Published by Blackwell Publishing Inc.

Basic cognitive mechanisms, such as the abilities to briefly maintain, focus, and process information, decline with age. Related fields of cognitive aging research have been ad-vancing rapidly, but mostly in-dependently, at the biological, information processing, and behavioral levels. To facilitate integration, this article re-views research on cognitive ag-ing at the different levels, and describes a recent integrative theory postulating that aging-related deficiencies in neu-rotransmission cause increased noise in information process-ing and less distinctive cortical representation, which in turn lead to cognitive deficits. Ag-ing-related attenuation of cate-cholaminergic modulation can be modeled by lowering a neu-ral network parameter to re-duce the signal-to-noise ratio of information processing. The performance of such models is consistent with benchmark phenomena observed in hu-mans, ranging from age dif-ferences in learning rate, asymptotic performance, and interference susceptibility to intra- and interindividual vari-ability and ability dedifferenti-ation. Although the details of the conjectured sequence of ef-fects linking neuromodulation to cognitive aging deficits await further empirical validation, cross-level theorizing of the kind illustrated here could foster the coevolution of related fields through cross-level data synthe-sis and hypothesis testing