Therapeutic strategies that target the accumulation and toxicity of Aβ in the brain during Alzheimer's disease may offer significant promise for the treatment of this neurodegenerative disorder [2, 5, 58]. In particular, focus upon central nervous system microglia, immune cell sentinels that can sequester Aβ[4, 9, 14-16], may offer great promise for new therapies. Furthermore, identification of microglial cytoprotective pathways for entities such as EPO and Wnt1 [59-61] may synergistically enhance the development of treatments for Alzheimer's disease.
We show that EPO protects microglia against Aβ exposure during both early and late phases of apoptotic cell injury similar to prior studies with other injury models in non-neuronal cells [33, 34, 62].
http://impactaging.com/papers/v4/n3/full/100440.html
