Now showing 1 - 10 of 16
  • 2016Journal Article
    [["dc.bibliographiccitation.artnumber","315"],["dc.bibliographiccitation.journal","Frontiers in Aging Neuroscience"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Rodriguez-Callejas, Juan D."],["dc.contributor.author","Fuchs, Eberhard"],["dc.contributor.author","Perez-Cruz, Claudia"],["dc.date.accessioned","2019-07-09T11:43:04Z"],["dc.date.available","2019-07-09T11:43:04Z"],["dc.date.issued","2016"],["dc.description.abstract","Common marmosets (Callithrix jacchus) have recently gained popularity in biomedical research as models of aging research. Basically, they confer advantages from other non-human primates due to their shorter lifespan with onset of appearance of aging at 8 years. Old marmosets present some markers linked to neurodegeneration in the brain such as amyloid beta (Ab)1􀀀42 and Ab1􀀀40. However, there are no studies exploring other cellular markers associated with neurodegenerative diseases in this non-human primate. Using immunohistochemistry, we analyzed brains of male adolescent, adult, old, and aged marmosets. We observed accumulation of Ab1 and A in the 􀀀40 b1􀀀42 cortex of aged subjects. Tau hyperphosphorylation was already detected in the brain of adolescent animals and increased with aging in a more fibrillary form. Microglia activation was also observed in the aging process, while a dystrophic phenotype accumulates in aged subjects. Interestingly, dystrophic microglia contained hyperphosphorylated tau, but active microglia did not. These results support previous findings regarding microglia dysfunctionality in aging and neurodegenerative diseases as Alzheimer’s disease. Further studies should explore the functional consequences of these findings to position this non-human primate as animal model of aging and neurodegeneration."],["dc.identifier.doi","10.3389/fnagi.2016.00315"],["dc.identifier.pmid","28066237"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14119"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/58818"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1663-4365"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Evidence of Tau Hyperphosphorylation and Dystrophic Microglia in the Common Marmoset"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]
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  • 2009Journal Article
    [["dc.bibliographiccitation.artnumber","e3659"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","PLoS ONE"],["dc.bibliographiccitation.volume","4"],["dc.contributor.author","Cooper, Ben"],["dc.contributor.author","Fuchs, Eberhard"],["dc.contributor.author","Fluegge, Gabriele"],["dc.date.accessioned","2018-11-07T08:33:25Z"],["dc.date.available","2018-11-07T08:33:25Z"],["dc.date.issued","2009"],["dc.description.abstract","It has been repeatedly shown that chronic stress changes dendrites, spines and modulates expression of synaptic molecules. These effects all may impair information transfer between neurons. The present study shows that chronic stress also regulates expression of M6a, a glycoprotein which is localised in axonal membranes. We have previously demonstrated that M6a is a component of glutamatergic axons. The present data reveal that it is the splice variant M6a-Ib, not M6a-Ia, which is strongly expressed in the brain. Chronic stress in male rats (3 weeks daily restraint) has regional effects: quantitative in situ hybridization demonstrated that M6a-Ib mRNA in dentate gyrus granule neurons and in CA3 pyramidal neurons is downregulated, whereas M6a-Ib mRNA in the medial prefrontal cortex is upregulated by chronic stress. This is the first study showing that expression of an axonal membrane molecule is differentially affected by stress in a region-dependent manner. Therefore, one may speculate that diminished expression of the glycoprotein in the hippocampus leads to altered output in the corresponding cortical projection areas. Enhanced M6a-Ib expression in the medial prefrontal cortex (in areas prelimbic and infralimbic cortex) might be interpreted as a compensatory mechanism in response to changes in axonal projections from the hippocampus. Our findings provide evidence that in addition to alterations in dendrites and spines chronic stress also changes the integrity of axons and may thus impair information transfer even between distant brain regions."],["dc.identifier.doi","10.1371/journal.pone.0003659"],["dc.identifier.isi","000265483100001"],["dc.identifier.pmid","19180239"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/5822"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/17571"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prĂĽfen"],["dc.notes.submitter","Najko"],["dc.publisher","Public Library Science"],["dc.relation.issn","1932-6203"],["dc.rights","CC BY 2.5"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.5"],["dc.title","Expression of the Axonal Membrane Glycoprotein M6a Is Regulated by Chronic Stress"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]
