Several studies have examined the neural effects of working memory practice, but due to different task demands, diverse patterns of neural changes have been reported. In the present study, we... Show moreSeveral studies have examined the neural effects of working memory practice, but due to different task demands, diverse patterns of neural changes have been reported. In the present study, we examined neural effects of practice using a task with different working memory demands within a single practice paradigm. Fifteen adults practiced during 6 weeks with a task that required maintenance and manipulation of information under low and high working memory loads. Functional magnetic resonance imaging (FMRI) data were acquired in the first week and last week of the practice period. Results were compared with results of a control group who did not practice the task. We demonstrated that practice was beneficial for both working memory maintenance and manipulation processes but that these processes were supported by different neural changes. While maintenance trials showed increased activation (i.e., less deactivation) in default-mode regions after practice, manipulation trials experienced increased activation in the striatum. Changes were also observed in left ventrolateral prefrontal cortex (VLPFC), bilateral dorsolateral prefrontal cortex (DLPFC) and left superior parietal cortex (SPC). However, for bilateral DLPFC and left SPC, these changes were not specific to the practice group. These findings illustrate the importance of controlling for test-retest effects in training or intervention studies. Behavioral follow-up tests demonstrated that practice effects lasted over a 6-month period, but the absence of transfer effects indicated that the acquired skills were specific for the practiced working memory task. (C) 2010 Elsevier Inc. All rights reserved. Show less
The altered iron concentration in many neurodegenerative diseases such as Alzheimer's disease (AD) has led to the development of MRI sequences that are sensitive to the accompanying changes in the... Show moreThe altered iron concentration in many neurodegenerative diseases such as Alzheimer's disease (AD) has led to the development of MRI sequences that are sensitive to the accompanying changes in the transverse relaxation rate. Heavily T-2*-weighted imaging sequences at high magnetic field strength (7 T and above), in particular, show potential for detecting small changes in iron concentration. However, these sequences require a long echo time in combination with a long scanning time for high resolution and are therefore prone to image artifacts caused by physiological fluctuations, patient motion or system instabilities. Many groups have found that the high image quality that was obtained using high resolution T-2*-weighted sequences at 7 T in healthy volunteers, could not be obtained in AD patients. In this study the source of the image artifacts was investigated in phantom and in healthy volunteer experiments by incorporating movement parameters and resonance frequency (f0) variations which were measured in AD patients. It was found that image degradation caused by typical f0 variations was a factor-of-four times larger than artifacts caused by movement characteristic of AD patients in the scanner. In addition to respiratory induced f0 variations, large jumps in the f0 were observed in AD patients. By implementing a navigator echo technique to correct for f0 variations, the image quality of high resolution T-2*-weighted images increased considerably. This technique was successfully applied in five AD patients and in five subjective memory complainers. Visual scoring showed improvements in image quality in 9 out of 10 subjects. Ghosting levels were reduced by 24 +/- 13%. (C) 2010 Elsevier Inc. All rights reserved. Show less
Zarei, M.; Patenaude, B.; Damoiseaux, J.; Morgese, C.; Smith, S.; Matthews, P.M.; ... ; Jenkinson, M. 2010
Recent models hypothesize that adolescents' risky behavior is the consequence of increased sensitivity to rewards in the ventral medial (VM) prefrontal cortex (PFC) and the ventral striatum (VS),... Show moreRecent models hypothesize that adolescents' risky behavior is the consequence of increased sensitivity to rewards in the ventral medial (VM) prefrontal cortex (PFC) and the ventral striatum (VS), paired with immature cognitive control abilities due to slow maturation of the dorsal anterior cingulate cortex (ACC) and lateral PFC. We tested this hypothesis with fMRI using a gambling task in which participants chose between Low-Risk gambles with a high probability of obtaining a small reward (1 Euro) and High-Risk gambles with a smaller probability of obtaining a higher reward (2, 4, 6, or 8 Euro). We examined neural responses during choice selection and outcome processing in participants from 4 age groups (pre-pubertal children, early adolescents, older adolescents and young adults). High-Risk choices increased with rewards for all ages, but risk-taking decreased with age for low reward gambles. The fMRI results confirmed that High-Risk choices were associated with activation in VMPFC, whereas Low-Risk choices were associated with activation in lateral PFC. Activation in dorsal ACC showed a linear decrease with age, whereas activation in VMPFC and VS showed an inverted U-shaped developmental pattern, with a peak in adolescence. In addition, behavioral differences in risk-taking propensity modulated brain activation in all age groups. These findings support the hypothesis that risky behavior in adolescence is associated with an imbalance caused by different developmental trajectories of reward and regulatory brain circuitry. (C) 2010 Elsevier Inc. All rights reserved. Show less
