Deregulated semantic cognition contributes to object-use deficits in Alzheimer's disease: A comparison with semantic aphasia and semantic dementia.

Executive control is impaired from the early stages of Alzheimer's Disease (AD) and this produces deregulated semantic cognition (Corbett, Jefferies, Burns, & Lambon Ralph, ; Perry, Watson, & Hodges, ). While control deficits should affect semantic retrieval across all modalities, previous studies have typically focused on verbal semantic tasks. Even when non-verbal semantic tasks have been used, these have typically employed simple picture-matching tasks, which may be influenced by abnormalities in covert naming.

Unpicking the semantic impairment in Alzheimer's disease: qualitative changes with disease severity.

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. We hypothesised and confirmed that the nature of semantic impairment in AD changes with disease severity.

Deregulated semantic cognition follows prefrontal and temporo-parietal damage: evidence from the impact of task constraint on nonverbal object use.

Semantic cognition, which encompasses all conceptually based behavior, is dependent on the successful interaction of two key components: conceptual representations and regulatory control. Qualitatively distinct disorders of semantic knowledge follow damage to the different parts of this system. Previous studies have shown that patients with multimodal semantic impairment following CVA--a condition referred to as semantic aphasia (SA)--perform poorly on a range of conceptual tasks due to a failure of executive control following prefrontal and/or temporo-parietal infarction [Jefferies, E.

Elucidating the nature of deregulated semantic cognition in semantic aphasia: evidence for the roles of prefrontal and temporo-parietal cortices.

Semantic cognition--semantically driven verbal and nonverbal behavior--is composed of at least two interactive principal components: conceptual representations and executive control processes that regulate and shape activation within the semantic system. Previous studies indicate that semantic dementia follows from a progressive yet specific degradation of conceptual knowledge. In contrast, multimodal semantic impairment in aphasic patients (semantic aphasia [SA]) reflects damage to the control component of semantic cognition [Jefferies, E.

Different impairments of semantic cognition in semantic dementia and semantic aphasia: evidence from the non-verbal domain.

Disorders of semantic cognition in different neuropsychological conditions result from diverse areas of brain damage and may have different underlying causes. This study used a comparative case-series design to examine the hypothesis that relatively circumscribed bilateral atrophy of the anterior temporal lobe in semantic dementia (SD) produces a gradual degradation of core semantic representations, whilst a deficit of cognitive control produces multi-modal semantic impairment in a subset of patients with stroke aphasia following damage involving the left prefrontal cortex or regions in and around the temporoparietal area; this condition, which transcends traditional aphasia classifications, is referred to as 'semantic aphasia' (SA). There have been very few direct comparisons of these patient groups to date and these previous studies have focussed on verbal comprehension.

Exploring multimodal semantic control impairments in semantic aphasia: evidence from naturalistic object use.

Semantic processing can break down in qualitatively distinct ways in different neuropsychological populations. Previous studies have shown that patients with multimodal semantic impairments following stroke - referred to as semantic aphasia (SA) - show deficits on a range of conceptual tasks due to a failure of semantic control processes in the context of prefrontal and/or temporoparietal infarction. Although a deficit of semantic control would be expected to impair performance in all modalities in parallel, most previous research in this patient group has focussed primarily on tasks employing words.