title: Rodent models of neuroinflammation for Alzheimer's disease.
abstract: 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.
authors.affiliation: Elmezzi Graduate School of Molecular Medicine, The Feinstein Institute for Medical Research, 350 Community drive, Manhasset, NY, 11030, USA. anazem@nshs.edu.
authors.forename: Amir
authors.initials: A
authors.lastname: Nazem
authors.affiliation: Elmezzi Graduate School of Molecular Medicine, The Feinstein Institute for Medical Research, 350 Community drive, Manhasset, NY, 11030, USA. rsankowski@nshs.edu.
authors.forename: Roman
authors.initials: R
authors.lastname: Sankowski
authors.affiliation: Institute of Immunology, Philipps University Marburg, Hans-Meerwein-Str., 35043, Marburg, Germany. bacher@staff.uni-marburg.de.
authors.forename: Michael
authors.initials: M
authors.lastname: Bacher
authors.affiliation: Center for Molecular Innovation, The Feinstein Institute for Medical Research, 350 Community drive, Manhasset, NY, 11030, USA. yalabed@nshs.edu.
authors.forename: Yousef
authors.initials: Y
authors.lastname: Al-Abed
mesh_terms: D000544:Alzheimer Disease / Q000150:complications* / Q000209:etiology*; D000818:Animals; D004195:Disease Models, Animal; D004660:Encephalitis / Q000209:etiology*; D006801:Humans