Ferreira, Diana Gabriela

[["dc.bibliographiccitation.firstpage","1876"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Molecular Psychiatry"],["dc.bibliographiccitation.lastpage","1900"],["dc.bibliographiccitation.volume","25"],["dc.contributor.author","Temido-Ferreira, Mariana"],["dc.contributor.author","Ferreira, Diana G."],["dc.contributor.author","Batalha, Vânia L."],["dc.contributor.author","Marques-Morgado, Inês"],["dc.contributor.author","Coelho, Joana E."],["dc.contributor.author","Pereira, Pedro"],["dc.contributor.author","Gomes, Rui"],["dc.contributor.author","Pinto, Andreia"],["dc.contributor.author","Carvalho, Sara"],["dc.contributor.author","Canas, Paula M."],["dc.contributor.author","Cuvelier, Laetitia"],["dc.contributor.author","Buée-Scherrer, Valerie"],["dc.contributor.author","Faivre, Emilie"],["dc.contributor.author","Baqi, Younis"],["dc.contributor.author","Müller, Christa E."],["dc.contributor.author","Pimentel, José"],["dc.contributor.author","Schiffmann, Serge N."],["dc.contributor.author","Buée, Luc"],["dc.contributor.author","Bader, Michael"],["dc.contributor.author","Outeiro, Tiago F."],["dc.contributor.author","Blum, David"],["dc.contributor.author","Cunha, Rodrigo A."],["dc.contributor.author","Marie, Hélène"],["dc.contributor.author","Pousinha, Paula A."],["dc.contributor.author","Lopes, Luísa V."],["dc.date.accessioned","2021-04-14T08:24:30Z"],["dc.date.available","2021-04-14T08:24:30Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1038/s41380-018-0110-9"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15577"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/81305"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.notes.intern","Merged from goescholar"],["dc.relation.eissn","1476-5578"],["dc.relation.issn","1359-4184"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Age-related shift in LTD is dependent on neuronal adenosine A2A receptors interplay with mGluR5 and NMDA receptors"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1399"],["dc.bibliographiccitation.journal","Brain"],["dc.bibliographiccitation.lastpage","1419"],["dc.bibliographiccitation.volume","140"],["dc.contributor.author","Miranda, Hugo Vicente"],["dc.contributor.author","Szego, Eva M."],["dc.contributor.author","Oliveira, Luis M. A."],["dc.contributor.author","Breda, Carlo"],["dc.contributor.author","Darendelioglu, Ekrem"],["dc.contributor.author","de Oliveira, Rita Machado"],["dc.contributor.author","Ferreira, Diana G."],["dc.contributor.author","Gomes, Marcos Antonio"],["dc.contributor.author","Rott, Ruth"],["dc.contributor.author","Oliveira, Marcia"],["dc.contributor.author","Munari, Francesca"],["dc.contributor.author","Enguita, Francisco Javier"],["dc.contributor.author","Simoes, Tania"],["dc.contributor.author","Rodrigues, Eva F."],["dc.contributor.author","Heinrich, Michael"],["dc.contributor.author","Martins, Ivo C."],["dc.contributor.author","Zamolo, Irina"],["dc.contributor.author","Riess, Olaf"],["dc.contributor.author","Cordeiro, Carlos"],["dc.contributor.author","Ponces-Freire, Ana"],["dc.contributor.author","Lashuel, Hilal Ahmed"],["dc.contributor.author","Santos, Nuno C."],["dc.contributor.author","Lopes, Luisa Vaqueiro"],["dc.contributor.author","Xiang, Wei"],["dc.contributor.author","Jovin, Thomas M."],["dc.contributor.author","Penque, Deborah"],["dc.contributor.author","Engelender, Simone"],["dc.contributor.author","Zweckstetter, Markus"],["dc.contributor.author","Klucken, Jochen"],["dc.contributor.author","Giorgini, Flaviano"],["dc.contributor.author","Quintas, Alexandre"],["dc.contributor.author","Outeiro, Tiago Fleming"],["dc.date.accessioned","2018-11-07T10:24:40Z"],["dc.date.available","2018-11-07T10:24:40Z"],["dc.date.issued","2017"],["dc.description.abstract","alpha-Synuclein misfolding and aggregation is a hallmark in Parkinson's disease and in several other neurodegenerative diseases known as synucleinopathies. The toxic properties of alpha-synuclein are conserved from yeast to man, but the precise underpinnings of the cellular pathologies associated are still elusive, complicating the development of effective therapeutic strategies. Combining molecular genetics with target-based approaches, we established that glycation, an unavoidable age-associated post-translational modification, enhanced alpha-synuclein toxicity in vitro and in vivo, in Drosophila and in mice. Glycation affected primarily the N-terminal region of alpha-synuclein, reducing membrane binding, impaired the clearance of alpha-synuclein, and promoted the accumulation of