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  1. AU="Luchena, Celia"
  2. AU="Jessica Martin"
  3. AU=Quesada Victor
  4. AU="Ting-Ann Wang"
  5. AU="Bancroft, Gregory J"
  6. AU="Michalkova, Hana"
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  1. Article ; Online: A nonlinear meccano for Alzheimer's emergence by amyloid β-mediated glutamatergic hyperactivity.

    Bonifazi, Giulio / Luchena, Celia / Gaminde-Blasco, Adhara / Ortiz-Sanz, Carolina / Capetillo-Zarate, Estibaliz / Matute, Carlos / Alberdi, Elena / De Pittà, Maurizio

    Neurobiology of disease

    2024  Volume 194, Page(s) 106473

    Abstract: The pathophysiological process of Alzheimer's disease (AD) is believed to begin many years before the formal diagnosis of AD dementia. This protracted preclinical phase offers a crucial window for potential therapeutic interventions, yet its ... ...

    Abstract The pathophysiological process of Alzheimer's disease (AD) is believed to begin many years before the formal diagnosis of AD dementia. This protracted preclinical phase offers a crucial window for potential therapeutic interventions, yet its comprehensive characterization remains elusive. Accumulating evidence suggests that amyloid-β (Aβ) may mediate neuronal hyperactivity in circuit dysfunction in the early stages of AD. At the same time, neural activity can also facilitate Aβ accumulation through intricate feed-forward interactions, complicating elucidating the conditions governing Aβ-dependent hyperactivity and its diagnostic utility. In this study, we use biophysical modeling to shed light on such conditions. Our analysis reveals that the inherently nonlinear nature of the underlying molecular interactions can give rise to the emergence of various modes of hyperactivity. This diversity in the mechanisms of hyperactivity may ultimately account for a spectrum of AD manifestations.
    MeSH term(s) Humans ; Amyloid beta-Peptides ; Alzheimer Disease ; Neurons/physiology ; Cell Communication
    Chemical Substances Amyloid beta-Peptides
    Language English
    Publishing date 2024-03-15
    Publishing country United States
    Document type Journal Article
    ZDB-ID 1211786-9
    ISSN 1095-953X ; 0969-9961
    ISSN (online) 1095-953X
    ISSN 0969-9961
    DOI 10.1016/j.nbd.2024.106473
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 4444: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

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  2. Article: A Neuron, Microglia, and Astrocyte Triple Co-culture Model to Study Alzheimer's Disease.

    Luchena, Celia / Zuazo-Ibarra, Jone / Valero, Jorge / Matute, Carlos / Alberdi, Elena / Capetillo-Zarate, Estibaliz

    Frontiers in aging neuroscience

    2022  Volume 14, Page(s) 844534

    Abstract: Glial cells are essential to understand Alzheimer's disease (AD) progression, given their role in neuroinflammation and neurodegeneration. There is a need for reliable and easy to manipulate models that allow studying the mechanisms behind neuron and ... ...

    Abstract Glial cells are essential to understand Alzheimer's disease (AD) progression, given their role in neuroinflammation and neurodegeneration. There is a need for reliable and easy to manipulate models that allow studying the mechanisms behind neuron and glia communication. Currently available models such as co-cultures require complex methodologies and/or might not be affordable for all laboratories. With this in mind, we aimed to establish a straightforward
    Language English
    Publishing date 2022-04-14
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2558898-9
    ISSN 1663-4365
    ISSN 1663-4365
    DOI 10.3389/fnagi.2022.844534
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Sephin1 Protects Neurons against Excitotoxicity Independently of the Integrated Stress Response.

    Ruiz, Asier / Zuazo, Jone / Ortiz-Sanz, Carolina / Luchena, Celia / Matute, Carlos / Alberdi, Elena

    International journal of molecular sciences

    2020  Volume 21, Issue 17

    Abstract: Sephin1 is a derivative of guanabenz that inhibits the dephosphorylation of the eukaryotic initiation factor 2 alpha (eIF2α) and therefore may enhance the integrated stress response (ISR), an adaptive mechanism against different cellular stresses, such ... ...

    Abstract Sephin1 is a derivative of guanabenz that inhibits the dephosphorylation of the eukaryotic initiation factor 2 alpha (eIF2α) and therefore may enhance the integrated stress response (ISR), an adaptive mechanism against different cellular stresses, such as accumulation of misfolded proteins. Unlike guanabenz, Sephin1 provides neuroprotection without adverse effects on the α2-adrenergic system and therefore it is considered a promising pharmacological therapeutic tool. Here, we have studied the effects of Sephin1 on N-methyl-D-aspartic acid (NMDA) receptor signaling which may modulate the ISR and contribute to excitotoxic neuronal loss in several neurodegenerative conditions. Time-course analysis of peIF2α levels after NMDA receptor overactivation showed a delayed dephosphorylation that occurred in the absence of activating transcription factor 4 (ATF4) and therefore independently of the ISR, in contrast to that observed during endoplasmic reticulum (ER) stress induced by tunicamycin and thapsigargin. Similar to guanabenz, Sephin1 completely blocked NMDA-induced neuronal death and was ineffective against AMPA-induced excitotoxicity, whereas it did not protect from experimental ER stress. Interestingly, both guanabenz and Sephin1 partially but significantly reduced NMDA-induced cytosolic Ca
    MeSH term(s) Animals ; Calcium/metabolism ; Cells, Cultured ; Cytoprotection/drug effects ; Embryo, Mammalian ; Endoplasmic Reticulum Stress/drug effects ; Guanabenz/analogs & derivatives ; Guanabenz/pharmacology ; N-Methylaspartate/metabolism ; N-Methylaspartate/pharmacology ; Neurons/drug effects ; Neurons/metabolism ; Neurons/physiology ; Neuroprotective Agents/pharmacology ; Neurotoxicity Syndromes/metabolism ; Neurotoxicity Syndromes/pathology ; Rats ; Rats, Sprague-Dawley ; Signal Transduction/drug effects ; Stress, Physiological/drug effects
    Chemical Substances Neuroprotective Agents ; N-Methylaspartate (6384-92-5) ; sephin1 (9M998304JB) ; Guanabenz (GGD30112WC) ; Calcium (SY7Q814VUP)
    Language English
    Publishing date 2020-08-24
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms21176088
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Corrigendum to "Contribution of Neurons and Glial Cells to Complement-Mediated Synapse Removal during Development, Aging and in Alzheimer's Disease".

