Journal
NEUROTOXICITY RESEARCH
Volume 34, Issue 3, Pages 477-488Publisher
SPRINGER
DOI: 10.1007/s12640-018-9905-3
Keywords
Alzheimer's disease; L-3-n-Butylphthalide; Neural stem cells; Neurogenesis; BDNF; CREB; Akt
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Funding
- National Natural Sciences Foundation of China [81473200, 81673420]
- CAMS Innovation Fund for Medical Sciences [2017-I2M-2-004]
- Key Laboratory of Neurodegenerative Diseases (Capital Medical University), Ministry of Education of China
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Alzheimer's disease (AD) is characterized by extracellular accumulation of beta-amyloid peptides (A beta) and intracellular neurofibrillary tangles, along with cognitive decline and neurodegeneration. The cognitive deficit is considered to be due to the dysfunction of hippocampal neurogenesis. Although L-3-n-butylphthalide (L-NBP) has been shown beneficial effects in multiple AD animal models, the underlying molecular mechanisms are still elusive. In this study, we investigated the effects of L-NBP on neurogenesis both in vitro and in vivo. L-NBP promoted proliferation and migration of neural stem cells and induced neuronal differentiation in vitro. In APP/PS1 mice, L-NBP induced neurogenesis in the dentate gyrus and improved cognitive functions. In addition, L-NBP significantly increased the expressions of BDNF and NGF, tyrosine phosphorylation of its cognate receptor, and phosphorylation of Akt as well as CREB at Ser133 in the hippocampus of APP/PS1 mice. These results indicated that L-NBP might stimulate the proliferation, migration, and differentiation of hippocampal neural stem cells and reversed cognitive deficits in APP/PS1 mice. BDNF/TrkB/CREB/Akt signaling pathway might be involved.
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