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We could downregulate EP2 in microglia in response to AB (same as we are planning for BACE1 currently). Since they will only be in microglia, the shouldn't cause problems with other cells. The system should shut down without AB signalling.
6/26/14
I found this paper from Nature (Targeting gene-modified hematopoietic cells to the centralnervous system: Use of green fluorescent protein uncovers microglial engraftment) which showed:
mice which had undergone a bone marrow transplant with GFP-expressing bone marrow cells had GFP-expressing microglia in their brains at a substantial level after four months, which means there is a circulating microglial precursor in our blood (Ly6Chi CCR2+, according to another paper). Engraftment increased and was directed to specific areas of the brain if their was some sort of damage to that area of the brain.Other interesting things, though (from first paper):
IMPORTANT: "The decreased propensity of the MSCV promoter to transcriptional silencing in vivo is of particular relevance in the CNS where gene silencing is pertinent." *red-flag, red-flag!*
Not so important: "Recently, cells derived from bone marrow (BM) were found to enter the brain in adult life to differentiate into microglia, astrocytes and neurons2–4"