Connectivity between the amygdala, insula (Amygdala-aI) and ventral medial prefrontal cortex (Amygdala-vmPFC) have been implicated in individual variability in fear and vulnerability to psychiatric disorders. However, it is currently unknown to what extent connectivity between these regions in the newborn period is relevant for the development of fear and other aspects of negative emotionality (NE), such as sadness. Here, we investigate newborn Am-Ins and Am-vmPFC resting state functional connectivity in relation to developmental trajectories of fear and sadness over the first two years of life using data from the Infant Behavior Questionnaire Revised (IBQ-R) and Early Childhood Behavior Questionnaire (ECBQ) (N=62). Stronger newborn amygdala connectivity predicts higher fear and sadness at 6-months-of-age and less change from 6 to 24-months-of-age. Interestingly, Am-Ins connectivity was specifically relevant for fear and not sadness, while Am-vmPFC was associated only with sadness. Associations remained consistent after considering variation in maternal sensitivity and maternal postnatal depressive symptomology. Already by the time of birth, individual differences in amygdala connectivity are relevant for the expression of fear over the first two-years-of-life. Additionally, specificity is observed, such that connections relevant for fear development are distinct from those predicting sadness trajectories.
The gut microbiota emerged as a potential modulator of brain connectivity in health and disease. This systematic review details current evidence on the gut-brain axis and its influence on brain connectivity. The initial set of studies included 532 papers, updated to January 2024.
Co-activation of distinct brain areas provides a valuable measure of functional interaction, or connectivity, between them. One well-validated way to investigate the co-activation patterns of a precise area is meta-analytic connectivity modeling (MACM), which performs a seed-based meta-analysis on task-based functional magnetic resonance imaging (task-fMRI) data. While MACM stands as a powerful automated tool for constructing robust models of whole-brain human functional connectivity, its inherent limitation lies in its inability to capture the distinct interrelationships among multiple brain regions.
Caloric depletion leads to behavioral changes that help an animal find food and restore its homeostatic balance. Hunger increases exploration and risk-taking behavior, allowing an animal to forage for food despite risks; however, the neural circuitry underlying this change is unknown. Here, we characterize how hunger restructures an animal's spontaneous behavior as well as its directed exploration of a novel object.
Department of Neurology, Oregon Health & Science University, Portland, OR, United States; APDM Precision Motion, Clario, Portland, Oregon, United States. Electronic address:
Fatigue in people with Multiple Sclerosis (PwMS) is a poorly understood, complex, and disabling symptom. We hypothesized that the perception of fatigue in PwMS results from increased information processing in cortical areas responsible for the perception of bodily states and decreased information processing in the cortico-basal ganglia network involved in the perception of motor performance. We investigated whether PwMS who perceive excessive fatigue would have increased resting-state functional connectivity (rsFC) between interoceptive brain areas (amygdala, anterior cingulate cortex [ACC], and insula) and decreased rsFC between cortico-basal ganglia premotor network compared to PwMS not reporting fatigue.
Background: The co-occurrence of metabolic dysfunction and neurodegenerative diseases suggests a genetic link, yet the shared genetic architecture and causality remain unclear. We aimed to comprehensively characterise these genetic relationships.
Methods: We investigated genetic correlations among four neurodegenerative diseases and seven metabolic dysfunctions, followed by bidirectional Mendelian randomisation (MR) to assess potential causal relationships.