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  • 2014Journal Article
    [["dc.bibliographiccitation.firstpage","31"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Cell and Tissue Research"],["dc.bibliographiccitation.lastpage","41"],["dc.bibliographiccitation.volume","357"],["dc.contributor.author","Fluegge, Gabriele"],["dc.contributor.author","Araya-Callis, Carolina"],["dc.contributor.author","Garea-Rodriguez, Enrique"],["dc.contributor.author","Stadelmann-Nessler, Christine"],["dc.contributor.author","Fuchs, Eberhard"],["dc.date.accessioned","2018-11-07T09:38:14Z"],["dc.date.available","2018-11-07T09:38:14Z"],["dc.date.issued","2014"],["dc.description.abstract","The protein NDRG2 (N-myc downregulated gene 2) is expressed in astrocytes. We show here that NDRG2 is located in the cytosol of protoplasmic and fibrous astrocytes throughout the mammalian brain, including Bergmann glia as observed in mouse, rat, tree shrew, marmoset and human. NDRG2 immunoreactivity is detectable in the astrocytic cell bodies and excrescencies including fine distal processes. Glutamatergic and GABAergic nerve terminals are associated with NDRG2 immunopositive astrocytic processes. Muller glia in the retina displays no NDRG2 immunoreactivity. NDRG2 positive astrocytes are more abundant and more evenly distributed in the brain than GFAP (glial fibrillary acidic protein) immunoreactive cells. Some regions with very little GFAP such as the caudate nucleus show pronounced NDRG2 immunoreactivity. In white matter areas, NDRG2 is less strong than GFAP labeling. Most NDRG2 positive somata are immunoreactive for S100 but not all S100 cells express NDRG2. NDRG2 positive astrocytes do not express nestin and NG2 (chondroitin sulfate proteoglycan 4). The localization of NDRG2 overlaps only partially with that of aquaporin 4, the membrane-bound water channel that is concentrated in the astrocytic endfeet. Reactive astrocytes at a cortical lesion display very little NDRG2, which indicates that expression of the protein is reduced in reactive astrocytes. In conclusion, our data show that NDRG2 is a specific marker for a large population of mature, non-reactive brain astrocytes. Visualization of NDRG2 immunoreactive structures may serve as a reliable tool for quantitative studies on numbers of astrocytes in distinct brain regions and for high-resolution microscopy studies on distal astrocytic processes."],["dc.identifier.doi","10.1007/s00441-014-1837-5"],["dc.identifier.isi","000338759900003"],["dc.identifier.pmid","24816982"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/10233"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/33027"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prĂĽfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","1432-0878"],["dc.relation.issn","0302-766X"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","NDRG2 as a marker protein for brain astrocytes"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]
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  • 2012Journal Article
    [["dc.bibliographiccitation.firstpage","113"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Behavioural Brain Research"],["dc.bibliographiccitation.lastpage","123"],["dc.bibliographiccitation.volume","235"],["dc.contributor.author","Hoffmann, Kerstin"],["dc.contributor.author","Coolen, Alex"],["dc.contributor.author","Schlumbohm, Christina"],["dc.contributor.author","Meerlo, Peter"],["dc.contributor.author","Fuchs, Eberhard"],["dc.date.accessioned","2018-11-07T09:03:09Z"],["dc.date.available","2018-11-07T09:03:09Z"],["dc.date.issued","2012"],["dc.description.abstract","Initial studies in the day active marmoset monkey (Callithrix jacchus) indicate that the sleep-wake cycle of these non-human primates resembles that of humans and therefore conceivably represent an appropriate model for human sleep. The methods currently employed for sleep studies in marmosets are limited. The objective of this study was to employ and validate the use of specific remote monitoring system technologies that enable accurate long-term recordings of sleep-wake rhythms and the closely related rhythms of core body temperature (CBT) and locomotor activity in unrestrained group-housed marmosets. Additionally, a pilot sleep deprivation (SD) study was performed to test the recording systems in an applied experimental setup. Our results show that marmosets typically exhibit a monophasic sleep pattern with cyclical alternations between NREM and REM sleep. CBT displays a pronounced daily rhythm and locomotor activity is primarily restricted to the light phase. SD caused an immediate increase in NREM sleep time and EEG slow-wave activity as well as a delayed REM sleep rebound that did not fully compensate for REM sleep that had been lost during SD. In