Objective-Many neurologically-constrained models of semantic memory have been informed by two primary temporal lobe pathologies: Alzheimer's Disease (AD) and Semantic Dementia (SD). However, controversy persists regarding the nature of the semantic impairment associated with these patient populations. Some argue that AD presents as a disconnection syndrome in which linguistic impairment reflects difficulties in lexical or perceptual means of semantic access. In contrast, there is a wider consensus that SD reflects loss of core knowledge that underlies word and object meaning. Object naming provides a window into the integrity of semantic knowledge in these two populations.Method-We examined naming accuracy, errors and the correlation of naming ability with neuropsychological measures (semantic ability, executive functioning, and working memory) in a large sample of patients with AD (n=36) and SD (n=21).Results-Naming ability and naming errors differed between groups, as did neuropsychological predictors of naming ability. Despite a similar extent of baseline cognitive impairment, SD patients were more anomic than AD patients.Conclusions-These results add to a growing body of literature supporting a dual impairment to semantic content and active semantic processing in AD, and confirm the fundamental deficit in semantic content in SD. We interpret these findings as supporting of a model of semantic memory premised upon dynamic interactivity between the process and content of conceptual knowledge. KeywordsAlzheimer's Disease; Semantic Dementia; Semantic Memory; Naming; Error Types; Naming Errors; Error Analysis Object naming relies on the integrity of a series of discrete yet highly interactive cognitive processes working in concert to access meaning, assign a corresponding symbolic word form, and encode an appropriate lexical-phonological output sequence. Naming impairment Address Correspondence To: Jamie Reilly, Ph.D., University of Florida, Speech, Language, and Hearing Sciences, P.O. Box 100174, Gainesville, Florida 32610, jjreilly@phhp.ufl.edu, Fax: (352) Tel: (352) 273-6161. Publisher's Disclaimer: The following manuscript is the final accepted manuscript. It has not been subjected to the final copyediting, fact-checking, and proofreading required for formal publication. It is not the definitive, publisher-authenticated version. The American Psychological Association and its Council of Editors disclaim any responsibility or liabilities for errors or omissions of this manuscript version, any version derived from this manuscript by NIH, or other third parties. The published version is available at www.apa.org/pubs/journals/neu NIH Public Access Author ManuscriptNeuropsychology. Author manuscript; available in PMC 2012 July 1. NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript (i.e., anomia) can potentially result from a number of etiologies affecting input, output, or core conceptual knowledge that supports word meaning. From the standpoint of cognitive neuropsychology, two p...

Background-It has been proposed that anomia following left inferior temporal lobe lesions may have two different underlying mechanisms with distinct neural substrates. Specifically, naming impairment following damage to more posterior regions (BA 37) has been considered to result from a disconnection between preserved semantic knowledge and phonological word forms (pure anomia), whereas anomia following damage to anterior temporal regions (BAs 38, 20/21) has been attributed to the degradation of semantic representations (semantic anomia). However, the integrity of semantic knowledge in patients with pure anomia has not been demonstrated convincingly, nor were lesions in these cases necessarily confined to BA 37. Furthermore, evidence of semantic anomia often comes from individuals with bilateral temporal lobe damage, so it is unclear whether unilateral temporal lobe lesions are sufficient to produce significant semantic impairment.

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