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Brian was  excited about macrophages/microglia as chassis idea.  Relevant paper: Microglia in the adult brain arise from Ly-6ChiCCR2+ monocytes only under defined host conditions

6/23/14

EP2 and phagocytosis of AB.pdf

EP2 potential target for AD. Knocking out EP2 increases phagocytosis of AB-immunoreactive material (hence, AB) by a LOT, and microglia lacking EP2 do not cause neurodegeneration. EP2 has been associated with other brain disorders and I could not find papers that show that EP2-/- has detrimental effects on the brain (only thing I found: Salt−sensitive hypertension and reduced fertility in mice lacking the prostaglandin EP2 receptor)
We could downregulate EP2 in microglia in response to AB (same as we are planning for BACE1 currently). The paper thinks EP2 could be a potential target for AD treatment.