conclusion, the combination of two innovative technical approaches allows for simultaneous measurements of CBT, sleep cycles and activity in multiple subjects. The employment of these systems represents a significant refinement in terms of animal welfare and will enable many future applications and longitudinal studies of circadian rhythms in marmosets. (C) 2012 Elsevier B.V. All rights reserved."],["dc.identifier.doi","10.1016/j.bbr.2012.07.033"],["dc.identifier.isi","000309801400002"],["dc.identifier.pmid","22850608"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/11319"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/24842"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prĂĽfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.relation.issn","0166-4328"],["dc.rights","CC BY-NC-ND 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-nd/3.0"],["dc.title","Remote long-term registrations of sleep-wake rhythms, core body temperature and activity in marmoset monkeys"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]
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  • 2009Journal Article
    [["dc.bibliographiccitation.firstpage","1115"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Hypertension"],["dc.bibliographiccitation.lastpage","1122"],["dc.bibliographiccitation.volume","54"],["dc.contributor.author","Bramlage, Carsten Paul"],["dc.contributor.author","Schlumbohm, Christina"],["dc.contributor.author","Pryce, Christopher Robert"],["dc.contributor.author","Mirza, Serkan"],["dc.contributor.author","Schnell, Christian"],["dc.contributor.author","Amann, Kerstin"],["dc.contributor.author","Amstrong, Victor William"],["dc.contributor.author","Eitner, Frank"],["dc.contributor.author","Zapf, Antonia"],["dc.contributor.author","Feldon, Joram"],["dc.contributor.author","Oellerich, Michael"],["dc.contributor.author","Fuchs, Eberhard"],["dc.contributor.author","Mueller, Gerhard Anton"],["dc.contributor.author","Strutz, Frank M."],["dc.date.accessioned","2018-11-07T11:22:44Z"],["dc.date.available","2018-11-07T11:22:44Z"],["dc.date.issued","2009"],["dc.description.abstract","The influence of prenatal factors on the development of arterial hypertension has gained considerable interest in recent years. Prenatal dexamethasone exposure was found to induce hypertension and to alter nephron number and size in rodents and sheep. However, it is not clear whether these findings are applicable to nonhuman primates. Thus, we examined the effects of prenatal dexamethasone treatment on blood pressure (BP) and nephron number in marmoset monkeys. Fifty-two marmosets were allotted to 3 groups according to the gestational stage during which their mothers were exposed to oral 5-mg/kg dexamethasone for 7 days (gestation period: 20 weeks): (1) the early dexamethasone group at week 7; (2) the late dexamethasone group at week 13; and (3) the control group. BP was determined by telemetric (n = 12) or cuff measurements (n = 30), along with cystatin C, proteinuria, and body weight. All of the animals were euthanized at the age of 24 months, and glomerular number and volume were determined. Prenatal exposure to dexamethasone did not lead to a significant difference between the groups with regard to BP, kidney morphology and function, or body weight. BP correlated significantly with body weight, relative kidney weight, and mean glomerular volume and the body weight with the glomerular volume regardless of dexamethasone treatment. In conclusion, prenatal exposure to dexamethasone in marmosets does not, in contrast to other mammals studied, result in hypertension or changes in kidney morphology. Our data support the role of body weight as a predictor of elevated glomerular volume and BP development rather than prenatal dexamethasone exposure. (Hypertension. 2009;54:1115-1122.)"],["dc.identifier.doi","10.1161/HYPERTENSIONAHA.109.136580"],["dc.identifier.isi","000270992100031"],["dc.identifier.pmid","19770406"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6183"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/56040"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prĂĽfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.relation.issn","0194-911X"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Prenatal Dexamethasone Exposure Does Not Alter Blood Pressure and Nephron Number in the Young Adult Marmoset Monkey"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]
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  • 2007Journal Article