toxic oligomers that impaired neuronal synaptic transmission. Strikingly, using glycation inhibitors, we demonstrated that normal clearance of alpha-synuclein was re-established, aggregation was reduced, and motor phenotypes in Drosophila were alleviated. Altogether, our study demonstrates glycation constitutes a novel drug target that can be explored in synucleinopathies as well as in other neurodegenerative conditions."],["dc.identifier.doi","10.1093/brain/awx056"],["dc.identifier.isi","000400069900026"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/42703"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Oxford Univ Press"],["dc.relation.haserratum","/handle/2/103764"],["dc.relation.issn","1460-2156"],["dc.relation.issn","0006-8950"],["dc.title","Glycation potentiates alpha-synuclein-associated neurodegeneration in synucleinopathies"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","e58"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Brain"],["dc.bibliographiccitation.lastpage","e58"],["dc.bibliographiccitation.volume","144"],["dc.contributor.author","Miranda, Hugo Vicente"],["dc.contributor.author","Szegő, Éva M."],["dc.contributor.author","Oliveira, Luís M. A."],["dc.contributor.author","Breda, Carlo"],["dc.contributor.author","Darendelioglu, Ekrem"],["dc.contributor.author","de Oliveira, Rita M."],["dc.contributor.author","Ferreira, Diana G."],["dc.contributor.author","Gomes, Marcos A."],["dc.contributor.author","Rott, Ruth"],["dc.contributor.author","Oliveira, Márcia"],["dc.contributor.author","Outeiro, Tiago Fleming"],["dc.date.accessioned","2022-03-01T11:46:42Z"],["dc.date.available","2022-03-01T11:46:42Z"],["dc.date.issued","2021"],["dc.identifier.doi","10.1093/brain/awab175"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/103764"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-531"],["dc.relation.eissn","1460-2156"],["dc.relation.iserratumof","/handle/2/42703"],["dc.relation.issn","0006-8950"],["dc.title","Erratum to: Glycation potentiates α-synuclein-associated neurodegeneration in synucleinopathies"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.subtype","erratum_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","718"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Cerebral Cortex"],["dc.bibliographiccitation.lastpage","730"],["dc.bibliographiccitation.volume","27"],["dc.contributor.author","Ferreira, Diana G."],["dc.contributor.author","Batalha, Vania L."],["dc.contributor.author","Vicente Miranda, Hugo"],["dc.contributor.author","Coelho, Joana E."],["dc.contributor.author","Gomes, Rui"],["dc.contributor.author","Goncalves, Francisco Q."],["dc.contributor.author","Real, Joana I."],["dc.contributor.author","Rino, Jose"],["dc.contributor.author","Albino-Teixeira, Antonio"],["dc.contributor.author","Cunha, Rodrigo A."],["dc.contributor.author","Outeiro, Tiago Fleming"],["dc.contributor.author","Lopes, Luisa Vaqueiro"],["dc.date.accessioned","2018-11-07T10:28:45Z"],["dc.date.available","2018-11-07T10:28:45Z"],["dc.date.issued","2017"],["dc.description.abstract","Abnormal accumulation of aggregated alpha-synuclein (aSyn) is a hallmark of sporadic and familial Parkinson's disease (PD) and related synucleinopathies. Recent studies suggest a neuroprotective role of adenosine A(2A) receptor (A(2A)R) antagonists in PD. Nevertheless, the precise molecular mechanisms underlying this neuroprotection remain unclear. We assessed the impact of A(2A)R blockade or genetic deletion (A(2A)R KO) on synaptic plasticity and neuronal cell death induced by aSyn oligomers. We found that impairment of LTP associated with aSyn exposurewas rescued in A(2A)R KO mice or upon A(2A)R blockade, through an NMDA receptor-dependent mechanism. The mechanisms underlying these effects were evaluated in SH-SY5Y cells overexpressing aSyn and rat primary neuronal cultures exposed to aSyn. Cell death in both conditions was prevented by selective A(2A)R antagonists. Interestingly, blockade of these receptors did not interfere with aSyn oligomerization but, instead, reduced the percentage of cells displaying aSyn inclusions. Altogether, our data raise the possibility that the well-documented effects of A(2A)R antagonists involve the control of the latter stages of aSyn aggregation, thereby preventing the associated neurotoxicity. These findings suggest that A(2A)R represent an important target for the development of effective drugs for the treatment of PD and related