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Background: Social restrictions and vaccination seem to have shaped the pandemic development in Europe, but the influence of geographical position is still debated. This study aims to verify whether the pandemic spread through Europe following a particular direction, during the period between the start of the pandemic and November 2021. The existence of a spatial gradient for epidemic intensity is also hypothesized. Methods: Daily COVID-19 epidemiological data were extracted from Our World in Data COVID-19 database, which also included vaccination and non-pharmacological interventions data. Latitude and longitude of each country's centroid were used as geographic variables. Epidemic periods were delimited from epidemic surge data. Multivariable linear and Cox's regression models were performed for each epidemic period to test if geographical variables influenced surge dates. Generalized additive models (GAM) were used to test the spatial gradient hypothesis with three epidemic intensity measures. Results: Linear models suggest a possible west-east shift in the first epidemic period and features a significant association of NPIs with epidemic surge delay. Neither latitude nor longitude had significant associations with epidemic surge timing in both second and third periods. Latitude displays strong negative associations with all epidemic intensity measures in GAM models. Vaccination was also negatively associated with intensity. Conclusions: A longitudinal spread of the pandemic in Europe seems plausible, particularly concerning the first wave. However, a recurrent trend was not observed. Southern Europe countries may have experienced increased transmissibility and incidence, despite climatic conditions apparently unfavourable to the virus. [ABSTRACT FROM AUTHOR]

Abstract: Previous studies have associated Attention‐Deficit/Hyperactivity Disorder (ADHD) with a maturational lag of brain functional networks. Functional connectivity of the human brain changes from primarily local to more distant connectivity patterns during typical development. Under the maturational lag hypothesis, we expect children with ADHD to exhibit increased local connectivity and decreased distant connectivity compared with neurotypically developing (ND) children. We applied a graph‐theory method to compute local and distant connectivity levels and cross‐sectionally compared them in a sample of 120 children with ADHD and 120 age‐matched ND children (age range = 7–17 years). In addition, we measured if potential group differences in local and distant connectivity were stable across the age range considered. Finally, we assessed the clinical relevance of observed group differences by correlating the connectivity levels and ADHD symptoms severity separately for each group. Children with ADHD exhibited more local connectivity than age‐matched ND children in multiple brain regions, mainly overlapping with default mode, fronto‐parietal and ventral attentional functional networks (p < .05‐ threshold free‐cluster enhancement–family‐wise error). We detected an atypical developmental pattern of local connectivity in somatomotor regions, that is, decreases with age in ND children, and increases with age in children with ADHD. Furthermore, local connectivity within somatomotor areas correlated positively with clinical severity of ADHD symptoms, both in ADHD and ND children. Results suggest an immature functional state of multiple brain networks in children with ADHD. Whereas the ADHD diagnosis is associated with the integrity of the system comprising the fronto‐parietal, default mode and ventral attentional networks, the severity of clinical symptoms is related to atypical functional connectivity within somatomotor areas. Additionally, our findings are in line with the view of ADHD as a disorder of deviated maturational trajectories, mainly affecting somatomotor areas, rather than delays that normalize with age. [ABSTRACT FROM AUTHOR]

Neuronal failure leading to dementia in neurodegenerative diseases is evidenced in vivo by functional and structural changes in the brain such as reductions of glucose consumption and volume of grey matter. The earliest phase of cognitive decline and presymptomatic stages of these diseases are heralded by specific patterns of hypometabolism, even in the absence of atrophy, which are currently considered as diagnostic biomarkers. Atrophy is less consistently found as an initial marker of these diseases and is invariably present in moderate to severe stages with a disease-related topography. The relationship between these two markers is not uniform, but in the two diseases in which they have been directly compared, Alzheimer's and Parkinson's disease, altered hypometabolism precedes and exceeds atrophy in most regions. This suggests a two-step degenerative process. In contrast to these findings, the hippocampus skips this pattern and is more structurally than functionally affected, thereby suggesting a different pathological mechanism in this particular area. More studies are needed to disentangle the mechanisms underlying both markers and their relationship in neurodegenerative diseases. [ABSTRACT FROM AUTHOR]