Among the difficulties associated with Autism Spectrum Disorder (ASD) are those related to adaptation to changes and new situations, as well as anxious-depressive symptoms frequently related to excessive environmental requirements. The main objective of this research is to study the psychological impact of the lockdown due to the social emergency situation (COVID-19) in children/adolescents and adults diagnosed with ASD. Participants were 37 caregivers of children/adolescents with ASD, also 35 ASD adults and 32 informants. Evaluation was conducted through a web survey system and included standardized clinical questionnaires (CBCL and SCL-90-R), which were compared with results before lockdown start, and a brief self-reported survey addressing the subjective perception of changes in daily functioning areas. The results revealed a reduction of psychopathological symptoms in both age groups, but only reaching statistical significance in the adult group, except for Somatization, Anxiety, and Obsessive-Compulsive domains. ASD severity Level 2 showed greater improvement after lockdown onset in the children/adolescent group when compared to ASD Level 1 participants. Younger adults (18-25 yoa) reported greater improvement than older adults (=>25 yoa). Survey results indicate an improvement of feeding quality and a reduction in the number of social initiations during the lockdown. Adult ASD participants perceived a decrease in stress levels after the lockdown onset, whereas caregivers reported higher stress levels at the same point in both age groups. Limitations included the small number of participants and a heterogeneous evaluation window between measures. Pyschopathological status after two months of social distancing and lockdown seems to improve in ASD young adult population.

Low-grade inflammation plays a role not only in the pathogenesis of major depressive disorder (MDD) but probably also in the poor responsiveness to regular antidepressants. There are also indications that anti-inflammatory agents improve the outcomes of antidepressants. Aim: To study whether the presence of low-grade inflammation predicts the outcome of antidepressants, anti-inflammatory agents, or combinations thereof. Methods: We carried out a systematic review of the literature on the prediction capability of the serum levels of inflammatory compounds and/or the inflammatory state of circulating leukocytes for the outcome of antidepressant/anti-inflammatory treatment in MDD. We compared outcomes of the review with original data (collected in two limited trials carried out in the EU project MOODINFLAME) on the prediction capability of the inflammatory state of monocytes (as measured by inflammatory gene expression) for the outcome of venlafaxine, imipramine, or sertraline treatment, the latter with and without celecoxib added. Results: Collectively, the literature and original data showed that: 1) raised serum levels of pro-inflammatory compounds (in particular of CRP/IL-6) characterize an inflammatory form of MDD with poor responsiveness to predominately serotonergic agents, but a better responsiveness to antidepressant regimens with a) (add-on) noradrenergic, dopaminergic, or glutamatergic action or b) (add-on) anti-inflammatory agents such as infliximab, minocycline, or eicosapentaenoic acid, showing—next to anti-inflammatory—dopaminergic or lipid corrective action; 2) these successful anti-inflammatory (add-on) agents, when used in patients with low serum levels of CRP/IL-6, decreased response rates in comparison to placebo. Add-on aspirin, in contrast, improved responsiveness in such “non-inflammatory” patients; 3) patients with increased inflammatory gene expression in circulating leukocytes had a poor responsiveness to serotonergic/noradrenergic agents. Conclusions: The presence of inflammation in patients with MDD heralds a poor outcome of first-line antidepressant therapies. Immediate step-ups to dopaminergic or glutamatergic regimens or to (add-on) anti-inflammatory agents are most likely indicated. However, at present, insufficient data exist to design protocols with reliable inflammation parameter cutoff points to guide such therapies, the more since detrimental outcomes are possible of anti-inflammatory agents in “non-inflamed” patients.