Recent studies of patients with Korsakoff's amnesia suggest that central noradrenergic (NE) activity is diminished by the brainstem and diencephalic lesions associated with this disease. Similarly, there is a body of evidence that experimental manipulations of central NE activity affect the ability of animals to learn and remember some conditioned behaviors. The relationship between brain NE activity and human amnesia is underscored by evidence of comparable behavioral deficits in animals with NE depleting lesions and in humans with Korsakoff's psychosis. We argue that diminished NE activity impairs cognitive activation and that this limits processes related to attention and to the information processing capacity of patients with Korsakoff's psychosis.