    Luchena, Celia / Zuazo-Ibarra, Jone / Alberdi, Elena / Matute, Carlos / Capetillo-Zarate, Estibaliz

    Mediators of inflammation

    2019  Volume 2019, Page(s) 7539620

    Abstract: This corrects the article DOI: 10.1155/2018/2530414.]. ...

    Abstract [This corrects the article DOI: 10.1155/2018/2530414.].
    Language English
    Publishing date 2019-01-29
    Publishing country United States
    Document type Published Erratum
    ZDB-ID 1137605-3
    ISSN 1466-1861 ; 0962-9351
    ISSN (online) 1466-1861
    ISSN 0962-9351
    DOI 10.1155/2019/7539620
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 3575: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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    Jg. 1995 - 2021: Lesesall (2.OG)
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  5. Article ; Online: Amyloid β / PKC-dependent alterations in NMDA receptor composition are detected in early stages of Alzheimer´s disease.

    Ortiz-Sanz, Carolina / Balantzategi, Uxue / Quintela-López, Tania / Ruiz, Asier / Luchena, Celia / Zuazo-Ibarra, Jone / Capetillo-Zarate, Estibaliz / Matute, Carlos / Zugaza, José L / Alberdi, Elena

    Cell death & disease

    2022  Volume 13, Issue 3, Page(s) 253

    Abstract: Amyloid beta (Aβ)-mediated synapse dysfunction is an early event in Alzheimer's disease (AD) pathogenesis and previous studies suggest that NMDA receptor (NMDAR) dysregulation may contribute to these pathological effects. Although Aβ peptides impair ... ...

    Abstract Amyloid beta (Aβ)-mediated synapse dysfunction is an early event in Alzheimer's disease (AD) pathogenesis and previous studies suggest that NMDA receptor (NMDAR) dysregulation may contribute to these pathological effects. Although Aβ peptides impair NMDAR expression and activity, the mechanisms mediating these alterations in the early stages of AD are unclear. Here, we observed that NMDAR subunit NR2B and PSD-95 levels were aberrantly upregulated and correlated with Aβ
    MeSH term(s) Alzheimer Disease/metabolism ; Amyloid beta-Peptides/metabolism ; Animals ; Hippocampus/metabolism ; Humans ; Integrin beta1/metabolism ; Mice ; N-Methylaspartate ; Protein Kinase C/metabolism ; Receptors, N-Methyl-D-Aspartate/metabolism ; Synapses/metabolism
    Chemical Substances Amyloid beta-Peptides ; Integrin beta1 ; Receptors, N-Methyl-D-Aspartate ; N-Methylaspartate (6384-92-5) ; Protein Kinase C (EC 2.7.11.13)
    Language English
    Publishing date 2022-03-19
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2541626-1
    ISSN 2041-4889 ; 2041-4889
    ISSN (online) 2041-4889
    ISSN 2041-4889
    DOI 10.1038/s41419-022-04687-y
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Contribution of Neurons and Glial Cells to Complement-Mediated Synapse Removal during Development, Aging and in Alzheimer's Disease.

    Luchena, Celia / Zuazo-Ibarra, Jone / Alberdi, Elena / Matute, Carlos / Capetillo-Zarate, Estibaliz

    Mediators of inflammation

    2018  Volume 2018, Page(s) 2530414

    Abstract: Synapse loss is an early manifestation of pathology in Alzheimer's disease (AD) and is currently the best correlate to cognitive decline. Microglial cells are involved in synapse pruning during development via the complement pathway. Moreover, recent ... ...

    Abstract Synapse loss is an early manifestation of pathology in Alzheimer's disease (AD) and is currently the best correlate to cognitive decline. Microglial cells are involved in synapse pruning during development via the complement pathway. Moreover, recent evidence points towards a key role played by glial cells in synapse loss during AD. However, further contribution of glial cells and the role of neurons to synapse pathology in AD remain not well understood. This review is aimed at comprehensively reporting the source and/or cellular localization in the CNS-in microglia, astrocytes, or neurons-of the triggering components (C1q, C3) of the classical complement pathway involved in synapse pruning in development, adulthood, and AD.
    MeSH term(s) Aging/physiology ; Alzheimer Disease/metabolism ; Animals ; Astrocytes/cytology ; Astrocytes/metabolism ; Humans ; Microglia/metabolism ; Neuroglia/metabolism ; Neurons/cytology ; Neurons/metabolism ; Synapses/metabolism
    Language English
    Publishing date 2018-11-11
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 1137605-3
    ISSN 1466-1861 ; 0962-9351
    ISSN (online) 1466-1861
    ISSN 0962-9351
    DOI 10.1155/2018/2530414
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Kategorien

    In stock of ZB MED Cologne/Königswinter

    Zs.A 3575: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

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