    [["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.issue","190"],["dc.bibliographiccitation.journal","BMC genomics"],["dc.bibliographiccitation.lastpage","9"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Datson, Nicole A."],["dc.contributor.author","Morsink, Maarten C."],["dc.contributor.author","Atanasova, Srebrena"],["dc.contributor.author","Armstrong, Victor W."],["dc.contributor.author","Zischler, Hans"],["dc.contributor.author","Schlumbohm, Christina"],["dc.contributor.author","Dutilh, Bas E."],["dc.contributor.author","Huynen, Martijn A."],["dc.contributor.author","Waegele, Brigitte"],["dc.contributor.author","Ruepp, Andreas"],["dc.contributor.author","Kloet, E. Ronald"],["dc.contributor.author","Fuchs, Eberhard"],["dc.date.accessioned","2019-07-10T08:13:00Z"],["dc.date.available","2019-07-10T08:13:00Z"],["dc.date.issued","2007"],["dc.description.abstract","Background: The common marmoset monkey (Callithrix jacchus), a small non-endangered New World primate native to eastern Brazil, is becoming increasingly used as a non-human primate model in biomedical research, drug development and safety assessment. In contrast to the growing interest for the marmoset as an animal model, the molecular tools for genetic analysis are extremely limited.Results: Here we report the development of the first marmoset-specific oligonucleotide microarray (EUMAMA) containing probe sets targeting 1541 different marmoset transcripts expressed in hippocampus. These 1541 transcripts represent a wide variety of different functional gene classes. Hybridisation of the marmoset microarray with labelled RNA from hippocampus, cortex and a panel of 7 different peripheral tissues resulted in high detection rates of 85% in the neuronal tissues and on average 70% in the non-neuronal tissues. The expression profiles of the 2 neuronal tissues, hippocampus and cortex, were highly similar, as indicated by a correlation coefficient of 0.96. Several transcripts with a tissue-specific pattern of expression were identified. Besides the marmoset microarray we have generated 3215 ESTs derived from marmoset hippocampus, which have been annotated and submitted to GenBank [GenBank: EF214838 EF215447, EH380242 EH382846]. Conclusion: We have generated the first marmoset-specific DNA microarray and demonstrated its use to characterise large-scale gene expression profiles of hippocampus but also of other neuronal and non-neuronal tissues. In addition, we have generated a large collection of ESTs of marmoset origin, which are now available in the public domain. These new tools will facilitate molecular genetic research into this non-human primate animal model."],["dc.identifier.fs","91281"],["dc.identifier.ppn","560256167"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/4367"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/61097"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.orgunit","Universitätsmedizin Göttingen"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.subject.ddc","610"],["dc.title","Development of the first marmoset-specific DNA microarray (EUMAMA): a new genetic tool for large-scale expression profiling in a non-human primate"],["dc.title.alternative","Research article"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]
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  • 2012Journal Article
    [["dc.bibliographiccitation.artnumber","e43709"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","PLoS ONE"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Seehase, Sophie"],["dc.contributor.author","Lauenstein, Hans-Dieter"],["dc.contributor.author","Schlumbohm, Christina"],["dc.contributor.author","Switalla, Simone"],["dc.contributor.author","Neuhaus, Vanessa"],["dc.contributor.author","Förster, Christine"],["dc.contributor.author","Fieguth, Hans-Gerd"],["dc.contributor.author","Pfennig, Olaf"],["dc.contributor.author","Fuchs, Eberhard"],["dc.contributor.author","Kaup, Franz-Josef"],["dc.contributor.author","Bleyer, Martina"],["dc.contributor.author","Hohlfeld, Jens M."],["dc.contributor.author","Braun, Armin"],["dc.contributor.author","Sewald, Katherina"],["dc.contributor.author","Knauf, Sascha"],["dc.date.accessioned","2019-07-09T11:53:43Z"],["dc.date.available","2019-07-09T11:53:43Z"],["dc.date.issued","2012"],["dc.description.abstract","Increasing incidence and substantial morbidity and mortality of respiratory diseases requires the development of new human-specific anti-inflammatory and disease-modifying therapeutics. Therefore, new predictive animal models that closely reflect human lung pathology are needed. In the current study, a tiered acute lipopolysaccharide (LPS)-induced inflammation model was established in marmoset monkeys (Callithrix jacchus) to reflect crucial features of inflammatory lung diseases. Firstly, in an ex vivo approach marmoset and, for the purposes of comparison, human precision-cut lung slices (PCLS) were stimulated with LPS in the presence or absence of the phosphodiesterase-4 (PDE4) inhibitor roflumilast. Proinflammatory cytokines including tumor necrosis factor-alpha (TNF-a) and macrophage inflammatory protein-1 beta (MIP- 1b) were measured. The corticosteroid dexamethasone was used as treatment control. Secondly, in an in vivo approach marmosets were pre-treated with