Rodent models of neuroinflammation for Alzheimer's disease

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. © nazem et al.; licensee biomed central.