Recently, transgenic mice expressing Aβ4-42 (Tg4-42 transgenic line) have been generated (Bouter et al., 2013) as a transgenic mouse model of Alzheimer’s disease (AD). These mutants developed a massive CA1 pyramidal neuron loss in the hippocampus. This hippocampal neurodegeneration was associated with age-dependent spatial learning deficits in the Morris water-maze. In the present project, we wish to extend these findings by investigating different types of Alzheimer-relevant cognitive domains, object memory including novel object recognition, object-place memory, temporal order memory (TOM) and episodic-like memory (ELM). We will also examine whether chronic erythropoietin (EPO) treatment would be effective in ameliorating cognitive deficits in these mice. In all experiments, we will in parallel test mice of the 5xFAD transgenic line as an established Alzheimer model. The aim of this project is to investigate whether pre- or early symptomatic EPO treatment can block or delay the cognitive deficits in two transgenic mouse models of Alzheimer’s disease. These findings could help to identify novel pharmacological targets to develop better medications that could protect against neurodegeneration as well as cognitive decline in Alzheimer’s disease.