roflumilast or dexamethasone and unilaterally challenged with LPS. Ipsilateral bronchoalveolar lavage (BAL) was conducted 18 hours after LPS challenge. BAL fluid was processed and analyzed for neutrophils, TNF-a, and MIP-1b. TNF-a release in marmoset PCLS correlated significantly with human PCLS. Roflumilast treatment significantly reduced TNF-a secretion ex vivo in both species, with comparable half maximal inhibitory concentration (IC50). LPS instillation into marmoset lungs caused a profound inflammation as shown by neutrophilic influx and increased TNF-a and MIP-1b levels in BAL fluid. This inflammatory response was significantly suppressed by roflumilast and dexamethasone. The close similarity of marmoset and human lungs regarding LPS-induced inflammation and the significant anti-inflammatory effect of approved pharmaceuticals assess the suitability of marmoset monkeys to serve as a promising model for studying anti-inflammatory drugs."],["dc.identifier.doi","10.1371/journal.pone.0043709"],["dc.identifier.fs","593143"],["dc.identifier.pmid","22952743"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/7903"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/60479"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.rights","CC BY 2.5"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.5"],["dc.title","LPS-Induced Lung Inflammation in Marmoset Monkeys – An Acute Model for Anti-Inflammatory Drug Testing"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]
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  • 2007Journal Article
    [["dc.bibliographiccitation.artnumber","46276"],["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.journal","Neural plasticity"],["dc.bibliographiccitation.lastpage","14"],["dc.contributor.author","Perez-Cruz, Claudia"],["dc.contributor.author","MĂĽller-Keuker, Jeanine I. H."],["dc.contributor.author","Heilbronner, Urs"],["dc.contributor.author","Fuchs, Eberhard"],["dc.contributor.author","FlĂĽgge, Gabriele"],["dc.date.accessioned","2019-07-09T11:52:28Z"],["dc.date.available","2019-07-09T11:52:28Z"],["dc.date.issued","2007"],["dc.description.abstract","The prefrontal cortex (PFC) plays an important role in the stress response. We filled pyramidal neurons in PFC layer III with neurobiotin and analyzed dendrites in rats submitted to chronic restraint stress and in controls. In the right prelimbic cortex (PL) of controls, apical and distal dendrites were longer than in the left PL. Stress reduced the total length of apical dendrites in right PL and abolished the hemispheric difference. In right infralimbic cortex (IL) of controls, proximal apical dendrites were longer than in left IL, and stress eliminated this hemispheric difference. No hemispheric difference was detected in anterior cingulate cortex (ACx) of controls, but stress reduced apical dendritic length in left ACx. These data demonstrate interhemispheric differences in the morphology of pyramidal neurons in PL and IL of control rats and selective effects of stress on the right hemisphere. In contrast, stress reduced dendritic length in the left ACx."],["dc.identifier.doi","10.1155/2007/46276"],["dc.identifier.fs","207216"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/4359"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/60197"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1687-5443"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.subject.ddc","610"],["dc.subject.ddc","599.8"],["dc.title","Morphology of Pyramidal Neurons in the Rat Prefrontal Cortex: Lateralized Dendritic Remodeling by Chronic Stress"],["dc.title.alternative","Research Article"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]
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  • 2017Journal Article
    [["dc.bibliographiccitation.firstpage","15"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Acta Neuropathologica"],["dc.bibliographiccitation.lastpage","34"],["dc.bibliographiccitation.volume","134"],["dc.contributor.author","Lagumersindez-Denis, Nielsen"],["dc.contributor.author","Wrzos, Claudia"],["dc.contributor.author","Mack, Matthias"],["dc.contributor.author","Winkler, Anne"],["dc.contributor.author","van der Meer, Franziska"],["dc.contributor.author","Reinert, Marie-Christine"],["dc.contributor.author","Hollasch, Heiko"],["dc.contributor.author","Flach, Anne"],["dc.contributor.author","Bruehl, Hilke"],["dc.contributor.author","Cullen, Eilish"],["dc.contributor.author","Schlumbohm, Christina"],["dc.contributor.author","Fuchs, Eberhard"],["dc.contributor.author","Linington, Christopher"],["dc.contributor.author","Barrantes-Freer, Alonso"],["dc.contributor.author","Metz, Imke"],["dc.contributor.author","Wegner, Christiane"],["dc.contributor.author","Liebetanz, David"],["dc.contributor.author","Prinz, Marco R."],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Nessler, Stefan"],["dc.date.accessioned","2018-11-07T10:22:07Z"],["dc.date.available","2018-11-07T10:22:07Z"],["dc.date.issued","2017"],["dc.description.abstract","Cortical