Academic Journal

Adult Neural Stem Cell Migration Is Impaired in a Mouse Model of Alzheimer's Disease

التفاصيل البيبلوغرافية
العنوان: Adult Neural Stem Cell Migration Is Impaired in a Mouse Model of Alzheimer's Disease
المؤلفون: Esteve, Daniel, Molina-Navarro, María Micaela, Giraldo-Reboloso, Esther, Martínez-Varea, Noelia, Blanco-Gandia, Mari Carmen, Rodríguez-Arias, Marta, García-Verdugo, Jose Manuel, Viña, José, Lloret, Ana
المساهمون: Universitat Politècnica de València. Escuela Técnica Superior de Ingeniería Agronómica y del Medio Natural - Escola Tècnica Superior d'Enginyeria Agronòmica i del Medi Natural, European Commission, Generalitat Valenciana, Universitat de València, Instituto de Salud Carlos III, Agencia Estatal de Investigación, European Regional Development Fund
بيانات النشر: Springer-Verlag
سنة النشر: 2022
المجموعة: Universitat Politécnica de Valencia: RiuNet / Politechnical University of Valencia
مصطلحات موضوعية: Subventricular zone, Beta-amyloid toxicity, Neurogenesis, Senescence, Olfaction, BIOLOGIA CELULAR
الوصف: [EN] Neurogenesis in the adult brain takes place in two neurogenic niches: the ventricular-subventricular zone (V-SVZ) and the subgranular zone. After differentiation, neural precursor cells (neuroblasts) have to move to an adequate position, a process known as neuronal migration. Some studies show that in Alzheimer's disease, the adult neurogenesis is impaired. Our main aim was to investigate some proteins involved both in the physiopathology of Alzheimer's disease and in the neuronal migration process using the APP/PS1 Alzheimer's mouse model. Progenitor migrating cells are accumulated in the V-SVZ of the APP/PS1 mice. Furthermore, we find an increase of Cdh1 levels and a decrease of Cdk5/p35 and cyclin B1, indicating that these cells have an alteration of the cell cycle, which triggers a senescence state. We find less cells in the rostral migratory stream and less mature neurons in the olfactory bulbs from APP/PS1 mice, leading to an impaired odour discriminatory ability compared with WT mice. Alzheimer's disease mice present a deficit in cell migration from V-SVZ due to a senescent phenotype. Therefore, these results can contribute to a new approach of Alzheimer's based on senolytic compounds or pro-neurogenic factors. ; Open Access funding provided thanks to the CRUE-CSIC agreement with Springer Nature. This work was supported by the following grants: Instituto de Salud Carlos III CB16/10/00435 (CIBER-FES), (PID2019-110906RB-I00/AEI/10.13039/501100011033) from the Spanish Ministry of Innovation and Science, PROMETEO/2019/097 from `Conselleria, de Sanitat de la Generalitat Valenciana' and EU Funded H2020-DIABFRAIL-LATAM (Ref: 825546), European Joint Programming Initiative `A Healthy Diet for a Healthy Life' (JPI HDHL) and of the ERA-NET Cofound ERA-HDHL (GA No 696295 of the EU Horizon 2020 Research and Innovation Programme). Part of the equipment employed in this work has been funded by Generalitat Valenciana and co-financed with ERDF funds (OP ERDF of Comunitat Valenciana 2014-2020). Special Research ...
نوع الوثيقة: article in journal/newspaper
اللغة: English
تدمد: 0893-7648
Relation: Molecular Neurobiology; info:eu-repo/grantAgreement/AEI/Plan Estatal de Investigación Científica y Técnica y de Innovación 2017-2020/PID2019-110906RB-I00/ES/NUEVAS INTERVENCIONES TERAPEUTICAS MULTIDOMINIO PARA RETRASAR LA FRAGILIDAD Y LA DISCAPACIDAD. IDENTIFICACION DE MECANISMOS MOLECULARES CON RELEVANCIA TRASLACIONAL/; info:eu-repo/grantAgreement/GVA//PROMETEO%2F2019%2F097/; info:eu-repo/grantAgreement/EC/H2020/696295/EU; info:eu-repo/grantAgreement/ISCIII//CB16%2F10%2F00435//CIBER-FES/; info:eu-repo/grantAgreement/EC/H2020/825546/EU; info:eu-repo/grantAgreement/UV//UV-INV-AE-1546096/; https://doi.org/10.1007/s12035-021-02620-6; urn:issn:0893-7648; http://hdl.handle.net/10251/195605; PMC8857127
DOI: 10.1007/s12035-021-02620-6
الاتاحة: http://hdl.handle.net/10251/195605
https://doi.org/10.1007/s12035-021-02620-6
Rights: http://creativecommons.org/licenses/by/4.0/ ; info:eu-repo/semantics/openAccess
رقم الانضمام: edsbas.EC42F2F0
قاعدة البيانات: BASE
الوصف
تدمد:08937648
DOI:10.1007/s12035-021-02620-6