Affiliations: University of Manchester, Manchester, UK | University of York, York, UK | Neuroscience and Aphasia Research Unit (NARU), School
of Psychological Sciences, Zochonis Building, University of Manchester,
Manchester, UK
Note: [] Corresponding author: Neuroscience and Aphasia Research Unit
(NARU), School of Psychological Sciences, Zochonis Building, University of
Manchester, Oxford Road, Manchester, M13 9PL, UK. Tel.: +44 161 275 2551; Fax:
+44 161 275 2873; E-mail: [email protected]
Abstract: Despite a vast literature examining semantic impairment in
Alzheimer's disease (AD), consensus regarding the nature of the deficit remains
elusive. We re-considered this issue in the context of a framework that assumes
semantic cognition can break down in two ways: (1) core semantic
representations can degrade or (2) cognitive control mechanisms can become
impaired [1]. We hypothesised and confirmed that the nature of semantic
impairment in AD changes with disease severity. Patients at mild or severe
stages of the disorder exhibited impairment across various semantic tasks but
the nature of those deficits differed qualitatively for the two groups.
Commensurate with early dysfunction of the cognitive control,
temporoparietal-frontal-cingulate network, characteristics of deregulated
semantic cognition were exhibited by the mild AD cases. In contrast, the severe
AD group reproduced features of additional degradation of core semantic
representations. These results suggest that spread of pathology into lateral
anterior temporal lobes in later stage AD produces degradation of semantic
representations, exacerbating the already deregulated system. Moreover, the
dual nature of severe patients' impairment was highlighted by
disproportionately poor performance on tasks placing high demand on both
conceptual knowledge and control processes – e.g., category fluency.
