Jonathan Edwards
Senior Member (Voting Rights)
One thing I'm a bit worried about is if the main pathology of this disease is in the CNS, how do we study this? If the core of the disease mechanisms are happening in the brain rather than peripheral tissues, then where do we start?
Note that although we have treated RA on the basis that we think autoantibodies are causing inflammation by forming complexes and ligating FcRIIIa we have never actually measured that in patients. You cannot find complexes triggering TNF release inside a joint. You have to set up in vitro model systems. Animal studies are by and large useless for studying disease, although animal studies are useful for understanding normal mechanisms.
Much of our understanding of pathophysiology comes from inference.