Amyloid in the Brain

Clinical Feasibility of Molecular Imaging of Plaque Inflammation in Atherosclerosis M olecular imaging of various components of atherosclerotic plaques has been proposed, and proof of principle has been demonstrated in experimental models of disease (1). These preclinical studies have predominantly targeted plaque inflammation with the premise that the extent of inflammation would determine the vulnerability of the plaque to rupture. Plaque inflammation has been detected by targeting alterations in monocytes that facilitate their migration to the neointima, ensure efficient scavenging of insudated lipid, oversee their transformation to foam cells or mediate cell death (1). Molecular targets have also included events that are associated with or consequent to inflammation, such as production of cytokines and metalloproteinases. Although these experimental molecular imaging studies have offered significant promise, translational data in the clinical setting has just started to emerge. Clinical studies of molecular targeting are the major