The misfolded pro-inflammatory protein S100A9 disrupts memory via neurochemical remodelling instigating an Alzheimer’s disease-like cognitive deficit
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- 作者：Marina A. Grudena ; Tatiana V. Davydovab ; Chao Wangc ; Victor B. Narkevichd ; Valentina G. Fominab ; Vladimir S. Kudrind ; Ludmilla A. Morozova-Rochec ; Robert D.E. Sewelle ; sewell@cardiff.ac.uk" class="auth_mail" title="E-mail the corresponding author
- 关键词：S100A9 ; Amyloid ; Neuroinflammation ; Memory ; Passive avoidance task ; Neurotransmitters ; Alzheimer&rsquo ; s disease
- 刊名：Behavioural Brain Research
- 出版年：2016
- 出版时间：1 June 2016
- 年：2016
- 卷：306
- 期：Complete
- 页码：106-116
- 全文大小：1893 K
文摘
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Protein S100A9 oligomers and/or fibrils were given intranasally for 14 days in mice.
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S100A9 oligomers and fibrils but not their mixture evoked passive avoidance amnesia.
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The dopaminergic system was the primary disrupted target of S100A9 species amnesia.
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Native S100A9 had no amnestic effect but disrupted brain monoamine neurochemistry.
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The new findings are relevant to dementia management via a neuroprotective strategy.