Publication: BDNF-, IGF-1- and GDNF-secreting human neural progenitor cells rescue amyloid β-induced toxicity in cultured rat septal neurons
Issued Date
2012-01-01
Resource Type
ISSN
15736903
03643190
03643190
Other identifier(s)
2-s2.0-84856279659
Rights
Mahidol University
Rights Holder(s)
SCOPUS
Bibliographic Citation
Neurochemical Research. Vol.37, No.1 (2012), 143-152
Suggested Citation
Narisorn Kitiyanant, Yindee Kitiyanant, Clive N. Svendsen, Wipawan Thangnipon BDNF-, IGF-1- and GDNF-secreting human neural progenitor cells rescue amyloid β-induced toxicity in cultured rat septal neurons. Neurochemical Research. Vol.37, No.1 (2012), 143-152. doi:10.1007/s11064-011-0592-1 Retrieved from: https://repository.li.mahidol.ac.th/handle/123456789/13842
Research Projects
Organizational Units
Authors
Journal Issue
Thesis
Title
BDNF-, IGF-1- and GDNF-secreting human neural progenitor cells rescue amyloid β-induced toxicity in cultured rat septal neurons
Other Contributor(s)
Abstract
Alzheimer's disease (AD) is characterized by the depositions of amyloid-β (Aβ) 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 Aβ 1-42 peptide. Oligomeric Aβ 1-42 , (10 μM) 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 Aβ 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. © 2011 Springer Science+Business Media, LLC.