Cited by 52Alzheimer's disease research and treatmentsNeuroinflammation and Neurodegeneration MechanismsNeurological Disease Mechanisms and Treatments

Atorvastatin attenuates cognitive deficits and neuroinflammation induced by Aβ1-42 involving modulation of TLR4/TRAF6/NF-κB Pathway

Wang, Shan, Zhang, Xiaowei, Zhai, Liuyu, Sheng, Xiaona, Zheng, Weina, Chu, Hongshan, Zhang, Guohua·2018·Journal of Molecular Neuroscience

Abstract

Inflammatory damage aggravates the progression of Alzheimer's disease (AD) and the mechanism of inflammatory damage may provide a new therapeutic window for the treatment of AD. Toll-like receptor 4 (TLR4)-mediated signaling can regulate the inflammatory process. However, changes in TLR4 signaling pathway induced by beta-amyloid (Aβ) have not been well characterized in brain, especially in the hippocampus. In the present study, we explored the changes of TLR4 signaling pathway induced by Aβ in the hippocampus and the role of atorvastatin in modulating this signal pathway and neurotoxicity induced by Aβ. Experimental AD rats were induced by intrahippocampal injection of Aβ 1-42 , and the rats were treated with atorvastatin by oral gavage from 3 weeks before to 6 days after injections of Aβ 1-42 . To determine the spatial learning and memory ability of rats in the AD models, Morris water maze (MWM) was performed. The expression of the glial fibrillary acidic protein (GFAP), ionized calcium binding adapter molecule-1 (Iba-1), TLR4, tumor necrosis factor receptor-associated factor 6 (TRAF6), and nuclear transcription factor (NF)-κB (NF-κB) protein in the hippocampus was detected by immunohistochemistry and Western blot. Compared to the control group, increased expression of TLR4, TRAF6, and NF-κB was observed in the hippocampus at 7 days post-injection of Aβ (P < 0.01). Furthermore, atorvastatin treatment significantly ameliorated cognitive deficits of rats, attenuated microglia…

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Crossref · 10.1007/s12031-018-1032-3

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  • The fibrillar and oligomeric Aβ-amyloid-induced neuroinflammatory response has been linked to TLR4.

    “Similarly, the fibrillar and oligomeric A β -amyloid-induced neuroinflammatory response has been linked to TLR4 as well (Reed-Geaghan et al., 2009; Wang et al., 2018).”

    From TET2 Regulates the Neuroinflammatory Response in Microglia (2019) · cites this paper as Wang et al., 2018

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Authors
Wang, S., Zhang, X., Zhai, L., Sheng, X., Zheng, W., Chu, H., & Zhang, G.
Affiliations
Second Hospital of Hebei Medical University (CN)
Corresponding author
Sheng, Xiaona
Venue
Journal of Molecular Neuroscience
Published
2018-02-07
Volume
64
Issue
3
Pages
363-373
ISSN
  • 0895-8696 (ISSN-L)
  • 1559-1166
OpenAlex
W2787684810
Cited by
52
References
66
Citations by year
2026: 3 · 2025: 7 · 2024: 5 · 2023: 7 · 2022: 6 · 2021: 6 · 2020: 9 · 2019: 7 · 2018: 2
FWCI
4.12
Type
journal article
Language
en
Open access
closed
Locations
  • Journal of Molecular Neuroscience (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • Hebei Natural Science Foundation (C2011206110)
  • The key project of Hebei medical science research (20150211)
Topics
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
Keywords
atorvastatin, Alzheimer's disease, amyloid-beta 42, neuroinflammation, TLR4 signaling, TRAF6, NF-κB, hippocampus, cognitive impairment, microglial activation, astrocyte activation, apoptosis, spatial learning and memory, statins
MeSH terms
Atorvastatin, Animals, Anti-Inflammatory Agents, Male, Peptide Fragments, Amyloid beta-Peptides, NF-kappa B, Rats, Sprague-Dawley, Neuroprotective Agents, TNF Receptor-Associated Factor 6, Toll-Like Receptor 4, Rats, Cognitive Dysfunction

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