PMID- 21909955
OWN - NLM
STAT- MEDLINE
DCOM- 20120509
LR  - 20211020
IS  - 1573-6903 (Electronic)
IS  - 0364-3190 (Linking)
VI  - 37
IP  - 1
DP  - 2012 Jan
TI  - BDNF-, IGF-1- and GDNF-secreting human neural progenitor cells rescue amyloid 
      beta-induced toxicity in cultured rat septal neurons.
PG  - 143-52
LID - 10.1007/s11064-011-0592-1 [doi]
AB  - Alzheimer's disease (AD) is characterized by the depositions of amyloid-beta (Abeta) 
      proteins, resulting in a reduction of choline acetyltransferase (ChAT) activity 
      of AD brain in the early stages of the disease. Several growth factors, including 
      brain-derived neurotrophic factor (BDNF), insulin-like growth factor (IGF)-1 and 
      glial cell-derived neurotrophic factor (GDNF) are known to protect neuronal cell 
      death in several neurodegenerative both in vitro and in vivo models. In this 
      study, septal neurons were prepared from septal nucleus of embryonic (day 16-17) 
      rat brain and treated with monomeric, oligomeric or fibrillar Abeta(1-42) peptide. 
      Oligomeric Abeta(1-42), (10 muM) was the most potent at sublethal dose. Septal neuron 
      cultures treated with BDNF, IGF-1 or GDNF or co-cultured with genetically 
      modified human neural progenitor cells (hNPCs) secreting these neurotrophic 
      factors (but not allowing contact between the two cell types), were protected 
      from oligomeric Abeta(1-42) peptide-induced cell death, and these trophic factors 
      enhanced cholinergic functions by increasing ChAT expression level. These results 
      indicate the potential of employing transplanted hNPCs for treatment of AD.
FAU - Kitiyanant, Narisorn
AU  - Kitiyanant N
AD  - Research Center for Neuroscience, Institute of Molecular Biosciences, Mahidol 
      University, Nakhon Pathom 73170, Thailand.
FAU - Kitiyanant, Yindee
AU  - Kitiyanant Y
FAU - Svendsen, Clive N
AU  - Svendsen CN
FAU - Thangnipon, Wipawan
AU  - Thangnipon W
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20110911
PL  - United States
TA  - Neurochem Res
JT  - Neurochemical research
JID - 7613461
RN  - 0 (Amyloid beta-Peptides)
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Glial Cell Line-Derived Neurotrophic Factor)
RN  - 0 (Peptide Fragments)
RN  - 0 (amyloid beta-protein (1-42))
RN  - 67763-96-6 (Insulin-Like Growth Factor I)
RN  - EC 2.3.1.6 (Choline O-Acetyltransferase)
SB  - IM
MH  - Amyloid beta-Peptides/*toxicity
MH  - Animals
MH  - Brain-Derived Neurotrophic Factor/*metabolism
MH  - Cells, Cultured
MH  - Choline O-Acetyltransferase/metabolism
MH  - Coculture Techniques
MH  - Female
MH  - Glial Cell Line-Derived Neurotrophic Factor/*metabolism
MH  - Humans
MH  - Insulin-Like Growth Factor I/*metabolism
MH  - Neurons/*metabolism
MH  - Peptide Fragments/*toxicity
MH  - Pregnancy
MH  - Rats
MH  - Rats, Transgenic
MH  - Rats, Wistar
MH  - Septum of Brain/cytology/*drug effects
MH  - Stem Cells/*metabolism
EDAT- 2011/09/13 06:00
MHDA- 2012/05/10 06:00
CRDT- 2011/09/13 06:00
PHST- 2011/07/05 00:00 [received]
PHST- 2011/08/29 00:00 [accepted]
PHST- 2011/08/18 00:00 [revised]
PHST- 2011/09/13 06:00 [entrez]
PHST- 2011/09/13 06:00 [pubmed]
PHST- 2012/05/10 06:00 [medline]
AID - 10.1007/s11064-011-0592-1 [doi]
PST - ppublish
SO  - Neurochem Res. 2012 Jan;37(1):143-52. doi: 10.1007/s11064-011-0592-1. Epub 2011 
      Sep 11.