Different underlying mechanisms for deficits in concept formation in dementia

Abstract

We investigated the different mechanisms that may underlie deficits in verbal concept formation among patients with Alzheimer's disease (AD) and ischaemic vascular dementia (IVD) associated with periventricular and deep white matter alterations. Concept formation was assessed with the WAIS-R Similarities subtest (SIM). Two types of errors were re-coded from the 0-point responses as scored by the WAIS-R manual. In set errors (e.g., dog-lion "they're alive") were coded when patients reported a very vague superordinate concept for the word pair. Out of set responses (e.g., dog-lion "the lion roars and the dog barks") were coded when a response was clearly out of mental set, i.e., when participants were unable to provide a superordinate concept for the word pair. Between-group comparisons demonstrated no difference in SIM test performance according to the scoring system described in the WAIS-R manual. Nonetheless, AD patients produced a greater proportion of in set errors, while IVD patients produced a greater proportion of out of set errors. Out of set errors were highly associated with measures of executive function, while in set errors were associated with measures related to delayed recognition memory and semantic intrusion errors. We conclude that the underlying deficits that contribute to poor concept formation differ between AD and IVD patients. In IVD impaired concept formation is related to deficits in the executive systems necessary to monitor responses and sustain mental set. In AD, by contrast, the deficit appears to be secondary to impaired verbal response selection.

Everyday action in dementia: Evidence for differential deficits in Alzheimer's diseaseversussubcortical vascular dementia

“…AD is characterized by amyloid plaques and neurofibrillary tangles distributed in the entorhinal cortex, hippocampus, and association cortex (Murayama & Saito, 2004). This pathology has been linked to deficits in declarative systems, particularly episodic memory (Libon et al, 1996) and semantic knowledge (Giovannetti et al, 1997(Giovannetti et al, , 2001Saffran & Schwartz, 1994). Executive deficits are often present, but are not considered the primary impairment (Knopman & Selnes, 2003).…”

Alterations in working memory as a function of leukoaraiosis in dementia

“…This result suggests that High LA participants' impaired mental manipulation within working memory may be due, in part, to being unable to disengage from or inhibit over-learned and automatic procedural memories (Lamar et al, 1997;Stuss et al, 1995). Across several neuropsychological tests, the production of capture errors has been associated with a combination of higher order executive dysfunction as well as lower level disinhibition of more automatic behaviors (Giovannetti et al, 2001;. Furthermore, across a variety of paradigms, capture errors have been associated with frontal lobe damage (Della Malva, Stuss, D'Alton, & Willmer, 1993;Reverberi, Lavaroni, Gigli, Skrap, & Shallice, 2005).…”

“…The cognitive and executive dysfunction associated with LA may be induced by corticalsubcortical and cortical-cortical disconnections (Catani & ffytche, 2005). Previous work in our laboratory suggests that pervasive executive dysfunction seen in dementia (e.g., deficits encompassing both higher-level and more basic executive skills), may be associated with pervasive disease-related neuropathology affecting afferent and efferent connections linking the prefrontal cortices with other areas of brain involved in these processes (Freeman et al, 2000;Giovannetti et al, 2001;Lamar et al, 1997;Lamar, Swenson, Kaplan, & Libon, 2004). This theory, based on the work of Luria (1980) and Goldberg and Bilder (1987), does not require frank frontal lobe lesions for the manifestation of varying levels of executive dysfunction in dementia despite the fact that specific aspects of executive dysfunction such as working memory have been ascribed to regions within the prefrontal cortex.…”

“A mosquito bites and a butterfly flies": a specific response type of frontal patients in a similarity task

“…The proportion of concrete similarity responses was similar in both patient groups (AD and frontal patients), and was therefore nonspecific as to the neurodegenerative disease. Various mechanisms may explain these responses: deficit in abstract thinking abilities (Garcin et al, 2012), impaired semantic knowledge (T Giovannetti et al, 2001) and deficits in response selection (T Giovannetti et al, 2001). The mechanisms explaining concrete similarities errors may differ in frontal patients and AD, and their neural substrate have to be determined.…”

“…However, the reasons why frontal patients present with categorization difficulties are not well understood. Categorization is a complex neurocognitive function, relying on semantic knowledge and executive functions (T Giovannetti et al, 2001), including similarity detection in objects that are physically different, abstraction, and response selection according to the rule (Garcin, Volle, Dubois, & Levy, 2012). Each of these processes may contribute to the deficit and lead to distinct types of categorization problems.…”