Abstract
Alzheimer's disease (AD), characterized by memory loss, cognitive decline, and dementia, is a progressive neurodegenerative disease. Although the long noncoding RNAs (lncRNAs) have recently been identified to play a role in the pathogenesis of AD, the specific effects of lncRNAs in AD remain unclear. In present study, we have investigated the expression profiles of lncRNAs in hippocampal of intranasal LPS-mediated Alzheimer's disease models in mice by microarray method. A total of 395 lncRNAs and 123 mRNAs was detected to express differently in AD models and controls (>2.0 folds, p<0.05). The microarray expression was validated by Quantitative Real-Time-PCR (qRT-PCR). The pathway analysis showed the mRNAs that correlated with lncRNAs were involved in inflammation, apoptosis, and nervous system related pathways. The lncRNA-TFs network analysis suggested the lncRNAs were mostly regulated by HMGA2, ONECUT2, FOXO1, and CDC5L. Additionally, lncRNA-target-TFs network analysis indicated the FOXL1, CDC5L, ONECUT2, and CDX1 to be the TFs most likely to regulate the production of these lncRNAs. This is the first study to investigate lncRNAs expression pattern in intranasal LPS-mediated Alzheimer's disease model in mice. And these results may facilitate the understanding of the pathogenesis of AD targeting lncRNAs.
Highlights
Alzheimer’s disease (AD), with principal clinical manifestations of memory loss, cognitive decline, and dementia, is a common progressive neurodegenerative disease in aging people worldwide [1, 2]
Mice with chronic intranasal LPS instillation spent significantly more time to travel into the fourth quadrant, where the hidden platform was previously placed, than the controls did (Figures 1(c) and 1(d)), which revealed weaker spatial memory ability in the AD model than controls
To examine further the influence of intranasal LPS instillation in inducing systemic or locus immune response, we detected the levels of IL1-β, IL6, IL10, and TNF-α in peripheral blood of AD models and controls, as well as in cerebrospinal fluid (CSF) and PB of AD models
Summary
Alzheimer’s disease (AD), with principal clinical manifestations of memory loss, cognitive decline, and dementia, is a common progressive neurodegenerative disease in aging people worldwide [1, 2]. The main neuropathic characteristics of AD are marked by extracellular amyloid-β (Aβ) deposition, neurofibrillary tangles (NFTs), loss of neuron, and synaptic and dystrophic neuritis [3,4,5]. The pathogenesis of AD is largely unknown. Multiple factors such as genetics, free radical injury, apoptosis, and inflammation were considered to be involved in the development of AD [6,7,8]. The recent associatedgenes could not explain the whole pathogenesis of AD
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