Alzheimer's

Information

A stereotaxic injection of amyloid-β peptide (1-42) into the hippocampus of C57Bl/6 mice produces marked neuronal loss and inflammation within the CA1 region. Deficits in working memory manifest within one week following administration of amyloid-β peptide and can be assessed using the Morris water maze and novel object recognition task. These endpoints are sufficient to rapidly determine whether a therapeutic warrants further investigation before investing in lengthy transgenic AD mouse models that feature a broader spectrum of neuropathology.

Related Information

Kim, H. G. et al. Donepezil inhibits the amyloid-beta oligomer-induced microglial activation in vitro and in vivo. Neurotoxicology 40, 23–32 (2014).

Lee, H. E. et al. Neuroprotective effect of sinapic acid in a mouse model of amyloid beta 1-42 protein-induced Alzheimer’s disease. Pharmacol. Biochem. Behav. 103, 260–266 (2012).

McLarnon, J. G. & Ryu, J. K. Relevance of abeta1-42 intrahippocampal injection as an animal model of inflamed Alzheimer’s disease brain. Curr. Alzheimer Res. 5, 475–80 (2008).

Choi, J. G. et al. Gami-Chunghyuldan ameliorates memory impairment and neurodegeneration induced by intrahippocampal Aβ 1-42 oligomer injection. Neurobiol. Learn. Mem. 96, 306–14 (2011).