synucleinopathies."],["dc.identifier.doi","10.1093/cercor/bhv268"],["dc.identifier.isi","000397064800058"],["dc.identifier.pmid","26534909"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/43496"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Oxford Univ Press Inc"],["dc.relation.issn","1460-2199"],["dc.relation.issn","1047-3211"],["dc.title","Adenosine A(2A) Receptors Modulate alpha-Synuclein Aggregation and Toxicity"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1569"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Nature Neuroscience"],["dc.bibliographiccitation.lastpage","1579"],["dc.bibliographiccitation.volume","20"],["dc.contributor.author","Ferreira, Diana G"],["dc.contributor.author","Temido-Ferreira, Mariana"],["dc.contributor.author","Vicente Miranda, Hugo"],["dc.contributor.author","Batalha, Vânia L"],["dc.contributor.author","Coelho, Joana E"],["dc.contributor.author","Szegö, Éva M"],["dc.contributor.author","Marques-Morgado, Inês"],["dc.contributor.author","Vaz, Sandra H"],["dc.contributor.author","Rhee, Jeong Seop"],["dc.contributor.author","Schmitz, Matthias"],["dc.contributor.author","Zerr, Inga"],["dc.contributor.author","Lopes, Luísa V"],["dc.contributor.author","Outeiro, Tiago F"],["dc.date.accessioned","2020-12-10T18:09:32Z"],["dc.date.available","2020-12-10T18:09:32Z"],["dc.date.issued","2017"],["dc.identifier.doi","10.1038/nn.4648"],["dc.identifier.eissn","1546-1726"],["dc.identifier.issn","1097-6256"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/73681"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","α-synuclein interacts with PrPC to induce cognitive impairment through mGluR5 and NMDAR2B"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","31493"],["dc.bibliographiccitation.journal","Scientific Reports"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Batalha, Vania L."],["dc.contributor.author","Ferreira, Diana G."],["dc.contributor.author","Coelho, Joana E."],["dc.contributor.author","Valadas, Jorge S."],["dc.contributor.author","Gomes, Rui"],["dc.contributor.author","Temido-Ferreira, Mariana"],["dc.contributor.author","Shmidt, Tatiana"],["dc.contributor.author","Baqi, Younis"],["dc.contributor.author","Buée, Luc"],["dc.contributor.author","Mueller, Christa E."],["dc.contributor.author","Hamdane, Malika"],["dc.contributor.author","Outeiro, Tiago Fleming"],["dc.contributor.author","Bader, Michael"],["dc.contributor.author","Meijsing, Sebastiaan H."],["dc.contributor.author","Sadri-Vakili, Ghazaleh"],["dc.contributor.author","Blum, David"],["dc.contributor.author","Lopes, Luisa Vaqueiro"],["dc.date.accessioned","2018-11-07T10:10:14Z"],["dc.date.available","2018-11-07T10:10:14Z"],["dc.date.issued","2016"],["dc.description.abstract","Caffeine is associated with procognitive effects in humans by counteracting overactivation of the adenosine A(2A) receptor (A(2A)R), which is upregulated in the human forebrain of aged and Alzheimer's disease (AD) patients. We have previously shown that an anti-A(2A)R therapy reverts age-like memory deficits, by reestablishment of the hypothalamic-pituitary-adrenal (HPA) axis feedback and corticosterone circadian levels. These observations suggest that A(2A)R over-activation and glucocorticoid dysfunction are key events in age-related hippocampal deficits; but their direct connection has never been explored. We now show that inducing A(2A)R overexpression in an aging-like profile is sufficient to trigger HPA-axis dysfunction, namely loss of plasmatic corticosterone circadian oscillation, and promotes reduction of GR hippocampal levels. The synaptic plasticity and memory deficits triggered by finally, we demonstrate that A(2A)R act on GR nuclear translocation and GR-dependent transcriptional regulation. We provide the first demonstration that A(2A)R is a major regulator of GR function and that this functional interconnection may be a trigger to age-related memory deficits. This supports the idea that the procognitive effects of A(2A)R antagonists, namely caffeine, on Alzheimer's and age-related cognitive impairments may rely on its ability to modulate GR actions."],["dc.identifier.doi","10.1038/srep31493"],["dc.identifier.isi","000381189100001"],["dc.identifier.pmid","27510168"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13682"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/39814"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.relation.issn","2045-2322"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","The caffeine-binding adenosine A(2A) receptor induces age-like HPA-axis dysfunction by targeting glucocorticoid receptor function"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]