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.

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