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In Alzheimer's disease (AD), brain atrophy has been proposed to be left lateralized. Here, we reinvestigated the asymmetry and lateralization (i.e., asymmetry directed toward one hemisphere) of grey-matter (GM) distribution in 35 patients with AD, 24 patients with amnestic mild cognitive impairment (aMCI, a state of increased risk for AD), and 30 age-matched healthy controls (HC). We analyzed GM distribution by applying voxel-based morphometry (VBM) including analyses for asymmetry and lateralization. When comparing MCI with AD patients, VBM revealed GM loss in the entorhinal, temporoparietal, dorsofrontal, and occipital cortices as well as in the precuneus; when comparing HCs with MCI patients, we found similar differences, which were less pronounced especially within the temporoparietal cortex and precuneus. Analyses of regional asymmetry and regional lateralization as well as global lateralization did not yield significant results. However, lobar asymmetry of the temporal, parietal, and occipital lobes increased from HC to AD. Moreover, in aMCI and AD patients, performance of language-based neuropsychological tests correlated with lateralization of GM loss to the left hemisphere. We conclude that, in principle, brain atrophy in AD is asymmetric rather than lateralized. At the individual level however, asymmetry contributes to cognitive deficits.

Background: In MS, the relationship between lesions within cerebral white matter (WM) and atrophy within deep gray matter (GM) is unclear. Objective: To investigate the spatial relationship between WM lesions and deep GM atrophy. Methods: We performed a cross-sectional structural magnetic resonance imaging (MRI) study (3 Tesla) in 249 patients with clinically-isolated syndrome or relapsing-remitting MS (Expanded Disability Status Scale score: median, 1.0; range, 0-4) and in 49 healthy controls. Preprocessing of T1-weighted and fluid-attenuated T2-weighted images resulted in normalized GM images and WM lesion probability maps. We performed two voxel-wise analyses: 1. We localized GM atrophy and confirmed that it is most pronounced within deep GM; 2. We searched for a spatial relationship between WM lesions and deep GM atrophy; to this end we analyzed WM lesion probability maps by voxel-wise multiple regression, including four variables derived from maxima of regional deep GM atrophy (caudate and pulvinar, each left and right). Results: Atrophy of each deep GM region was explained by ipsilateral WM lesion probability, in the area most densely connected to the respective deep GM region. Conclusion: We demonstrated that WM lesions and deep GM atrophy are spatially related. Our results are best compatible with the hypothesis that WM lesions contribute to deep GM atrophy through axonal pathology.

UCCA is mainly determined by brain volume as well as by WM content of cerebrospinal tracts.

Genetics of the variability of normal and diseased brain structure largely remains to be elucidated. Expansions of certain trinucleotide repeats cause neurodegenerative disorders of which Huntington's disease constitutes the most common example. Here, we test the hypothesis that variation within the IT15 gene on chromosome 4, whose expansion causes Huntington's disease, influences normal human brain structure. In 278 normal subjects, we determined CAG repeat length within the IT15 gene on chromosome 4 and analyzed high-resolution T1-weighted magnetic resonance images by the use of voxel-based morphometry. We found an increase of GM with increasing long CAG repeat and its interaction with age within the pallidum, which is involved in Huntington's disease. Our study demonstrates that a certain trinucleotide repeat influences normal brain structure in humans. This result may have important implications for the understanding of both the healthy and diseased brain.

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Introduction Previous research has found that emotionally intense stimuli are better remembered than neutral stimuli, especially after a period of sleep. However, few studies have examined memory for experienced emotional events, especially fearful ones. The purpose of the current study was to investigate the impact of sleep on memory consolidation using a fearful emotion induction task. Methods Thirty-three young adults (18.94±1.06 years; 64% female) were randomly assigned to either a fearful or neutral emotion induction condition. Participants were induced into their assigned emotion by visualizing each of eight emotion-congruent scenarios while corresponding music played in the background. Emotional state was measured using the Affect Grid before and after the emotion induction procedure. Twelve hours later, spanning either a day of wakefulness (wake group) or night of sleep (sleep group), participants were asked to recall the previously presented scenarios. Results A 2 x 2 ANOVA examined differences in the number of scenarios recalled between the conditions. A significant main effect of sleep was found, F(1,29)=8.41, p=.007, η 2p=.23, reflecting better recall in the sleep (3.21±1.78) vs. the wake group (1.79±1.72). There was also a main effect of emotion, F(1,29)=22.17, p<.001, η 2p=.43, reflecting better recall in the fear (3.58±1.54) vs. the neutral condition (1.29±1.44). However, there was no interaction. Results were similar for the number of details recalled between the conditions. The sleep group (12.74±9.09) recalled more details than the wake group (5.50±5.81), F(1,29)=8.05, p=.008, η 2p=.22. More details were also recalled in the fear condition (13.16±8.73) than the neutral condition (4.93±5.77), F(1,29)=10.54, p=.003, η 2p=.27. There was again no interaction. Conclusion Results demonstrate that both sleep and fearful emotion facilitate memory consolidation. This work both supports and extends existing research by examining emotional memory consolidation through the manipulation of experienced events, which may more closely approximate real world learning than previous methods. Support N/A