VAP1, upregulated in response to inflammation, is a cell adhesion protein that participates in lymphocyte recirculation, by mediating the binding of lymphocytes to peripheral lymph node vascular endothelial cells, in an L selectin independent fashion. VAP1 also displays a monoamine oxidase activity, catalyzing the deamination of methylamine to produce formaldehyde. Upregulation of VAP1 has been reported in Alzheimer's disease, where increased levels of formaldehyde are responsible for b amyloid cross linkage and plaque formation, significantly contributing to the pathogenesis of this disease.