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

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    0580370 - ÚEM 2024 RIV DE eng J - Journal Article
    Esteve, D. - Molina-Navarro, M.M. - Giraldo, E. - Martinez-Varea, Noelia - Blanco-Gandia, M.C. - Rodriguez-Arias, M. - Garcia-Verdugo, J.M. - Vina, J. - Lloret, A.
    Adult Neural Stem Cell Migration Is Impaired in a Mouse Model of Alzheimer's Disease.
    Molecular Neurobiology. Roč. 59, č. 2 (2022), s. 1168-1182. ISSN 0893-7648. E-ISSN 1559-1182
    Institutional support: RVO:68378041
    Keywords : subventricular zone * beta-amyloid toxicity * neurogenesis * senescence * olfaction
    OECD category: Neurosciences (including psychophysiology
    Impact factor: 5.1, year: 2022
    Method of publishing: Open access
    https://link.springer.com/article/10.1007/s12035-021-02620-6

    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.
    Permanent Link: https://hdl.handle.net/11104/0350407

     
     
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