Salivary α-amylase as a marker of stress reduction in individuals with intellectual disability and autism in response to occupational and music therapy.

BACKGROUND: Although the benefits of a range of disability-centric therapies have been well studied, little remains known about how they work, let alone how to monitor these benefits in a precise and reliable way. METHODS: Here, in two independent studies, we examine how sessions consisting of occupational or music therapy, both widely recognised for their effectiveness, modulate levels of salivary α-amylase (sAA), a now time- and cost-efficient marker of stress, in individuals with intellectual disability and autism spectrum disorder. Pre-session and post-session levels of sAA were compared in both groups in response to therapy and control sessions. RESULTS: In comparison to control sessions, occupational therapy significantly dampened rises in sAA levels while music therapy significantly decreased baseline sAA levels, highlighting the ability of both types of therapy to reduce stress and by proxy contribute to enhancing overall well-being. CONCLUSIONS: Not only do these results confirm the stress-reducing nature of two types of multisensory therapy, but they support the use of sAA as a potential tool for evaluating stress levels in individuals with intellectual disability and autism spectrum disorder, providing an important physiological lens that may guide strategies in clinical and non-clinical care for individuals with disabilities.

Parenting Stress Undermines Mother-Child Brain-to-Brain Synchrony: A Hyperscanning Study.

Synchrony refers to the coordinated interplay of behavioural and physiological signals that reflect the bi-directional attunement of one partner to the other's psychophysiological, cognitive, emotional, and behavioral state. In mother-child relationships, a synchronous pattern of interaction indicates parental sensitivity. Parenting stress has been shown to undermine mother-child behavioural synchrony. However, it has yet to be discerned whether parenting stress affects brain-to-brain synchrony during everyday joint activities. Here, we show that greater parenting stress is associated with less brain-to-brain synchrony in the medial left cluster of the prefrontal cortex when mother and child engage in a typical dyadic task of watching animation videos together. This brain region overlaps with the inferior frontal gyrus, the frontal eye field, and the dorsolateral prefrontal cortex, which are implicated in inference of mental states and social cognition. Our result demonstrates the adverse effect of parenting stress on mother-child attunement that is evident at a brain-to-brain level. Mother-child brain-to-brain asynchrony may underlie the robust association between parenting stress and poor dyadic co-regulation. We anticipate our study to form the foundation for future investigations into mechanisms by which parenting stress impairs the mother-child relationship.

Epitope mapping of CCR5 reveals multiple conformational states and distinct but overlapping structures involved in chemokine and coreceptor function.

The chemokine receptor CCR5 is the major coreceptor for R5 human immunodeficiency virus type-1 strains. We mapped the epitope specificities of 18 CCR5 monoclonal antibodies (mAbs) to identify domains of CCR5 required for chemokine binding, gp120 binding, and for inducing conformational changes in Env that lead to membrane fusion. We identified mAbs that bound to N-terminal epitopes, extracellular loop 2 (ECL2) epitopes, and multidomain (MD) epitopes composed of more than one single extracellular domain. N-terminal mAbs recognized specific residues that span the first 13 amino acids of CCR5, while nearly all ECL2 mAbs recognized residues Tyr-184 to Phe-189. In addition, all MD epitopes involved ECL2, including at least residues Lys-171 and Glu-172. We found that ECL2-specific mAbs were more efficient than NH2- or MD-antibodies in blocking RANTES or MIP-1beta binding. By contrast, N-terminal mAbs blocked gp120-CCR5 binding more effectively than ECL2 mAbs. Surprisingly, ECL2 mAbs were more potent inhibitors of viral infection than N-terminal mAbs. Thus, the ability to block virus infection did not correlate with the ability to block gp120 binding. Together, these results imply that chemokines and Env bind to distinct but overlapping sites in CCR5, and suggest that the N-terminal domain of CCR5 is more important for gp120 binding while the extracellular loops are more important for inducing conformational changes in Env that lead to membrane fusion and virus infection. Measurements of individual antibody affinities coupled with kinetic analysis of equilibrium binding states also suggested that there are multiple conformational states of CCR5. A previously described mAb, 2D7, was unique in its ability to effectively block both chemokine and Env binding as well as coreceptor activity. 2D7 bound to a unique antigenic determinant in the first half of ECL2 and recognized a far greater proportion of cell surface CCR5 molecules than the other mAbs examined. Thus, the epitope recognized by 2D7 may represent a particularly attractive target for CCR5 antagonists.