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ABSTRACT Importance Digital technology is now widely available for the interventions of autism, but its validity and feasibility remain to be proved. Objective This study aimed to investigate the effectiveness of digital health interventions (DHIs) in improving core symptoms or intelligence quotient in patients with autism spectrum disorder (ASD). Methods Three databases including PubMed, Cochrane, and Scopus, were searched on November 15, 2022. Randomized clinical trials that enrolled patients with ASD who received DHIs and a control group without DHI treatment were included. Cochrane risk of bias tool (RoB 2) was applied to assess the risk of bias. Results A total of 33 studies, involving 1285 participants (658 [51.2%] in DHI groups and 627 [48.8%] in control groups), were analyzed to investigate the differences between DHI groups and control groups. Significantly greater improvements in the overall performance of ASD were observed in the DHI groups compared to the control groups (including active, waitlist, treatment‐as‐usual, and no treatment) with an effect size of 1.89 (Cohen's d 95% confidence interval [CI]: 1.26–2.52). Studies with treatment‐as‐usual, waitlist, and no treatment control demonstrated large effect sizes of Cohen's d 3.41 (95% CI: 0.84–5.97), Cohen's d 4.27 (95% CI: 1.95–6.59), and Cohen's d 4.52 (95% CI: 2.98–6.06) respectively. In contrast, studies with active control revealed insignificant effect sizes (Cohen's d 0.73, 95% CI: 0.12–1.33). Interpretation This meta‐analysis found significantly greater improvements in core symptoms or intelligence quotient in ASD patients receiving DHIs compared to those in control conditions. ASD patients may benefit from the DHIs and reduce the economic burden.

The mechanism of learning and memory impairment induced by the combination of fluorine and aluminum (FA) is not fully understood. The results of our previous research demonstrated that miR-29b-3p is a differentially expressed miRNA in the hippocampi of rat offspring exposed to FA; this miRNA is related to learning and memory and apoptosis. Based on these findings, in vitro studies were designed to assess the role of miR-29b-3p in neuronal apoptosis caused by the coexistence of FA. In the present study, the viability of mouse neuroblastoma–rat glioma hybrid cell (NG108–15 cell) was analyzed using Cell Counting Kit-8 (CCK-8). Apoptosis was detected by a Novocyte Flow Cytometer. Relative mRNA and protein expression levels were evaluated by real-time fluorescence quantitative PCR (qRT-PCR) and Western blotting (WB), respectively. The results showed that FA aggravated NG108–15 cell apoptosis by inhibiting dual-specificity phosphatase-2 (Dusp2) via increased miR-29b-3p. Accordingly, a dual-luciferase reporter assay showed that miR-29b-3p modulated Dusp2 protein levels by targeting its 3′-untranslated region. These findings show, for the first time, that miR-29b-3p is involved in neuronal apoptosis triggered by FA by targeting Dusp2.