As a graduate student in David Holtzman’s group at Washington University in St. Louis, I studied how the strongest genetic risk factor for Alzheimer’s disease influences metabolism of the pathogenic amyloid beta peptide from brain interstitial fluid. I used in vivo microdialysis to show in behaving mice that clearance of this peptide is impeded by the presence of APOE4 whereas clearance in the context of more protective forms is faster. During my postdoctoral training in Tony Wyss-Coray’s group at Stanford University, I became engrossed in characterizing factors in the periphery that reverse features of brain aging, finding that systemic umbilical cord plasma treatment revitalizes hippocampal function in aged mice. My laboratory now focuses on characterizing the activity of blood-borne proteins like TIMP2 that mediate long-range effects on circuits in the brain in the context of Alzheimer’s disease.