Effects of neural stem cells on synaptic proteins and memory in a mouse model of Alzheimer's disease

Transplanting neural stem cells (NSC) to the damaged brain has been regarded as a potential treatment for neurodegenerative diseases such as Alzheimer's disease (AD), a condition characterized by memory loss. We hypothesized that transplantation of NSC into the hippocampal regions of APP + PS1...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:Journal of neuroscience research 2014-02, Vol.92 (2), p.185-194
Hauptverfasser: Zhang, W., Wang, G.M., Wang, P.J., Zhang, Q., Sha, S.H.
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
Beschreibung
Zusammenfassung:Transplanting neural stem cells (NSC) to the damaged brain has been regarded as a potential treatment for neurodegenerative diseases such as Alzheimer's disease (AD), a condition characterized by memory loss. We hypothesized that transplantation of NSC into the hippocampal regions of APP + PS1 transgenic (Tg) mice, a well‐established model of AD, would enhance the expression of synaptic proteins, which may be helpful for improving cognitive function. Our results showed that NSC transplantation significantly improved spatial learning and memory function in Tg mice. The results obtained by real‐time RT‐PCR, immunofluorescence, and Western blot analyses demonstrated that the expression of synaptophysin (SYN) and that of growth‐associated protein‐43 (GAP‐43) in Tg‐NSC mice, 8 weeks after transplantation, were significantly improved compared with what was observed in Tg‐Veh (control) mice. This finding was confirmed by the increase in the number of synapses in Tg‐NSC mice as observed via electron microscopy. Our results suggest that NSC‐induced changes can recover memory loss in APP + PS1 transgenic mice, possibly by establishing new neural circuits resulting from the engrafted NSC. © 2013 Wiley Periodicals, Inc.
ISSN:0360-4012
1097-4547
DOI:10.1002/jnr.23299