Impact des altérations de la substance blanche sur la mémoire prospective time-based dans le vieillissement normal : étude en imagerie par tenseur de diffusion

International audienc

Impact des altérations de la substance blanche sur la mémoire prospective time-based dans le vieillissement normal :étude en imagerie par tenseur de diffusion

International audienc

Contribution of funtional and diffusion imaging to better understand the decline of prospective memory in normal aging

International audienc

Brain Substrates of Time-Based Prospective Memory Decline in Aging: A Voxel-Based Morphometry and Diffusion Tensor Imaging Study: Neural substrates of prospective memory decline in aging

International audienceTime-based prospective memory (TBPM) allows us to remember to perform intended actionsat a specific time in the future. TBPM is sensitive to the effects of age, but the neural substrates of thisdecline are still poorly understood. The aim of the present study was thus to better characterize thebrain substrates of the age-related decline in TBPM, focusing on macrostructural gray-matter andmicrostructural white-matter integrity. We administered a TBPM task to 22 healthy young (26 ± 5.2years) and 23 older (63 ± 5.9 years) participants, who also underwent volumetric magnetic resonanceimaging and diffusion tensor imaging scans. Neuroimaging analyses revealed lower gray-mattervolumes in several brain areas in older participants, but these did not correlate with TBPMperformance. By contrast, an age-related decline in fractional anisotropy in several white-matter tractsconnecting frontal and occipital regions did correlate with TBPM performance, while there was nosignificant correlation in healthy young subjects. According to the literature, these tracts are connectedto the anterior prefrontal cortex and the thalamus, two structures involved in TBPM. These resultsconfirm the view that a disconnection process occurs in aging and contributes to cognitive decline

Trimethylamine N-oxide (TMAO) and indoxyl sulfate concentrations in patients with Alcohol Use Disorder

International audienceBackground: Trimethylamine N-oxide (TMAO) and indoxyl sulfate (IS) are produced by the microbiota and the liver, and can contribute to brain aging and impaired cognitive function. This study aims to examine serum TMAO and IS concentrations in patients with alcohol-use disorder (AUD) at the entry for alcohol withdrawal, and the relationships with several biological, neuropsychological, and clinical parameters. Methods: TMAO and IS were quantified in thirty AUD inpatients and fifteen healthy controls (HC). The severities of AUD and alcohol withdrawal syndrome (AWS), and general cognitive abilities were assessed in AUD patients. Results: TMAO concentrations did not differ between HC and AUD patients. Several biomarkers assessing nutritional status and liver function were significantly different in AUD patients with the lowest TMAO concentrations compared to other AUD patients. IS concentration was significantly lower in AUD patients and a significant positive predictor of serum prealbumin variation during the acute phase of alcohol withdrawal. No relationship was observed between the concentrations of these metabo-23 lites and the severities of alcohol dependence, AWS, or cognitive deficits. Conclusions: Our data 24 suggest that AUD patients with low concentrations of TMAO or IS should probably benefit from a 25 personalized refeeding program during the acute phase of alcohol withdrawal

Insular volumetry in severe alcohol use disorder and Korsakoff's syndrome through an anatomical parcellation: Let us go back to basics

International audienceAbstract Functional neuroimaging has demonstrated the key role played by the insula in severe alcohol use disorder (sAUD), notably through its involvement in craving and body signals processing. However, the anatomical counterpart of these functional modifications in sAUD patients with and without neurological complications remains largely unexplored, especially using state‐of‐the‐art parcellation tools. We thus compared the grey matter volume of insular subregions (form anterior to posterior: anterior inferior cortex, anterior short gyrus, middle short gyrus, posterior short gyrus, anterior long gyrus, posterior long gyrus) in 50 recently detoxified patients with sAUD, 19 patients with Korsakoff's syndrome (KS) and 36 healthy controls (HC). We used a mixed linear model analysis to explore group differences in the six subregions grey matter volume and lateralization differences. Insular macrostructure was globally affected to the same extent in sAUD with and without KS, indicating that these brain abnormalities may be related to alcohol consumption per se, rather than to the presence of alcohol‐related neurological complications. Insular atrophy showed a right‐sided lateralization effect and was especially marked in the posterior insula, a region associated with visceral information processing and the embodiment effect of a substance, from which craving arises. Anatomical damages might thus underlie the previously reported altered insular activations and their behavioural counterparts

