; Prasad D; Singh SB
[Ad] Address:Neurobiology Division, Defence Institute of Physiology and Allied Sciences, Lucknow Road, Timarpur, Delhi- 54, India....
[Ti] Title:Neuroprotective Role of L-NG-Nitroarginine Methyl Ester (L-NAME) against Chronic Hypobaric Hypoxia with Crowding Stress (CHC) Induced Depression-Like Behaviour.
[So] Source:PLoS One;11(4):e0153371, 2016.
[Is] ISSN:1932-6203
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Improper neuroimmune responses following chronic stress exposure have been reported to cause neuronal dysfunctions leading to memory impairment, anxiety and depression like behaviours. Though several factors affecting microglial activation and consequent alteration in neuro-inflammatory responses have been well studied, role of NO and its association with microglia in stress induced depression model is yet to be explored. In the present study, we validated combination of chronic hypobaric hypoxia and crowding (CHC) as a stress model for depression and investigated the role of chronic stress induced elevated nitric oxide (NO) level in microglia activation and its effect on neuro-inflammatory responses in brain. Further, we evaluated the ameliorative effect of L-NG-Nitroarginine Methyl Ester (L-NAME) to reverse the stress induced depressive mood state. Four groups of male Sprague Dawley rat were taken and divided into control and CHC stress exposed group with and without treatment of L-NAME. Depression like behaviour and anhedonia in rats were assessed by Forced Swim Test (FST) and Sucrose Preference Test (SPT). Microglial activation was evaluated using Iba-1 immunohistochemistry and proinflammatory cytokines were assessed in the hippocampal region. Our result showed that exposure to CHC stress increased the number of active microglia with corresponding increase in inflammatory cytokines and altered behavioural responses. The inhibition of NO synthesis by L-NAME during CHC exposure decreased the number of active microglia in hippocampus as evident from decreased Iba-1 positive cells. Further, L-NAME administration decreased pro-inflammatory cytokines in hippocampus and improved behaviour of rats. Our study demonstrate that stress induced elevation of NO plays pivotal role in altered microglial activation and consequent neurodegenerative processes leading to depression like behaviour in rat.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1604
[Cu] Class update date: 160423
[Lr] Last revision date:160423
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1371/journal.pone.0153371

  9 / 280032 MEDLINE  
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[PMID]: 27082629
[Au] Autor:Simons CJ; Bartels-Velthuis AA; Pijnenborg GH; Genetic Risk and Outcome of Psychosis (GROUP) Investigators
[Ad] Address:GGzE, Institute for Mental Health Care Eindhoven and De Kempen, Eindhoven, The Netherlands....
[Ti] Title:Cognitive Performance and Long-Term Social Functioning in Psychotic Disorder: A Three-Year Follow-Up Study.
[So] Source:PLoS One;11(4):e0151299, 2016.
[Is] ISSN:1932-6203
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:OBJECTIVE: Studies have linked cognitive functioning to everyday social functioning in psychotic disorders, but the nature of the relationships between cognition, social cognition, symptoms, and social functioning remains unestablished. Modelling the contributions of non-social and social cognitive ability in the prediction of social functioning may help in more clearly defining therapeutic targets to improve functioning. METHOD: In a sample of 745 patients with a non-affective psychotic disorder, the associations between cognition and social cognition at baseline on the one hand, and self-reported social functioning three years later on the other, were analysed. First, case-control comparisons were conducted; associations were subsequently further explored in patients, investigating the potential mediating role of symptoms. Analyses were repeated in a subsample of 233 patients with recent-onset psychosis. RESULTS: Information processing speed and immediate verbal memory were stronger associated with social functioning in patients than in healthy controls. Most cognition variables significantly predicted social functioning at follow-up, whereas social cognition was not associated with social functioning. Symptoms were robustly associated with follow-up social functioning, with negative symptoms fully mediating most associations between cognition and follow-up social functioning. Illness duration did not moderate the strength of the association between cognitive functioning and follow-up social functioning. No associations were found between (social) cognition and follow-up social functioning in patients with recent-onset psychosis. CONCLUSIONS: Although cognitive functioning is associated with later social functioning in psychotic disorder, its role in explaining social functioning outcome above negative symptoms appears only modest. In recent-onset psychosis, cognition may have a negligible role in predicting later social functioning. Moreover, social cognition tasks may not predict self-reported social functioning.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1604
[Cu] Class update date: 160423
[Lr] Last revision date:160423
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1371/journal.pone.0151299

  10 / 280032 MEDLINE  
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[PMID]: 27078155
[Au] Autor:Zhang Y; Xu C; Zheng H; Loh HH; Law PY
[Ad] Address:Department of Pharmacology, University of Minnesota, 6-120 Jackson Hall, 321 Church St. S.E., Minneapolis, Minnesota 55455-0217, United States of America....
[Ti] Title:Morphine Modulates Adult Neurogenesis and Contextual Memory by Impeding the Maturation of Neural Progenitors.
[So] Source:PLoS One;11(4):e0153628, 2016.
[Is] ISSN:1932-6203
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The regulation of adult neurogenesis by opiates has been implicated in modulating different addiction cycles. At which neurogenesis stage opiates exert their action remains unresolved. We attempt to define the temporal window of morphine's inhibition effect on adult neurogenesis by using the POMC-EGFP mouse model, in which newborn granular cells (GCs) can be visualized between days 3-28 post-mitotic. The POMC-EGFP mice were trained under the 3-chambers conditioned place preference (CPP) paradigm with either saline or morphine. We observed after 4 days of CPP training with saline, the number of EGFP-labeled newborn GCs in sub-granular zone (SGZ) hippocampus significantly increased compared to mice injected with saline in their homecage. CPP training with morphine significantly decreased the number of EGFP-labeled GCs, whereas no significant difference in the number of EGFP-labeled GCs was observed with the homecage mice injected with the same dose of morphine. Using cell-type selective markers, we observed that morphine reduced the number of late stage progenitors and immature neurons such as Doublecortin (DCX) and ßIII Tubulin (TuJ1) positive cells in the SGZ but did not reduce the number of early progenitors such as Nestin, SOX2, or neurogenic differentiation-1 (NeuroD1) positive cells. Analysis of co-localization between different cell markers shows that morphine reduced the number of adult-born GCs by interfering with differentiation of early progenitors, but not by inducing apoptosis. In addition, when NeuroD1 was over-expressed in DG by stereotaxic injection of lentivirus, it rescued the loss of immature neurons and prolonged the extinction of morphine-trained CPP. These results suggest that under the condition of CPP training paradigm, morphine affects the transition of neural progenitor/stem cells to immature neurons via a mechanism involving NeuroD1.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1604
[Cu] Class update date: 160423
[Lr] Last revision date:160423
[Js] Journal subset:IM
[St] Status:In-Data-Review
[do] DOI:10.1371/journal.pone.0153628


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