Autism spectrum disorder (ASD) is a neurodevelopmental condition characterized by a complex and multifaceted neurobehavioral syndrome. In the last decades, several studies highlighted an increased prevalence of sleep problems in ASD, which would be associated with autonomic system and circadian rhythm disruption. The present review aimed to summarize the available literature about sleep problems in ASD subjects and about the possible biological factors implicated in circadian rhythm and autonomic system deregulation in this population, as well as possible therapeutic approaches. Shared biological underpinnings between ASD symptoms and altered circadian rhythms/autonomic functions are also discussed. Studies on sleep showed how ASD subjects typically report more problems regarding insufficient sleep time, bedtime resistance and reduced sleep pressure. A link between sleep difficulties and irritability, deficits in social skills and behavioral problems was also highlighted. Among the mechanisms implicated, alteration in genes related to circadian rhythms, such as CLOCK genes, and in melatonin levels were reported. ASD subjects also showed altered hypothalamic pituitary adrenal (HPA) axis and autonomic functions, generally with a tendency towards hyperarousal and hyper sympathetic state. Intriguingly, some of these biological alterations in ASD individuals were not associated only with sleep problems but also with more autism-specific clusters of symptoms, such as communication impairment or repetitive behaviors Although among the available treatments melatonin showed promising results, pharmacological studies for sleep problems in ASD need to follow more standardized protocols to reach more repeatable and reliable results. Further research should investigate the issue of sleep problems in ASD in a broader perspective, taking into account shared pathophysiological mechanisms for core and associated symptoms of ASD.

Background The importance of recognizing different kinds of autism spectrum presentations among adults, including subthreshold forms and the broad autism phenotype (BAP), has been increasingly highlighted in recent studies. Meanwhile, the possible involvement of immune system deregulation and altered methylation/trans-sulfuration processes in autism spectrum disorder (ASD) is gaining growing attention, but studies in this field are mainly focused on children. In this framework, the aim of this study was to compare plasmatic concentrations of IL-6 and homocysteine (HCY) among adults with ASD, their first-degree relatives, and healthy controls (CTLs), investigating also possible correlations with specific autism symptoms. Methods Plasma concentrations of IL-6 and HCY were measured in a group of adult subjects with ASD, their first-degree relatives (BAP group), and healthy controls (CTL). All participants were also evaluated with psychometric instruments. Results IL-6 and HCY concentrations were significantly higher in the ASD group than in CTLs, while BAP subjects reported intermediate results. Significant correlations were reported between biochemical parameters and psychometric scales, particularly for the dimension of ruminative thinking. Conclusions These findings support the hypothesis of a key involvement of HCY-related metabolism and immune system alteration in autism spectrum pathophysiology. HCY and IL-6 seem to show different associations with specific autism dimensions.

Recently, vitamin D is considered a pleiotropic hormone, and as such, it has also become a topic of renewed interest in neuropsychiatry for its proposed role in the aetiology and pathophysiology of different psychiatric conditions, including mood disorders (MDs). This seems particularly crucial while considering the relatively high and often neglected prevalence of hypovitaminosis D in the general population and in specific groups, such as patients suffering from the most common type of MDs, which are major depression (MDD) and bipolar disorders (BDs). Therefore, in view of the controversial literature and findings on this topic and its potential therapeutic implications, the present study aimed at evaluating vitamin D levels in the plasma of a sample of inpatients fulfilling the DSM-5 criteria for mood episodes within BDs. The clinical picture was assessed by means of specific rating scales. The results showed that the vitamin D levels (mean ± SD, nM/L) of the bipolar patients of our sample were significantly lower (14.58 ± 11.27 nmol/L) than the normative values (>30 nmol/L). Eleven patients had sufficient values and only 4 had optimal, while 19 showed insufficient, 18 critical, and 17 severely critical levels. No differences emerged according to different socio-demographic or clinical features. In our opinion, the present findings strengthen previous research highlighting decreased vitamin D levels in bipolar patients and support the role of this pleiotropic hormone in BDs. Nevertheless, further studies should follow to corroborate the data of this preliminary study and to address the potential benefits of vitamin D supplementation in the treatment of MDs.

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Post-traumatic stress disorder (PTSD) is a psychopathological condition with a heterogeneous clinical picture that is complex and challenging to treat. Its multifaceted pathophysiology still remains an unresolved question and certainly contributes to this issue. The pharmacological treatment of PTSD is mainly empirical and centered on the serotonergic system. Since the therapeutic response to prescribed drugs targeting single symptoms is generally inconsistent, there is an urgent need for novel pathogenetic hypotheses, including different mediators and pathways. This paper was conceived as a narrative review with the aim of debating the current pharmacological treatment of PTSD and further highlighting prospective targets for future drugs. The authors accessed some of the main databases of scientific literature available and selected all the papers that fulfilled the purpose of the present work. The results showed that most of the current pharmacological treatments for PTSD are symptom-based and show only partial benefits; this largely reflects the limited knowledge of its neurobiology. Growing, albeit limited, data suggests that the hypothalamic-pituitary-adrenal axis, opioids, glutamate, cannabinoids, oxytocin, neuropeptide Y, and microRNA may play a role in the development of PTSD and could be targeted for novel treatments. Indeed, recent research indicates that examining different pathways might result in the development of novel and more efficient drugs.