PMID- 24481678
OWN - NLM
STAT- MEDLINE
DCOM- 20150911
LR  - 20211021
IS  - 1559-1182 (Electronic)
IS  - 0893-7648 (Linking)
VI  - 50
IP  - 2
DP  - 2014 Oct
TI  - Neural stem cell transplants improve cognitive function without altering amyloid 
      pathology in an APP/PS1 double transgenic model of Alzheimer's disease.
PG  - 423-37
LID - 10.1007/s12035-014-8640-x [doi]
AB  - Neural stem cells (NSCs) are capable of self-renewal and are multipotent. 
      Transplantation of NSCs may represent a promising approach for treating 
      neurodegenerative disorders associated with cognitive decline, such as Alzheimer 
      disease (AD) characterized by extensive loss of neurons. In this study, we 
      investigated the effect of NSC transplantation on cognitive function in the 
      amyloid precursor protein/presenilin-1 (APP/PS1) transgenic mouse, an AD mouse 
      model with age-dependent cognitive deficits. We found that NSCs bilaterally 
      transplanted into hippocampal regions improved spatial learning and memory 
      function in these mice, but did not alter Abeta pathology. Immunohistochemical 
      analyses determined that NSCs proliferated, migrated, and differentiated into 
      three neuronal cell types. The improvement in cognitive function was correlated 
      with enhanced long-term potentiation (LTP) and an increase in the neuron 
      expression of proteins related to cognitive function: N-methyl-D-aspartate (NMDA) 
      2B unit, synaptophysin (SYP), protein kinase C zeta subtypes (PKCzeta), tyrosine 
      receptor kinase B (TrkB), and brain-derived neurotrophic factor (BDNF). Taken 
      together, our data indicated that injected NSCs can rescue cognitive deficits in 
      APP/PS1 transgenic mice by replacing neuronal cell types expressing multiple 
      cognition-related proteins that enhance LTP.
FAU - Zhang, Wei
AU  - Zhang W
AD  - Department of Medical Imaging, Tongji Hospital, Medical School of Tongji 
      University, No. 389 Xincun Road, Putuo District, Shanghai, 200065, China.
FAU - Wang, Pei-Jun
AU  - Wang PJ
FAU - Sha, Hong-ying
AU  - Sha HY
FAU - Ni, Jiong
AU  - Ni J
FAU - Li, Ming-hua
AU  - Li MH
FAU - Gu, Guo-jun
AU  - Gu GJ
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20140131
PL  - United States
TA  - Mol Neurobiol
JT  - Molecular neurobiology
JID - 8900963
RN  - 0 (Amyloid beta-Protein Precursor)
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Presenilin-1)
RN  - 0 (presenilin 1, mouse)
SB  - IM
MH  - Alzheimer Disease/pathology/physiopathology/*therapy
MH  - Amyloid beta-Protein Precursor/genetics/metabolism
MH  - Animals
MH  - Brain-Derived Neurotrophic Factor/metabolism
MH  - Cell- and Tissue-Based Therapy/methods
MH  - Cognition/physiology
MH  - Disease Models, Animal
MH  - Long-Term Potentiation/physiology
MH  - Memory/physiology
MH  - Mice
MH  - Mice, Transgenic
MH  - Neural Stem Cells/*cytology/transplantation
MH  - Neurons/*cytology/metabolism
MH  - Presenilin-1/genetics/metabolism
MH  - *Stem Cell Transplantation
EDAT- 2014/02/01 06:00
MHDA- 2015/09/12 06:00
CRDT- 2014/02/01 06:00
PHST- 2013/10/25 00:00 [received]
PHST- 2014/01/02 00:00 [accepted]
PHST- 2014/02/01 06:00 [entrez]
PHST- 2014/02/01 06:00 [pubmed]
PHST- 2015/09/12 06:00 [medline]
AID - 10.1007/s12035-014-8640-x [doi]
PST - ppublish
SO  - Mol Neurobiol. 2014 Oct;50(2):423-37. doi: 10.1007/s12035-014-8640-x. Epub 2014 
      Jan 31.