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Dysregulated eating among children and adolescents is associated with a wide range of negative mental and physical health outcomes, including obesity. However, less is known regarding underlying neural mechanisms underlying such behaviors. Therefore, the present manuscript systematically reviewed neuroimaging research examining dysregulated eating behavior linked to excess weight in children and adolescents. A systematic literature search identified 23 eligible studies, the majority of which were cross-sectional functional magnetic resonance imaging (fMRI) studies and excluded participants with psychiatric disorders. Dysregulated eating was captured by measures of eating styles and eating self-regulation, eating disorder behaviors, food addiction, objective measures of non-homeostatic eating and caloric restriction. While preliminary, findings suggested eating dysregulation was related to aberrant functioning within the frontostriatal and frontoparietal regions involved in self-regulatory processes, as well as regions involved in satiety signaling and interoception. This heterogeneous body of research is continually growing and may have potential to inform future prevention and intervention approaches. Results also identified several important limitations to consider and highlight key areas for future research.Neuroimaging techniques to measure the function of the human brain such as electroencephalography (EEG), positron emission tomography (PET), and functional magnetic resonance imaging (fMRI), are powerful tools for understanding the underlying neural circuitry associated with alcohol use disorder (AUD) and obesity. The sensory (visual, taste and smell) paradigms used in neuroimaging studies represent an ideal platform to investigate the connection between the different neural circuits subserving the reward/executive control systems in these disorders, which may offer a translational mechanism for novel intervention predictions. Thus, the current review provides an integrated summary of the recent neuroimaging studies that have applied cue-reactivity paradigms and neuromodulation strategies to explore underlying alterations in neural circuitry as well in treatment strategies in AUD and obesity. Finally, we discuss literature on mechanisms associated with increased alcohol sensitivity post-bariatric surgery (BS) which offers guidance for future research to use sensory percepts in elucidating the relation of reward signaling in AUD development post-BS.Alcohol and other psychoactive drugs are oftentimes implicated in legal cases. A pertinent question herein is whether such substances might adversely affect testimonies of victims, eyewitnesses, or suspects by propelling the formation of false memory and increasing susceptibility to suggestion. In the current review, we amassed all available evidence on the effects of intoxication on false memory formation and suggestibility, including the substances alcohol, benzodiazepines, cannabis, stimulants, hallucinogens, and antipsychotics. Our review indicated that alcohol and cannabis under certain conditions increased the susceptibility to false memories and/or suggestion with effect sizes ranging from medium to large. When intoxicated during an event, alcohol is most likely to increase this susceptibility at high intoxication levels or after a delay, whereas cannabis exerts detrimental effects during acute intoxication but not necessarily once sober. For other substances, ecologically valid research separating different memory phases is needed. Overall, differences between substances regarding false memory effects exist, suggesting that a nuanced approach is needed when dealing with intoxicated individuals in a legal context.Major depressive disorder (MDD) is the leading cause of disability worldwide. Neurofeedback training has been suggested as a potential additional treatment option for MDD patients not reaching remission from standard care (i.e., psychopharmacology and psychotherapy). Here we systematically reviewed neurofeedback studies employing electroencephalography, or functional magnetic resonance-based protocols in depressive patients. Of 585 initially screened studies, 24 were included in our final sample (N = 480 patients in experimental and N = 194 in the control groups completing the primary endpoint). We evaluated the clinical efficacy across studies and attempted to group studies according to the control condition categories currently used in the field that affect clinical outcomes in group comparisons. In most studies, MDD patients showed symptom improvement superior to the control group(s). However, most articles did not comply with the most stringent study quality and reporting practices. We conclude with recommendations on best practices for experimental designs and reporting standards for neurofeedback training.Our understanding of the neural basis of somatosensation is based largely on studies of the whisker system of mice and rats and the hands of macaque monkeys. this website Results across these animal models are often interpreted as providing direct insight into human somatosensation. Work on these systems has proceeded in parallel, capitalizing on the strengths of each model, but has rarely been considered as a whole. This lack of integration promotes a piecemeal understanding of somatosensation. Here, we examine the functions and morphologies of whiskers of mice and rats, the hands of macaque monkeys, and the somatosensory neuraxes of these three species. We then discuss how somatosensory information is encoded in their respective nervous systems, highlighting similarities and differences. We reflect on the limitations of these models of human somatosensation and consider key gaps in our understanding of the neural basis of somatosensation.Epidemiological studies show a strong association between exposure to air pollution - and particularly to particulate matter (PM) -, increased prevalence of Multiple Sclerosis (MS) and higher rates of hospital admissions for MS and MS relapses. Besides having immunomodulatory effects and sustaining a systemic oxidative-inflammatory response, PM may participate in MS pathogenesis by targeting also Central Nervous System (CNS)-specific processes, such as myelin repair. Here we show that, in a mouse model of lysolecithin-induced demyelination of the subcortical white matter, post-injury exposure to fine PM hampers remyelination, disturbs oligodendroglia differentiation dynamics and promotes astroglia and microglia reactivity. These findings support the view that exposure to fine PM can contribute to demyelinating pathologies by targeting the endogenous regenerative capability of the CNS tissue.