Rodent models of neuroinflammation for Alzheimer’s disease

Journal of Neuroinflammation

Yousef Al-Abed¹  Michael Bacher³  Roman Sankowski²  Amir Nazem² 

[1] Center for Molecular Innovation, The Feinstein Institute for Medical Research, 350 Community drive, Manhasset 11030, NY, USA;Elmezzi Graduate School of Molecular Medicine, The Feinstein Institute for Medical Research, 350 Community drive, Manhasset 11030, NY, USA;Institute of Immunology, Philipps University Marburg, Hans-Meerwein-Str., Marburg, 35043, Germany

关键词: Tau protein;    Amyloid-β;    Innate immunity;    Animal models;    Neurodegeneration;    Neuroinflammation;    Alzheimer’s disease;   

Others  :  1226206
DOI  :  10.1186/s12974-015-0291-y

 received in 2015-02-07, accepted in 2015-03-27,  发布年份 2015

【 摘 要 】

Alzheimer’s disease remains incurable, and the failures of current disease-modifying strategies for Alzheimer’s disease could be attributed to a lack of in vivo models that recapitulate the underlying etiology of late-onset Alzheimer’s disease. The etiology of late-onset Alzheimer’s disease is not based on mutations related to amyloid-β (Aβ) or tau production which are currently the basis of in vivo models of Alzheimer’s disease. It has recently been suggested that mechanisms like chronic neuroinflammation may occur prior to amyloid-β and tau pathologies in late-onset Alzheimer’s disease. The aim of this study is to analyze the characteristics of rodent models of neuroinflammation in late-onset Alzheimer’s disease. Our search criteria were based on characteristics of an idealistic disease model that should recapitulate causes, symptoms, and lesions in a chronological order similar to the actual disease. Therefore, a model based on the inflammation hypothesis of late-onset Alzheimer’s disease should include the following features: (i) primary chronic neuroinflammation, (ii) manifestations of memory and cognitive impairment, and (iii) late development of tau and Aβ pathologies. The following models fit the pre-defined criteria: lipopolysaccharide- and PolyI:C-induced models of immune challenge; streptozotocin-, okadaic acid-, and colchicine neurotoxin-induced neuroinflammation models, as well as interleukin-1β, anti-nerve growth factor and p25 transgenic models. Among these models, streptozotocin, PolyI:C-induced, and p25 neuroinflammation models are compatible with the inflammation hypothesis of Alzheimer’s disease.

【 授权许可】

   
2015 Nazem et al.; licensee BioMed Central.

【 图 表 】

Figure 1.

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