Zarei, M.; Patenaude, B.; Damoiseaux, J.; Morgese, C.; Smith, S.; Matthews, P.M.; ... ; Jenkinson, M. 2010
Alzheimer's disease (AD) is associated with neuronal loss not only in the hippocampus and amygdala but also in the thalamus. Anterodorsal, centromedial, and pulvinar nuclei are the main sites of... Show moreAlzheimer's disease (AD) is associated with neuronal loss not only in the hippocampus and amygdala but also in the thalamus. Anterodorsal, centromedial, and pulvinar nuclei are the main sites of degeneration in AD. Here we combined shape analysis and diffusion tensor imaging (DTI) tractography to study degeneration in AD in the thalamus and its connections. Structural and diffusion tensor MRI scans were obtained from 16 AD patients and 22 demographically similar healthy Volunteers. The thalamus, hippocampus, and amygdala were automatically segmented using our locally developed algorithm, and group comparisons were carried out for each Surface vertex. We also employed Probabilistic diffusion tractography to obtain connectivity measures between individual thalamic voxels and hippocampus/amygdala voxels and to segment the internal medullary lamina (IML). Shape analysis showed significant bilateral regional atrophy in the dorsal-medial part of the thalamus in AD patients compared to controls. Probabilistic tractography demonstrated that these regions are mainly connected with the hippocampus, temporal, and prefrontal cortex. Intrathalamic FA comparisons showed reductions in the anterodorsal region of thalamus. Intrathalamic tractography from this region revealed that the IML was significantly smaller in AD patients than in controls. We suggest that these changes can be attributed to the degeneration of the anterodorsal and intralaminar nuclei, respectively. In addition, based on previous neuropathological reports, ventral and dorsal-medial shape change in the thalamus in AD patients is likely to be driven by IML atrophy. This combined shape and connectivity analysis provides MRI evidence of regional thalamic degeneration in AD. (c) 2009 Elsevier Inc. All rights reserved. Show less
Cremers, H.R.; Demenescu, L.R.; Aleman, A.; Renken, R.; Tol, M.J. van; Wee, N.J.A. van der; ... ; Roelofs, K. 2010
Neuroticism is associated with the experience of negative affect and the development of affective disorders. While evidence exists for a modulatory role of neuroticism on task induced brain... Show moreNeuroticism is associated with the experience of negative affect and the development of affective disorders. While evidence exists for a modulatory role of neuroticism on task induced brain activity, it is unknown how neuroticism affects brain connectivity, especially the crucial coupling between the amygdala and the prefrontal cortex. Here we investigate this relation between functional connectivity and personality in response to negative facial expressions. Sixty healthy control participants, from the Netherlands Study on Depression and Anxiety (NESDA), were scanned during an emotional faces gender decision task. Activity and functional amygdala connectivity (psycho-physiological interaction [PPI]) related to faces of negative emotional valence (angry, fearful and sad) was compared to neutral facial expressions, while neuroticism scores were entered as a regressor. Activity for fearful compared to neutral faces in the dorsomedial prefrontal (dmPFC) cortex was positively correlated with neuroticism scores. PPI analyses revealed that right amygdala-dmPFC connectivity for angry and fearful compared to neutral faces was positively correlated with neuroticism scores. In contrast, left amygdala-anterior cingulate cortex (ACC) connectivity for angry, fearful and sad compared to neutral faces was negatively related to neuroticism levels. DmPFC activity has frequently been associated with self-referential processing in social cognitive tasks. Our results therefore suggest that high neurotic participants display stronger self-referential processing in response to negative emotional faces. Second, in line with previous reports on ACC function, the negative correlation between amygdala-ACC connectivity and neuroticism scores might indicate that those high in neuroticism display diminished control function of the ACC over the amygdala. These connectivity patterns might be associated with vulnerability to developing affective disorders such as depression and anxiety. (C) 2009 Elsevier Inc. All rights reserved. Show less
