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

D. Esteve, MM. Molina-Navarro, E. Giraldo, N. Martínez-Varea, MC. Blanco-Gandia, M. Rodríguez-Arias, JM. García-Verdugo, J. Viña, A. Lloret

. 2022 ; 59 (2) : 1168-1182. [pub] 20211211

Language English Country United States

Document type Journal Article

Persistent link   https://www.medvik.cz/link/bmc22019444

Grant support
696295 horizon 2020
CB16/10/00435 instituto de salud carlos iii
PID2019-110906RB-I00 ministerio de ciencia, innovación y universidades
PROMETEO/2019/097 conselleria de sanitat universal i salut pública
825546 joint programming initiative a healthy diet for a healthy life
UV-INV-AE-1546096 Universitat de València

E-resources Online Full text

NLK ProQuest Central from 1997-02-01 to 1 year ago
Medline Complete (EBSCOhost) from 2010-02-01 to 1 year ago
Health & Medicine (ProQuest) from 1997-02-01 to 1 year ago
Psychology Database (ProQuest) from 1997-02-01 to 1 year ago

Links

PubMed 34894324
DOI 10.1007/s12035-021-02620-6
Knihovny.cz E-resources

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.

References provided by Crossref.org

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