Biomedical subjects

B Giffard

Publications and source records attributed to B Giffard.

5 recordsLinked to original sources

PubMed2006

[Alzheimer's disease and human memory].

Memory disorders observed in Alzheimer's disease gave rise, from the eighties, to a detailed analysis into the framework of cognitive neuropsychology which aimed at describing the deficits of very specific processes. Beyond their clinical interest, these studies contributed to the modelisation of human memory thanks to the characterization of different memory systems and their relationships. The first part of this paper gives an overview of the memory deficits in Alzheimer's disease and insists on particular cognitive phenomena. Hence, several examples are developed in the domains of semantic memory (such as hyperpriming and hypopriming effects) and autobiographical memory. Recent results highlight the existence of severe autobiographical amnesia observed in all neurodegenerative diseases, though with contrasting profiles: Ribot's gradient in Alzheimer's disease (showing that remote memories are better preserved than recent ones), reverse gradient in semantic dementia and no clear gradient in the frontal variant of frontotemporal dementia. The second part of this article presents advances in cognitive neuroscience searching to disclose the cerebral substrates of these cognitive deficits in Alzheimer's disease. The studies using functional imaging techniques are the most informative regarding this problematic. While showing the dysfunctions of an extended network, they emphasize the selectivity of cerebral damages that are at the root of very specific cognitive dysfunctions, coming close in that way to the conceptions of cognitive neuropsychology. These neuroimaging studies unravel the existence of compensatory mechanisms, which until recently were clearly missing in the literature on neurodegenerative diseases. These different researches lead to a wide conception of human memory, not just limited to simple instrumental processes (encoding, storage, retrieval), but necessarily covering models of identity and continuity of the subject, which interact in a dynamic way with eminently changing memory representations.

Alzheimer Disease↗

PubMed2001

Entorhinal cortex disruption causes memory deficit in early Alzheimer's disease as shown by PET.

Voxel-based mapping of the correlations between cognitive scores and resting-state brain glucose utilization measured by PET has recently emerged as a novel way to reveal in living patients with Alzheimer's disease (AD) the neural systems whose disruption underlies particular neuropsychological, especially mnemonic, deficits. We have now applied this approach using a novel cognitive paradigm designed to selectively assess verbal episodic memory, and show that in early AD disruption of the left entorhinal cortex underlies this memory deficit, consistent with post mortem data showing that this brain area is affected earliest and most severely by tau pathology in AD.

Aged↗

PubMed2001

The nature of semantic memory deficits in Alzheimer's disease: new insights from hyperpriming effects.

While semantic memory deficits are a common landmark of Alzheimer's disease, the nature of these impairments remains to be clarified. Implicit tasks which assess semantic priming effects are often used to understand semantic deficits in Alzheimer's disease, but they have led to unclear conclusions because of methodological problems such as intervention of attentional mechanisms. To explore the effects of semantic priming in Alzheimer's disease and their relationship with semantic memory deficits, we used two tasks, one implicit and the other explicit. The implicit task was a lexical decision task to assess semantic priming, and in which pairs of words had coordinate (tiger-lion) or attribute relationships (zebra-stripe). The explicit task was a semantic knowledge task composed of namings and questions involving superordinate categories and attribute knowledge of concepts. The two tasks systematically assessed the integrity of the same concepts. This protocol was given to 53 Alzheimer's disease patients with mild to moderate dementia and to 20 controls. The Alzheimer's disease group as a whole obtained significantly greater priming effects (hyperpriming) than controls in the coordinate condition, and equivalent priming in the attribute condition. In the coordinate condition, a subgroup of 26 patients, with attribute knowledge deficits, had larger priming effects than both a subgroup without semantic deficits and the control group. These results show that in Alzheimer's disease the semantic priming effects vary according to the degree of attribute loss, and the presence of hyperpriming would reflect semantic memory deficits. This study unravels the fine-grained structure of semantic memory disturbances in Alzheimer's disease with mild to moderate dementia, affecting initially the attributes of concepts within a hierarchical network in which superordinate concepts remain preserved.

Aged↗

PubMed2001

[Contribution of positron emission tomography to functional neuroimaging in Alzheimer's disease].

When combined with cognitive investigations, functional neuroimaging methods such as positron emission tomography allow to depict the neural substrates that underlie the neuropsychological alterations in Alzheimer's disease. Capitalising on the variance in both cognitive performances and resting cerebral metabolic rate of glucose (CMRGlc) in Alzheimer's disease, it is possible to correlate these two quantitative variables on a pixel-by-pixel basis and to generate maps showing the significant correlations in stereotaxic space. Some examples using this approach in the domain of memory disorders are presented in this brief review. We notably show that the localisation of the significant correlations differs from one memory system to another, as evaluated by clinical memory tasks. This approach also unravels the compensatory mechanisms that take place with evolution of the disease. Over and above its interest in clinical neuropsychology, this method constitutes a new source of inferences complementary to the classic activation paradigm in normal subjects, as the latter identifies the cerebral structures that are involved with, but not necessarily indispensable for, the normal execution of the task. This approach highlights the interest of combining functional neuroimaging and neuropsychology to better understand the neural substrates of cognitive deficits in both patients with memory disorders and elderly normal subjects.

Alzheimer Disease↗

PubMedDate not supplied

[Schizophrenia and semantic priming effects].

INTRODUCTION: This article is a review of studies using the semantic priming paradigm to assess the functioning of semantic memory in schizophrenic patients. CONTEXT: Semantic priming describes the phenomenon of increasing the speed with which a string of letters (the target) is recognized as a word (lexical decision task) by presenting to the subject a semantically related word (the prime) prior to the appearance of the target word. This semantic priming is linked to both automatic and controlled processes depending on experimental conditions (stimulus onset asynchrony (SOA), percentage of related words and explicit memory instructions). Automatic process observed with short SOA, low related word percentage and instructions asking only to process the target, could be linked to the "automatic spreading activation" through the semantic network. Controlled processes involve "semantic matching" (the number of related and unrelated pairs influences the subjects decision) and "expectancy" (the prime leads the subject to generate an expectancy set of potential target to the prime). These processes can be observed whatever the SOA for the former and with long SOA for the later, but both with only high related word percentage and explicit memory instructions. LITERATURE FINDINGS: Studies evaluating semantic priming effects in schizophrenia show conflicting results: schizophrenic patients can present hyperpriming (semantic priming effect is larger in patients than in controls), hypopriming (semantic priming effect is lower in patients than in controls) or equal semantic priming effects compared to control subjects. DISCUSSION: These results could be associated to a global impairment of controlled processes in schizophrenia, essentially to a dysfunction of semantic matching process. On the other hand, efficiency of semantic automatic spreading activation process is controversial. These discrepancies could be linked to the different experimental conditions used (duration of SOA, proportion of related pairs and instructions), which influence on the degree of involvement of controlled processes and therefore prevent to really assess its functioning. In addition, manipulations of the relation between prime and target (semantic distance, type of semantic relation and strength of semantic relation) seem to influence reaction times. However, the relation between prime and target (mediated priming) frequently used could not be the most relevant relation to understand the way of spreading of activation in semantic network in patients with schizophrenia. Finally, patients with formal thought disorders present particularly high priming effects relative to controls. CONCLUSION: These abnormal semantic priming effects could reflect a dysfunction of automatic spreading activation process and consequently an exaggerated diffusion of activation in the semantic network. In the future, the inclusion of different groups schizophrenic subjects could allow us to determine whether semantic memory disorders are pathognomonic or specific of a particular group of patients with schizophrenia.

Cerebral Cortex↗