Delivering in‐school interventions to improve dietary behaviours amongst 11‐ to 16‐year‐olds: A systematic review

Childhood obesity is a global health concern, which has both short‐and long‐term health consequences for the individual, and is a potential burden on health care services and the wider economy. The school environment is a setting where changes can be applied to dietary behaviours, as schools have direct and intensive contact with children. This systematic review evaluated school‐based interventions designed to improve dietary behaviours among adolescents (11‐to 16‐year‐olds). The aims were to review types of interventions delivered, dietary behaviours targeted, and interventions' effectiveness in improving dietary behaviour and associated intervention components. Twenty‐nine school‐based interventional studies with this population were identified for review. The data were synthesized by identifying and comparing individual studies' results, intervention components, and characteristics.Interventions appeared more effective when they involved peers, used educational media to deliver health messages, increased availability of healthy foods in school,and incorporated computer‐based individualized feedback with normative information on eating behaviours. A limitation of the review was the lack of description in cer-tain reviewed studies and the nonfeasibility of conducting a meta‐analysis owing to study heterogeneity. Future interventions with this population could consider including the aforementioned components, gender‐specific feedback, and both short‐and long‐term follow‐ups as change may not be apparent immediately and to determine if changes are sustained

Space and time in visual context

No sensory stimulus is an island unto itself; rather, it can only properly be interpreted in light of the stimuli that surround it in space and time. This can result in entertaining illusions and puzzling results in psychological and neurophysiological experiments. We concentrate on perhaps the best studied test case, namely orientation or tilt, which gives rise to the notorious tilt illusion and the adaptation tilt after-effect. We review the empirical literature and discuss the computational and statistical ideas that are battling to explain these conundrums, and thereby gain favour as more general accounts of cortical processing

Mitochondria at the neuronal presynapse in health and disease

Synapses enable neurons to communicate with each other and are therefore a prerequisite for normal brain function. Presynaptically, this communication requires energy and generates large fluctuations in calcium concentrations. Mitochondria are optimized for supplying energy and buffering calcium, and they are actively recruited to presynapses. However, not all presynapses contain mitochondria; thus, how might synapses with and without mitochondria differ? Mitochondria are also increasingly recognized to serve additional functions at the presynapse. Here, we discuss the importance of presynaptic mitochondria in maintaining neuronal homeostasis and how dysfunctional presynaptic mitochondria might contribute to the development of disease

mTOR signaling in proteostasis and its relevance to autism spectrum disorders

Proteins are extremely labile cellular components, especially at physiological temperatures. The appropriate regulation of protein levels, or proteostasis, is essential for all cells. In the case of highly polarized cells like neurons, proteostasis is also crucial at synapses, where quick confined changes in protein composition occur to support synaptic activity and plasticity. The accurate regulation of those cellular processes controlling protein synthesis and degradation is necessary for proteostasis, and its deregulation has deleterious consequences in brain function. Alterations in those cellular mechanisms supporting synaptic protein homeostasis have been pinpointed in autism spectrum disorders such as tuberous sclerosis, neurofibromatosis 1, PTEN-related disorders, fragile X syndrome, MECP2 disorders and Angelman syndrome. Proteostasis alterations in these disorders share the alterations in mechanistic/mammalian target of rapamycin (mTOR) signaling pathway, an intracellular pathway with key synaptic roles. The aim of the present review is to describe the recent literature on the major cellular mechanisms involved in proteostasis regulation in the synaptic context, and its association with mTOR signaling deregulations in various autism spectrum disorders. Altogether, the cellular and molecular mechanisms in synaptic proteostasis could be the foundation for novel shared therapeutic strategies that would take advantage of targeting common disorder mechanisms.This review was supported by grant BFU2015-68568-P (MINECO/FEDER, EU) to AO