Because of these characteristics, existing rodent models will fail to recapitulate aspects of human pathophysiology associated with B7-1–mediated p75NTR-dependent processes in a variety of pathological states, including EAE (21), acute traumatic injury (43), AD (15), and cerebral ischemia (44), which are all conditions characterized by p75NTR induction and by inflammatory changes, including accumulation of APCs. The gene discussed is NGFR; the disease is Cerebral ischemia.