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Wnt signaling pathway overcomes the disruption of neuronal differentiation of neural progenitor cells induced by oligomeric amyloid β‐peptide
Author(s) -
Shruster Adi,
EldarFinkelman Hagit,
Melamed Eldad,
Offen Daniel
Publication year - 2011
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.2010.07131.x
Subject(s) - neurogenesis , wnt signaling pathway , progenitor cell , neural stem cell , biology , hippocampal formation , microbiology and biotechnology , wnt3a , cellular differentiation , progenitor , neuroscience , stem cell , signal transduction , gene , biochemistry
J. Neurochem. (2011) 116 , 522–529. Abstract Neural stem cells give rise to new hippocampal neurons throughout adulthood. Defects in neurogenesis are associated with cognitive dysfunctions, such as Alzheimer disease (AD). Our understanding of the signals controlling this process is limited. The present in vitro study explored the manner in which the Wnt signaling pathway regulates the differentiation of hippocampal progenitors (HPs) into neurons under the influence of amyloid β 42 (Aβ 42 ). The results showed that oligomeric Aβ 42 reduced neuronal differentiation. This process was accompanied by a reduction in active β‐catenin levels and proneural gene expression. The addition of Wnt3a increased the neuronal differentiation of Aβ 42 ‐treated HPs, at the expense of astrocyte differentiation. The effect of Wnt signaling was attributable to progenitor cell differentiation to the neuronal lineage, and not to increased proliferation or rescue of neurons. The interruption of Wnt signaling by oligomeric Aβ 42 may have clinical implications for the treatment of impaired neurogenesis in AD.