Is cD45RB a novel molecular therapeutic target to inhibit Abeta peptide-induced microglial MAPK activation?
In summary, p38 MAPK is another novel signaling pathway, besides p44/42, in which CD45RB cross-linking negatively regulates microglial Abeta phagocytosis while increasing potentially neurotoxic inflammation. Therefore, agonism of CD45RB PTP activity may be an effective therapeutic target for novel agents to treat AD due to its Abeta lowering, and inflammation reducing, properties that are particularly targeted at microglial cells. Such treatments may be more effective with less potential to produce systemic side-effects than therapeutics which induce non-specific, systemic down-regulation of inflammation.
There is a high rate of acute PCS in both mTBI and non-brain injured trauma patients. PCS was not found to be specific to mTBI. The use of the term PCS may be misleading as it incorrectly suggests that the basis of PCS is a brain injury.