| Literature DB >> 31970651 |
Huan Li1,2,3, Xingli Xue1,2, Liang Li1,2, Yaqin Li1,2, Yanni Wang1,2, Tao Huang1,2, Yanhong Wang1,2, Huaxing Meng1, Baolong Pan1, Qiao Niu4,5,6.
Abstract
Aluminum (Al) is an environmental neurotoxin with extensive exposure by humans, but the molecular mechanism of its toxicity is still unclear. Several studies have indicated that exposure to aluminum can impair learning and memory function. The purpose of this study was to investigate the mechanism of LTP injury and the effect of aluminum exposure on related signal pathways. The results showed that the axonal dendrites of neurons in the hippocampal CA1 area of rats exposed to maltol aluminum showed neuritic beading and the dendritic spines were reduced. This resulted in dose-dependent LTP inhibition and led to impaired learning and memory function in rats. The PI3K-Akt-mTOR pathway may play a crucial role in this process.Entities:
Keywords: Aluminum; Mammalian target of rapamycin (mTOR); Phosphatidylinositol 3-kinase (PI3K); Protein kinase B (Akt); Synaptic plasticity
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Year: 2020 PMID： 31970651 DOI： 10.1007/s12640-020-00165-5
Source DB: PubMed Journal: Neurotox Res ISSN： 1029-8428 Impact factor: 3.911