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Objective: To evaluate the behaviour change techniques (BCT) of anxiety-related stand-alone apps accessible to individuals who wish to use apps to assist in the self-management of their anxiety. Methods: Apps that met the inclusion criterion were downloaded and subjected to content analysis. Specific categories were coded using the BCTTv1 (behaviour change technique taxonomy) and the Mobile Application Rating Scale: User version (uMARS). Results: Overall, the reviewed apps included low levels of BCTs, which moderately correlated with app quality. When comparing apps that claimed to facilitate self-management of anxiety symptoms and those which did not, there were no significant differences in the BCT and overall quality between the two groups. Three stand-alone anxiety-related apps were identified as of better quality than the others. They had higher scores on both the level of behaviour change content and overall quality. Conclusions: The BCTTv1 framework was a time efficient method for assessing the behaviour change content of the apps. Implications: The BCTTv1 framework allows psychologists to make evidence-based decisions about the type of anxiety-related stand-alone apps to recommend to their clients.

Abstract An increasing number of rare mutations linked to autism spectrum disorders have been reported in genes encoding for proteins involved in synapse formation and maintenance, such as the post-synaptic cell adhesion proteins neuroligins. Most of the autism-linked mutations in the neuroligin genes map on the extracellular protein domain. The autism-linked substitution R451C in Neuroligin3 (NLGN3) induces a local misfolding of the extracellular domain, causing defective trafficking and retention of the mutant protein in the endoplasmic reticulum (ER). The activation of the unfolded protein response (UPR), due to misfolded proteins accumulating in the ER, has been implicated in pathological and physiological conditions of the nervous system. It was previously shown that the over-expression of R451C NLGN3 in a cellular system leads to the activation of the UPR. Here, we have investigated whether this protective cellular response is detectable in the knock-in mouse model of autism endogenously expressing R451C NLGN3. Our data showed up-regulation of UPR markers uniquely in the cerebellum of the R451C mice compared to WT littermates, at both embryonic and adult stages, but not in other brain regions. Miniature excitatory currents in the Purkinje cells of the R451C mice showed higher frequency than in the WT, which was rescued inhibiting the PERK branch of UPR. Taken together, our data indicate that the R451C mutation in neuroligin3 elicits UPR in vivo , which appears to trigger alterations of synaptic function in the cerebellum of a mouse model expressing the R451C autism-linked mutation. Graphical abstract Unlabelled Image Highlights • In vivo , R451C NLGN3 is partially retained in the ER. • UPR is uniquely detected in the cerebellum of the R451C NLGN3 knock-in mouse • Higher frequency of mEPSCs are found in the Purkinje cells of the R451C mouse • Inhibiting UPR rescues the excitatory functional phenotype in the Purkinje cells • UPR modulates glutamate release in the cerebellum of the R451C NLGN3 mouse model [ABSTRACT FROM AUTHOR]