Abstract
An integrative theory relating cognitive aging deficits observed at the behavioral level with age-related deficiency in neuromodulation causing less distinctive cortical representations is tested in a series of neural network simulations. Age-related attenuation of catecholaminergic function is simulated by lowering the mean gain of the processing unit, which subsequently reduces responsivity and raises intra-network activation variability. Age differences in learning rate, asymptotic performance, interference susceptibility, complexity cost, intra- and inter-individual variability, and ability dedifferentiation can all be modeled. Together, the simulations illustrate catecholamine's role in regulating the fidelity of neural information processing and subsequent effects leading to cognitive aging deficits.
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