demyelination is a widely recognized hallmark of multiple sclerosis (MS) and correlate of disease progression and cognitive decline. The pathomechanisms initiating and driving gray matter damage are only incompletely understood. Here, we determined the infiltrating leukocyte subpopulations in 26 cortical demyelinated lesions of biopsied MS patients and assessed their contribution to cortical lesion formation in a newly developed mouse model. We find that conformation-specific anti-myelin antibodies contribute to cortical demyelination even in the absence of the classical complement pathway. T cells and natural killer cells are relevant for intracortical type 2 but dispensable for subpial type 3 lesions, whereas CCR2(+) monocytes are required for both. Depleting CCR2(+) monocytes in marmoset monkeys with experimental autoimmune encephalomyelitis using a novel humanized CCR2 targeting antibody translates into significantly less cortical demyelination and disease severity. We conclude that biologics depleting CCR2(+) monocytes might be attractive candidates for preventing cortical lesion formation and ameliorating disease progression in MS."],["dc.identifier.doi","10.1007/s00401-017-1706-x"],["dc.identifier.isi","000403235900002"],["dc.identifier.pmid","28386765"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14713"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/42218"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prĂĽfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Springer"],["dc.relation.issn","1432-0533"],["dc.relation.issn","0001-6322"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Differential contribution of immune effector mechanisms to cortical demyelination in multiple sclerosis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]
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  • 2012Journal Article
    [["dc.bibliographiccitation.firstpage","97"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Cytogenetic and Genome Research"],["dc.bibliographiccitation.lastpage","106"],["dc.bibliographiccitation.volume","136"],["dc.contributor.author","Schneider, E."],["dc.contributor.author","Jensen, L. R."],["dc.contributor.author","Farcas, R."],["dc.contributor.author","Kondova, I."],["dc.contributor.author","Bontrop, R. E."],["dc.contributor.author","Navarro, B."],["dc.contributor.author","Fuchs, E."],["dc.contributor.author","Kuss, A. W."],["dc.contributor.author","Haaf, T."],["dc.date.accessioned","2019-07-09T11:54:38Z"],["dc.date.available","2019-07-09T11:54:38Z"],["dc.date.issued","2012"],["dc.description.abstract","The human brain is distinguished by its remarkable size, high energy consumption, and cognitive abilities compared to all other mammals and non-human primates. However, little is known about what has accelerated brain evolution in the human lineage. One possible explanation is that the appearance of advanced communication skills and language has been a driving force of human brain development. The phenotypic adaptations in brain structure and function which occurred on the way to modern humans may be associated with specific molecular signatures in today’s human genome and/or transcriptome. Genes that have been linked to language, reading, and/or autism spectrum disorders are prime candidates when searching for genes for human-specific communication abilities. The database and genome-wide expression analyses we present here revealed a clustering of such communication-associated genes (COAG) on human chromosomes X and 7, in particular chromosome 7q31-q36. Compared to the rest of the genome, we found a high number of COAG to be differentially expressed in the cortices of humans and non-human primates (chimpanzee, baboon, and/or marmoset). The role of X-linked genes for the development of human-specific cognitive abilities is well known. We now propose that chromosome 7q31-q36 also represents a hot spot for the evolution of human-specific communication abilities. Selective pressure on the T cell receptor beta locus on chromosome 7q34, which plays a pivotal role in the immune system, could have led to rapid dissemination of positive gene variants in hitchhiking COAG."],["dc.format.extent","10"],["dc.identifier.doi","10.1159/000335465"],["dc.identifier.fs","593150"],["dc.identifier.pmid","22261840"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/9488"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/60698"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1424-859X"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","A High Density of Human Communication-Associated Genes in Chromosome 7q31-q36: Differential Expression in Human and Non-Human Primate Cortices"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]
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