Performing a goal-directed movement consists of a chain of complex preparatory mechanisms. Such planning requires especially integration (or binding) of various action features, a process that has been conceptualized in the "Theory of Event Coding". Theoretical considerations and empirical research suggest that these processes are subject to developmental effects from adolescence to adulthood. The aim of the current study is to investigate age-related modulations in action feature binding processes and to shed light on underlying neurophysiological development from pre-adolescence to early adulthood. We examined a group of healthy participants (n = 61) between 10 and 30 years of age, who performed a task which requires a series of bimanual response selections in an embedded paradigm. For an in-depth analysis of the underlying neural correlates, we applied EEG signal decomposition together with source localization analyses. Behavioural results across the whole group did not show binding effects in reaction times but in intra-individual response variability. From age ten to thirty, there was a decrease in reaction times and reaction time variability, but no age-related effect in action file binding. The latter were corroborated by Bayesian data analyses. On the brain level, the developmental effects on response selection were associated with activation modulations in the superior parietal cortex (BA7). The results show that mechanisms of action execution and speed, but not those of action feature binding, are subject to age-related changes between the age of 10 and 30 years.

Highlights Neurophysiology of developmental effects in event file coding is examined. Two distinct neurophysiological processes underlie developmental effects. Both processes are associated with the superior parietal cortex (BA7).

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In a large proportion of individuals with fronto-temporal lobar degeneration (FTLD), the underlying pathology is associated with the misfolding and aggregation of the microtubule associated protein tau (FTLD-tau). With disease progression, widespread protein accumulation throughout cortical and subcortical brain regions may be responsible for neurodegeneration. One of the syndromes of FTLD is the behavioral variant of frontotemporal dementia (bvFTD), in which the underlying pathology is heterogenous, with half of the cases being related to FTLD-tau. Currently, there are no approved disease-modifying treatments for FTLD-tau, therefore representing a major unmet therapeutic need. These descriptive, preliminary findings of the phase 1 open-label trial provide data to support the potential of sodium selenate to halt the cognitive and behavioral decline, as well as to reduce tau levels in a small group of participants with bvFTD (N = 11). All participants were treated with sodium selenate over a period of 52 weeks. Cognition was assessed with the Neuropsychiatry Unit Cognitive Assessment Tool (NUCOG, total scores), social cognition with the Revised Self-Monitoring Scale (RSMS, total scores), behavior with the Cambridge Behavioral Inventory (CBI), and carer burden with the Caregiver Buden Scale (CBS). Fluid biomarker measures include cerebrospinal fluid of total tau (t-tau), phosphorylated tau (p-tau181), NfL, p-tau181/t-tau, t-tau/Aβ1–42, and p-tau181/Aβ1–42 levels. After treatment at follow-up, cognition and behavior showed further negative change (based on a reliable change criterion cut-off of annual NUCOG decline) in the “progressors,” but not in the “non-progressors.” “Non-progressors” also showed elevated baseline CSF tau levels and no increase after treatment, indicating underlying tau pathology and a positive response to sodium selenate treatment. Significant changes in MRI were not observed. The findings provide useful information for future clinical trials to systematically assess the disease-modifying treatment effects of sodium selenate in randomized controlled designs for bvFTD and FTLD-tau pathologies.