A Dissociation of Frequency and Regularity Effects in Pronunciation Performance Across Young-Adults, Older Adults, and Individuals With Senile Dementia of the Alzheimer-Type

Abstract

The regularity of a given spelling-to-sound sequence in English primarily influences the ease of naming low-frequency words and produces little influence on the ease of naming high-frequency words. This frequency × regularity interaction has been accommodated within both a single-route connectionist model and dual-route models of pronunciation performance. Recent evidence presented by dual-route theorists suggests that the sublexical route in naming performance demands more attention than the lexical route. The present study further explores this possibility by investigating the word-frequency by regularity interaction across five different groups of subjects that have well-documented changes in attentional capacities. The five groups were healthy young adults, older adults between 60 and 80 years of age, older adults greater than 80 years of age, very mildly demented individuals with senile dementia of the Alzheimers Type (SDAT), and mild/moderately demented SDAT individuals. The response latency results from a simple word-naming experiment indicated that there was a consistent increase in the word-frequency effect across the five subject groups (from young to mildly demented individuals) without any corresponding increase in either the regularity effect or the frequency × regularity interaction. However, the results also indicated that there was an increased likelihood of regularization errors (e.g., pronouncing the word pint such that it rhymes with hint) across the subject groups. These results are viewed as most consistent with a model in which healthy young adults are especially slow to name low-frequency irregular words because they must inhibit inconsistent output from an assembled route and produce the correct output from the addressed route. We argue that the increased likelihood of regularization errors in the healthy aged individuals and to a greater extent in the SDAT individuals may be due to a breakdown in the inhibitory control of partially activated (assembled route) information.