载脂蛋白 L2 导致脑铁代谢紊乱，但不影响 J20 阿尔茨海默病小鼠模型的认知、斑块负荷和神经胶质激活。
Lipocalin 2 contributes to brain iron dysregulation but does not affect cognition, plaque load, and glial activation in the J20 Alzheimer mouse model.
机构信息
Department of Neurology and Alzheimer Research Center, University Medical Center Groningen, University of Groningen, Hanzeplein 1, Groningen, 9713 GZ, The Netherlands.
Department of Molecular Neurobiology, Groningen Institute for Evolutionary Life Sciences (GELIFES), University of Groningen, Nijenborgh 7, Groningen, 9747 AG, The Netherlands.
出版信息
J Neuroinflammation. 2018 Nov 30;15(1):330. doi: 10.1186/s12974-018-1372-5.
BACKGROUND
Lipocalin 2 (Lcn2) is an acute-phase protein implicated in multiple neurodegenerative conditions. Interestingly, both neuroprotective and neurodegenerative effects have been described for Lcn2. Increased Lcn2 levels were found in human post-mortem Alzheimer (AD) brain tissue, and in vitro studies indicated that Lcn2 aggravates amyloid-β-induced toxicity. However, the role of Lcn2 has not been studied in an in vivo AD model. Therefore, in the current study, the effects of Lcn2 were studied in the J20 mouse model of AD.
METHODS
J20 mice and Lcn2-deficient J20 (J20xLcn2 KO) mice were compared at the behavioral and neuropathological level.
RESULTS
J20xLcn2 KO and J20 mice presented equally strong AD-like behavioral changes, cognitive impairment, plaque load, and glial activation. Interestingly, hippocampal iron accumulation was significantly decreased in J20xLcn2 KO mice as compared to J20 mice.
CONCLUSIONS
Lcn2 contributes to AD-like brain iron dysregulation, and future research should further explore the importance of Lcn2 in AD.
背景
脂钙蛋白 2（Lcn2）是一种急性期蛋白，与多种神经退行性疾病有关。有趣的是，Lcn2 既有神经保护作用，也有神经退行性作用。在人类阿尔茨海默病（AD）死后脑组织和体外研究中发现 Lcn2 水平升高，并且表明 Lcn2 加重了淀粉样β诱导的毒性。然而，Lcn2 在体内 AD 模型中的作用尚未得到研究。因此，在本研究中，研究了 Lcn2 在 AD 的 J20 小鼠模型中的作用。
方法
比较了 J20 小鼠和 Lcn2 缺陷型 J20（J20xLcn2 KO）小鼠的行为和神经病理学水平。
结果
J20xLcn2 KO 和 J20 小鼠均表现出相似的 AD 样行为变化、认知障碍、斑块负荷和神经胶质激活。有趣的是，与 J20 小鼠相比，J20xLcn2 KO 小鼠的海马铁积累显著减少。
结论
Lcn2 有助于 AD 样脑铁失调，未来的研究应进一步探讨 Lcn2 在 AD 中的重要性。
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