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Individuals with alcohol use disorder (AUD) show elevated brain metabolism of acetate at the expense of glucose. We hypothesized that a shift in energy substrates during withdrawal may contribute to withdrawal severity and neurotoxicity in AUD and that a ketogenic diet (KD) may mitigate these effects. We found that inpatients with AUD randomized to receive KD (n = 19) required fewer benzodiazepines during the first week of detoxification, in comparison to those receiving a standard American (SA) diet (n = 14). Over a 3-week treatment, KD compared to SA showed lower “wanting” and increased dorsal anterior cingulate cortex (dACC) reactivity to alcohol cues and altered dACC bioenergetics (i.e., elevated ketones and glutamate and lower neuroinflammatory markers). In a rat model of alcohol dependence, a history of KD reduced alcohol consumption. We provide clinical and preclinical evidence for beneficial effects of KD on managing alcohol withdrawal and on reducing alcohol drinking.

Task switching is regularly required in our everyday life. To succeed in switching, it is important to inhibit the most recently performed task and instead activate the currently relevant task. The process that inhibits a recently performed task when a new task is to be performed is referred to as 'backward inhibition' (BI). While the BI effect has been subject to intense research in cognitive psychology, little is known about the neuronal mechanisms that are related to the BI effect and those that relate to differences in the magnitude of the BI effect. In the current study, we examined the system neurophysiological basis of BI processes using event-related potentials (ERPs) and sLORETA by also taking inter-individual differences in the magnitude of the BI into account. The results suggest that BI processes and inter-individual differences in them strongly depend upon attentional selection mechanisms (reflected by N1-ERP modulations in the current task/trial) mediated via networks consisting of extrastriate occipital areas, the temporo-parietal junction and the inferior frontal gyrus. Other processes and mechanisms related to conflict monitoring, response selection, or the updating, organization and implementation of a new task-set (i.e. N2 and P3 processes) were not shown to be modulated by BI processes and differences in their magnitude, as evoked with a common BI paradigm.

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Study Objectives Sleep deprivation and circadian disruptions impair brain function and cognitive performance, but few studies have examined the effect of sleep inconsistency. Here, we investigated how inconsistent sleep duration and sleep timing between weekends (WE) and weekdays (WD) correlated with changes in behavior and brain function during task and at rest in 56 (30 female) healthy human participants. Methods WE–WD differences in sleep duration and sleep midpoint were calculated using 1-week actigraphy data. All participants underwent 3 Tesla blood-oxygen-level-dependent functional Magnetic Resonance Imaging (fMRI) to measure brain activity during a visual attention task (VAT) and in resting-state condition. Results We found that WE–WD inconsistency of sleep duration and sleep midpoint were uncorrelated with each other (r = .08, p = .58) and influenced behavior and brain function differently. Our healthy participants showed relatively small WE–WD differences (WE–WD: 0.59 hours). Longer WE sleep duration (relative to WD sleep duration) was associated with better attentional performance (3-ball: β = .30, t = 2.35, p = .023; 4-ball: β = .30, t = 2.21, p = .032) and greater deactivation of the default mode network (DMN) during VAT (p < .05, cluster-corrected) and greater resting-state functional connectivity (RSFC) between anterior DMN and occipital cortex (p < .01, cluster-corrected). In contrast, later WE sleep timing (relative to WD sleep timing) (WE–WD: 1.11 hours) was associated with worse performance (4-ball: β = −.33, t = −2.42, p = .020) and with lower occipital activation during VAT and with lower RSFC within the DMN. Conclusions Our results document the importance of consistent sleep timing for brain function in particular of the DMN and provide evidence of the benefits of WE catch-up sleep in healthy adults.

Cognitive flexibility is a major facet of executive functions and often refers to sequential task control; that is, it is very likely that one may re‐encounter a task that has previously been abandoned to carry out a different task. In the context of sequential cognitive flexibility, the “backward inhibition (BI) effect” has been studied quite extensively. Here we ask whether there are age‐related differences between adolescents and adults to overcome BI and what system‐neurophysiological mechanisms underlie these modulations. This was examined using a system neurophysiological study procedure combining event‐related potentials data with source localization and EEG signal decomposition methods. We show that sequential cognitive flexibility, and the ability overcome backward inhibition, is inferior in adolescents compared with adults. Accounting for intra‐individual variability in the neurophysiological data, this data suggest that two partly inter‐related processes underlie the differences between adolescents than adults to overcome backward inhibition: One process refers to the suppression of the inhibitory effect of the n‐1 trial on the n‐2 trial during perceptual categorization of incoming information that is associated with right inferior frontal regions. The other process refers to immature response selection and conflict monitoring mechanisms associated with regions in the medial frontal cortex.

Neurobiological markers of stress symptom progression for healthy survivors from a disaster (e.g., an earthquake) would greatly help with early intervention to prevent the development of stress-related disorders. However, the relationship between the neurobiological alterations and the symptom progression over time is unclear. Here, we examined 44 healthy survivors of the Wenchuan earthquake in China in a longitudinal resting-state fMRI study to observe the alterations of brain functions related to depressive or anxiety symptom progression. Using multi-variate pattern analysis to the fMRI data, we successfully predicted the depressive or anxiety symptom severity for these survivors in short- (25 days) and long-term (2 years) and the symptom severity changes over time. Several brain areas (e.g., the frontolimbic and striatal areas) and the functional connectivities located within the fronto-striato-thalamic and default-mode networks were found to be correlated with the symptom progression and might play important roles in the adaptation to trauma.