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Background: The use of psychoactive substances to neuroenhance cognitive performance is prevalent. Neuroenhancement (NE) in everyday life and doping in sport might rest on similar attitudinal representations, and both behaviors can be theoretically modeled by comparable means-to-end relations (substance-performance). A behavioral (not substance-based) definition of NE is proposed, with assumed functionality as its core component. It is empirically tested whether different NE variants (lifestyle drug, prescription drug, and illicit substance) can be regressed to school stressors.
Findings: Participants were 519 students (25.8 +/- 8.4 years old, 73.1% female). Logistic regressions indicate that a modified doping attitude scale can predict all three NE variants. Multiple NE substance abuse was frequent. Overwhelming demands in school were associated with lifestyle and prescription drug NE.
Conclusions: Researchers should be sensitive for probable structural similarities between enhancement in everyday life and sport and systematically explore where findings from one domain can be adapted for the other. Policy makers should be aware that students might misperceive NE as an acceptable means of coping with stress in school, and help to form societal sensitivity for the topic of NE among our younger ones in general.
SIRT6 is a NAD(+)-dependent deacetylase that modulates chromatin structure and safeguards genomic stability. Until now, SIRT6 has been assigned to the nucleus and only nuclear targets of SIRT6 are known. Here, we demonstrate that in response to stress, C. elegans SIR-2.4 and its mammalian orthologue SIRT6 localize to cytoplasmic stress granules, interact with various stress granule components and induce their assembly. Loss of SIRT6 or inhibition of its catalytic activity in mouse embryonic fibroblasts impairs stress granule formation and delays disassembly during recovery, whereas deficiency of SIR-2.4 diminishes maintenance of P granules and decreases survival of C. elegans under stress conditions. Our findings uncover a novel, evolutionary conserved function of SIRT6 in the maintenance of stress granules in response to stress.