Insular volumetry in severe alcohol use disorder and Korsakoff's syndrome through an anatomical parcellation: Let us go back to basics

International audienceAbstract Functional neuroimaging has demonstrated the key role played by the insula in severe alcohol use disorder (sAUD), notably through its involvement in craving and body signals processing. However, the anatomical counterpart of these functional modifications in sAUD patients with and without neurological complications remains largely unexplored, especially using state‐of‐the‐art parcellation tools. We thus compared the grey matter volume of insular subregions (form anterior to posterior: anterior inferior cortex, anterior short gyrus, middle short gyrus, posterior short gyrus, anterior long gyrus, posterior long gyrus) in 50 recently detoxified patients with sAUD, 19 patients with Korsakoff's syndrome (KS) and 36 healthy controls (HC). We used a mixed linear model analysis to explore group differences in the six subregions grey matter volume and lateralization differences. Insular macrostructure was globally affected to the same extent in sAUD with and without KS, indicating that these brain abnormalities may be related to alcohol consumption per se, rather than to the presence of alcohol‐related neurological complications. Insular atrophy showed a right‐sided lateralization effect and was especially marked in the posterior insula, a region associated with visceral information processing and the embodiment effect of a substance, from which craving arises. Anatomical damages might thus underlie the previously reported altered insular activations and their behavioural counterparts

DISRUPTION IN NORMAL CORRELATIONAL PATTERNS OF METABOLIC NETWORKS IN THE LIMBIC CIRCUIT DURING TRANSIENT GLOBAL AMNESIA

International audienceAbstract Transient global amnesia is characterized by the sudden apparition of severe episodic amnesia, mainly anterograde, associated with emotional changes. Even though the symptoms are stereotyped, cerebral mechanism underlying transient global amnesia remains unexplained and previous studies using positron emission tomography do not show any clear results or consensus on cerebral regions impacted during transient global amnesia. This study included a group of 10 transient global amnesic patients who underwent 18F-fluorodeoxyglucose positron emission tomography during the acute or recovery phase of the episode and 10 paired healthy controls. Episodic memory was evaluated with the encoding-storage-retrieval paradigm and a story recall test of the Wechsler’s memory scale and anxiety was assessed with the Spielberger scale. We used statistical parametric mapping to identify modifications of whole-brain metabolism. Regarding hypometabolism, there was no brain region systematically affected in all transient global amnesic patients and the comparison between amnesic patients and controls did not show any significant differences. To better understand the specific implication of the limbic circuit in the pathophysiology of transient global amnesia, we then conducted a correlational analysis that included regions of this network. Our findings showed that in healthy controls, regions of the limbic circuit seem to operate in a synchronized way with all regions being highly correlated to each other. On the opposite, in transient global amnesic patients, we observed a clear disruption of this normal correlational patterns between regions with the medial temporal lobe (the hippocampus, parahippocampal gyrus and amygdala) included in one cluster and the orbitofrontal cortex, anterior and posterior cingulate gyrus and thalamus gathered in the other one. Given the individual variability in the time course of transient global amnesia, the direct comparison between a group of patients and controls does not seem to favour the identification of subtle and transient alterations in regional metabolism. The involvement of an extended network, such as the limbic circuit, seems more likely to explain the symptoms of patients. Indeed, the synchronization of regions within the limbic circuit seems to be altered during transient global amnesia, which could explain the amnesia and anxiety observed in transient global amnesic patients. The present study thus deepens our understanding of the mechanisms underlying not only amnesia but also the emotional component of transient global amnesia by considering it as a disruption in the normal correlational patterns within the limbic circuit